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Parental care is regulated by multiple endocrine mechanisms. Among these hormones, prolactin (PRL) is involved in the expression of parental behaviors. Despite the consensus that PRL mediates variation in parental effort with age and body condition, its role in the adjustment of parental effort to fluctuating environmental conditions, including changing predation pressure, still awaits further investigation. To shed light on this knowledge gap, we relied on a long-term monitoring of female common eiders Somateria mollissima (n = 1277 breeding attempts, 2012-2022) incubating under fluctuating predation risk to investigate the link between baseline PRL levels and female minimum age, body condition, clutch size, environmental parameters (predation pressure, climate, nest microhabitat) and hatching success. We predicted that PRL would be higher in older females, those in better condition or incubating larger clutches. We also predicted that females would reduce parental effort when nesting under challenging environmental conditions (high predation pressure or poor climatic conditions), translated into reduced baseline PRL levels. We also explored how variation in PRL levels, female characteristics and environmental parameters were related to hatching success. Following our predictions, PRL levels were positively associated with body condition and female age (before showing a senescent decline in the oldest breeders). However, we did not observe any population-level or individual-level reduction in PRL levels in response to increasing predation pressure. Population-level baseline PRL levels instead increased over the study period, coincident with rising predation threat, but also increasing female body condition and age. While we did not provide evidence for a direct association between baseline PRL levels and predation risk, our results support the idea that elevated baseline PRL levels promote hatching success under internal constraints (in young, inexperienced, breeders or those incubating a large clutch) or constraining environmental conditions (during years of high predation pressure or poor climatic and foraging conditions). Finally, the low repeatability of baseline PRL levels and high interannual variability highlight considerable within-individual flexibility in baseline PRL levels. Further research should explore flexibility in parental effort to changing environmental conditions, focusing on both baseline and stress-induced PRL levels., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

To maximize fitness, parents may trade-off time and energy between parental care and self-maintenance. In vertebrates, prolactin and corticosterone are two important hormones that regulate parental investment because they stimulate parental care and mobilize energy, respectively. Further, concentrations of both hormones change in response to disturbances. One of the most important parental care behaviors in birds is incubation, since small changes in egg temperature have large effects on offspring. We investigated how prolactin and corticosterone may mediate parental incubation constancy (i.e., the daily amount of time spent incubating eggs) and regulation of egg temperature. We collected blood samples from female wood ducks (Aix sponsa) near the start and end of the incubation period to measure baseline and stress-induced (30 min after capture and restraint) hormone concentrations. We also quantified incubation constancy and egg temperature using artificial egg temperature loggers. As expected, prolactin decreased and corticosterone increased after 30 min of capture and restraint. Corticosterone concentrations (baseline and stress-induced) were negatively related to body mass, but were not related to incubation constancy. In contrast, prolactin concentrations (baseline and stress-induced) were higher at the end than the start of the incubation period, and stress-induced prolactin concentrations were positively related to incubation constancy following a nest disturbance (i.e., capture). Further, prolactin (baseline and stress-induced) concentrations were positively related to egg temperatures, but only after the disturbance. These results suggest that prolactin may be associated with the regulation of parental incubation constancy and resulting heat-transfer after a disturbance, which may ultimately affect offspring development., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Nest shelter in incubating birds is of major importance in providing protection against unfavourable conditions such as harshness of the environment and exposure to predators. We examined the link between nest shelter, baseline corticosterone (CORT) levels and hatching success in common eiders (Somateria mollissima) incubating at nest sites with different levels of shelter. Since more sheltered nest sites could be occupied by better-quality females, we also used an experimental manipulation of nest shelter to separate the effects of the physical attributes of the nest site from those of individual quality. We compared birds with naturally sheltered nests, exposed nests and exposed nests provided with artificial nest shelters and measured clutch size, body condition, CORT levels at the end of incubation and hatching success. If nest shelter reduces CORT levels, we predicted that CORT levels would be highest at the least sheltered sites, and that the provision of artificial shelter would reduce CORT levels. We found that nest shelter was not related to CORT levels in incubating eiders. Nest shelter, however, affected body condition, with females at exposed sites losing more body mass during incubation than females at naturally and artificially sheltered nests. Interestingly however, in those birds nesting at the exposed sites, with and without artificial shelter, those with the highest CORT levels had the lowest hatching success. This relationship was not evident in females nesting at naturally sheltered sites. These results suggest that the level of nest shelter does not directly affect CORT levels in females. Instead, we suggest that the relationship between CORT levels and hatching success is state-dependent. Exposed sites are occupied by individuals that laid smaller clutches, and hence are likely to be of lower quality, and the negative effects of elevated CORT on hatching success are more pronounced in these females., (Published by Elsevier Inc.)

Melatonin (MT) inhibits salt gland secretion of Pekin ducks [Ching, A.C.T., Hughes, M.R., Poon, A.M.S., Pang, S.F., 1999. Melatonin receptors and melatonin inhibition of duck salt gland secretion. Gen. Comp. Endocrinol. 116, 229-240]. The present study examined simultaneous diurnal changes in plasma concentrations of MT and four osmoregulatory hormones of Pekin ducks to assess the possible interactions among these hormones that might contribute to inhibition of extrarenal salt secretion. The study compared diurnal changes in freshwater (FW) and saline-acclimated (SA) male and female ducks. We hypothesized plasma concentrations of osmoregulatory hormones: (1) differ between sexes (partially accepted); (2) vary diurnally (accepted, influenced by sex and treatment); (3) are correlated with MT (partially accepted); and their diurnal variation is affected by (4) sex (partially accepted); and (5) saline acclimation (partially accepted). We compared body mass, plasma osmolality (Osm(pl)), plasma volume, concentrations of plasma ions, and arginine vasotocin (AVT), angiotensin II (AII), prolactin, (PRL), and aldosterone (ALDO), in relation to plasma melatonin (MT). At night body mass increased in FW ducks and decreased in SA ducks. This likely reflects the higher plasma PRL concentration of female ducks and its middark increase only in SA ducks. Plasma volume increased at night in all but FW males. Plasma sodium and osmolality were higher in SA ducks and did not vary diurnally in either FW or SA ducks. Midday MT did not differ between males and females or between FW and SA ducks; at middark, all ducks, except FW females, increased MT. Midday AVT was higher in SA ducks. Only FW ducks increased AVT at middark. Changes in AVT and MT were positively correlated in males and negatively correlated in females. Males had higher AII and, at night, AII increased in SA ducks and decreased in FW ducks. AVT and AII were negatively correlated. ALDO was highly correlated with AII and unaffected by sex, saline, or time. At night, only AVT was elevated in FW ducks, while MT, AII, and PRL were elevated in SA ducks. FW and SA ducks appear to follow different, but equally effective, hormonal strategies to maintain osmotic homeostasis at night. We conclude that the effect of MT on salt gland secretion is probably a direct effect. These may be influenced by gender.

This paper describes some aspects of the pituitary gland, gonads, and secondary sex characters of unusual pintails, Anas acuta, found in the wild. They were demonstrated to be females with partially masculinized plumage; i.e., their plumage showed various degrees of intersex, but the genital organs, syrinx, and electrophoretic pattern of sex-specific DNA were of the female type. Their left ovary underwent a marked involution and was associated with the mesonephros (the Wolffian body), as was the degenerated right ovary. Neither testicular tissue nor ovotestis was found in the gonad of either side. The oviduct was anatomically normal and comparable to that of the control adult. The plasma concentration of estradiol-17beta (E2) was shown to be 5.7+/-0.5 (mean+/-SE)pg/ml in the masculinized birds, 7.0+/-0.7 pg/ml in control males, and 22.5+/-6.1 pg/ml in control females, whereas plasma testosterone (T) was below the detection level in all of the samples. As to the pituitary gland, hypertrophy and/or deformity of the pars distalis was evident in the majority of the masculinized birds. Among others, hyperactive gonadotrophs, mainly luteinizing hormone (LH)- and LH/follicle-stimulating hormone (FSH)-immunoreactive cells, were prominent in the entire gland; and typical signet ring cells (castration cells) or giant gonadotrophs were frequently observed. These changes in the gonadotrophs may have been caused by a feedback response to the physiologically ovariectomized condition in the masculinized birds. Causal factor(s) of the ovarian degeneration remain to be further investigated.

In the common eider only the females incubate while they fast for 25 days. Thus, since they rely entirely on their body reserves for successful incubation, they can be defined as capital incubators. To assess the potential effects of their initial body mass, the incubation duration, and depletion in body reserves on prolactinemia, blood samples of eiders were analyzed during the breeding cycle and an experimental manipulation of the duration of incubation. Levels of circulating prolactin increased at the onset of incubation and then reached a high and stable level during incubation before increasing sharply before hatching. The prolactin level decreased significantly upon hatching. Captive females deprived from their eggs exhibited a rapid decrease in prolactinemia, suggesting that egg stimuli are necessary to prolactin secretion. Aunts, i.e., helper females caring for conspecific young, presented prolactin levels higher than nonbreeding captive females but not significantly different from those of females at hatching. Plasma prolactin at hatch was directly related to body mass loss. Birds with shortened incubation have higher body masses and showed higher levels of prolactinemia at hatching than the control group, in accordance with the idea that circulant prolactin at hatching is linked to body condition. Females which underwent an extended incubation (and started to eat again) displayed a low body mass and a high prolactinemia. These data therefore suggest that refeeding, albeit increasing the risk of predation, enhances prolactin secretion and allows the bird to continue incubation despite that it has reached a poor body condition., ((C)2002 Elsevier Science (USA).)

Most of the NaCl ingested by marine birds is reabsorbed from renal filtrate and excreted by the cephalic salt glands as a hypertonic NaCl secretion (SGS). Ducks have salt glands and their kidney cells have melatonin receptors. Melatonin affects glomerular filtration rate and tubular uptake of sodium (Na(+)) in mammals. We hypothesized that (1) duck salt glands also have melatonin receptors and (2) melatonin affects extrarenal Na(+) secretion. Both hypotheses were accepted because putative melatonin receptors were identified by 2¿(125)Iĭodomelatonin binding in salt glands of Pekin ducks, Anas platyrhynchos, and because melatonin inhibited SGS in these ducks. Saline ingestion increased B(max), but not K(d), of salt gland receptors. The duration of NaCl infusion needed to stimulate SGS was positively related with preinfusion plasma melatonin concentration (¿mel(pl)). Raising ¿mel(pl) prior to NaCl infusion further delayed onset of secretion and decreased secretion rate and concentration without affecting plasma volume and Na(+) concentration. Abrupt increase in ¿mel(pl) during SGS immediately decreased the rate by 43%. Secretion rate remained lower than the control rate during the subsequent hour; secretion concentration was not affected. This is the first report of putative melatonin binding sites in avian salt glands. Melatonin slowed the onset of NaCl-induced salt gland secretion and decreased its rate., (Copyright 1999 Academic Press.)

Plasma catecholamines have been measured in chronically adrenalectomized (ADX) ducks, in chronically adrenal-denervated ducks (DNX), and in their respective shamoperated controls (SH-adx, SH-dnx) after 3 min forced submergence. The results showed that 100% of the plasma epinephrine (EP) and 70 to 80% of plasma norepinephrine (NE) released during the dive came from the adrenal glands. Only 20 to 30% of plasma NE came from the endings of the autonomic vascular sympathetic nerves which are strongly stimulated during diving. Adrenal catecholamines were released by nerve activation only; nonneural mechanisms did not play any role in their release. The action of adrenal catecholamines on the cardiovascular system during dives was investigated by measuring heart rate and arterial blood pressure in operated and sham-operated ducks. Cardiovascular adjustments, associated with 3 min of forced diving, were not affected by any differences in the levels of plasma catecholamines.

The plasma concentrations of prolactin were measured by radioimmunoassay throughout the breeding cycle in female domestic ducks. Prolactin levels increased significantly during egg laying from 5 to 15 ng/ml and again at the start of incubation to about 28 ng/ml. Prolactin levels remained consistently high throughout incubation and fell sharply around the time the eggs hatched. Local anaesthesia of the incubation patches of incubating females for 9 hr caused a significant decrease in plasma prolactin. It is suggested that tactile stimulation from the eggs in the nest may cause the rise in prolactin during the egg laying period and also maintain prolactin secretion during incubation.

In immature ducklings injected with hypertonic saline the volume of extrarenal salt gland secretion was unaffected by prior treatment (immediately or 4 hr before salt loading) with long-lasting adrenocorticotrophin (ACTH 100 iu/kg, im) or exogenous corticosterone (1.0 mg/kg, im). Pretreatment with metyrapone, an 11-beta-hydroxylase blocker, (80 mg/kg, im) 4 hr before salt loading did not effect the volume of salt gland secretion but delayed the onset of extrarenal excretion. Salt gland function was suppressed in birds pretreated with metyrapone immediately prior to salt loading. The intravenous administration of metyrapone after salt loading immediately reduced salt gland activity, which remained suppressed for at least 40-50 min thereafter. The inhibitory effect of metyrapone on salt gland activity was not counteracted by the subsequent or simultaneous administration of exogenous corticosterone to salt-loaded ducks. These results suggest that acute alterations in adrenocortical activity are not causally responsible for changes in salt gland function.

The 30-min infusion of somatostatin (SRIF)-14 or SRIF-28 (800 ng/kg/min) in 7- to 8-week-old ducklings reduced the basal level of plasma growth hormone (GH). The magnitude of the GH suppression induced by SRIF-14 was similar to that elicited by SRIF-28. "Rebound" GH secretion was observed 30 min after infusion, the GH concentration being elevated above the basal level. The increase in GH secretion after SRIF-14 infusion was greater than that induced by SRIF-28. Plasma insulin and free fatty acid (FFA) levels were similarly reduced after 10 and 30 min of SRIF-14 or SRIF-28 infusion. Following infusion the FFA levels returned to the pretreatment concentration, whereas the insulin concentration in both groups remained suppressed 30 min after infusion. The insulin level was still suppressed 60 min after SRIF-14 infusion, but not after SRIF-28 infusion. The infusion of SRIF-14 resulted in a marked, progressive increase in the glucagon concentration, which was reduced in birds infused with SRIF-28 and accompanied by hypoglycaemia. Following SRIF-28 infusion a "rebound" in the glucagon concentration occurred and remained elevated for at least 60 min. These results demonstrate comparative effects of SRIF-14 and SRIF-28 on the basal release of pituitary GH and pancreatic insulin and glucagon, and in particular they suggest that SRIF-28 is more potent in inhibiting pancreatic A cell activity.

Temporal changes in the levels of serum luteinizing hormone (LH), prolactin, estradiol, and progesterone associated with the reproductive patterns of 53 wild captive canvasback ducks were measured. The reproductive endocrinology of both laying and nonlaying females was compared in this 3-year study. Females that remained sexually inactive had ovaries with small, undeveloped follicles. Nonlaying ducks also had lower serum levels of LH (P less than 0.01), prolactin (P less than 0.05), estradiol, and progesterone than those of laying ducks in mid-April (during prelay), mid-May (on the fourth day of egg production), and mid-June (during postlay and incubation). Prolactin levels of both layers and nonlayers increased over this time interval (P less than 0.01) but levels of nonlayers were significantly lower than those of layers for the three blood-sampling dates. The low prolactin levels demonstrate that reproductive failure was not a result of inhibition by high serum prolactin levels. Intravenous injections of luteinizing hormone-releasing hormone (LHRH) in female canvasbacks resulted in significantly elevated (P less than 0.01) serum LH on the prelay blood sampling date. Lack of reproduction in nonbreeding canvasbacks was thus associated with low circulating serum LH levels but with LHRH-sensitive pituitary pools. These data suggest that lack of reproduction was a result of the failure of the hypothalamus to release releasing factors. The serum hormones of laying canvasbacks varied temporally with stages of the nesting cycle. LH levels increased prior to egg laying and fluctuated during the laying period. LH levels decreased at the onset of incubation but increased after loss of clutch, with renesting activity. Serum prolactin levels of layers were low prior to egg laying and increased gradually through laying of the first clutch, the renesting period, and laying of the second clutch. The highest prolactin levels occurred in ducks incubating their eggs. Prolactin levels decreased in ducks that failed to incubate their eggs. Serum estradiol levels increased sharply between 2 and 5 weeks prior to egg laying and remained high until the second day of egg production. Estradiol levels decreased when the fourth egg was produced, and remained low through the laying of the first clutch, the renesting period, and laying of the second clutch. Progesterone fluctuated widely through the nesting cycle, showing several major peaks before laying and another during incubation.

Asp1,Val5-angiotensin II (AII) caused dose-dependent increases in aortic blood pressure (BP) when injected into anesthetized Pekin ducks. Norepinephrine (NE) and epinephrine (E) concentrations in arterial plasma were found to be elevated 1 min after injection of AII, when BP was peaking, while plasma levels of unconjugated dopamine (DA) did not undergo any consistent change. Pretreatment with 6-hydroxydopamine (6-OHDA) rendered ducks supersensitive to the pressor effect of injections of NE, but did not affect adrenal chromaffin cell granulation, plasma NE and E concentrations, or pressor responses to tyramine and AII. Depletion of endogenous NE and E stores, following treatment with reserpine, did not affect pressor responses to NE, but diminished pressor responses to tyramine and AII. The discrepancies in the responses of 6-OHDA-treated ducks and reserpinized ducks to exogenous NE and AII indicate different pressor mechanisms for the two hormones. It is suggested that mobilization of endogenous NE and E contributes to the rise in BP observed following AII injection.

The habituation of the corticosterone response of ducks to treadmill exercise (1.1 km/hr 0 degrees incline for 60 min) has been determined over a 28-day period. In untrained birds 30 min of treadmill exercise resulted in a marked (P less than 0.001) increase in the basal plasma corticosterone level. After 60 min of exercise the corticosterone concentration remained elevated (P less than 0.001) in comparison with basal and control (nonexercised) levels but was less (P less than 0.01) than that at 30 min. Following exercise the concentration declined to basal levels within 60 min. After 7 days of daily training the peak (30 min) corticosterone response to exercise diminished by greater than 50% and was absent in birds trained for 21 days. This habituation of the corticosterone response may be due to adrenocortical stimulation by pituitary adrenocorticotrophin (ACTH) being reduced. As the stimulatory effect of ACTH administration (8 IU/kg) on corticosterone secretion does not habituate in birds treated daily (for 28 days), the reduced corticosterone response to exercise may be due to decreased ACTH release rather than to a reduction in adrenal ACTH sensitivity.

Fresh water-reared Aylesbury ducklings were given 0.1 or 0.2 M NaCl drinking water and variations in the plasma concentrations of thyroxine (T4), triiodothyronine (T3), corticosterone, and aldosterone were determined. Within 24 hr of being transferred to 0.2 M NaCl the corticosterone concentration was increased, whereas the levels of plasma T3 and aldosterone were reduced. The increase in corticosterone secretion persisted for at least 7 days, but the T3 and aldosterone concentrations had returned to control levels within 5 days. The concentrations of plasma aldosterone and T3 were similarly affected in birds transferred to 0.1 M NaCl, although corticosterone levels increased only after the birds were maintained on 0.1 M NaCl for 7 days. Plasma concentrations of T4 were increased in 1- to 2-week-old (but not 7-week-old) birds 7 days after their transfer to 0.1 and 0.2 M NaCl. In birds maintained on saline for 6 weeks the basal concentration of each hormone was not significantly different from that in fresh water-reared controls. When saline-reared birds were returned to freshwater conditions the plasma aldosterone and T3 concentrations were increased over a 5-day period. Transfer to saline consistently reduced body weight and food intake, whereas the transfer of saline-reared birds to fresh water stimulated body weight gain. Consequently, although these endocrine responses during saltwater adaptation might be expected to minimise the loss of body reserves and to facilitate the extra renal excretion of sodium, these alterations in endocrine function may be partly due to salt water-induced changes in food intake.

Endocrine profiles of wild mallards (Anas platyrhynchos) and canvasbacks (Aythya valisineria) were determined during the spring and the summer. Males and females of each species were treated with a single intravenous injection of 12 micrograms of synthetic luteinizing hormone-releasing hormone (LHRH). Preinjection and postinjection blood samples were collected and LH levels were determined by radioimmunoassay. LHRH evoked a brisk and significant elevation in serum LH in all ducks indicating the pituitary glands of both species contain readily releasable pools of LH. In March, the preinjection baseline levels of LH in the two groups did not differ. However, mallards responded to LHRH with a twofold increase in serum LH, while canvasbacks responded with a fourfold increase (F = 17.1, P less than 0.001). At the summer blood sampling period, mallards had significantly higher circulating levels of serum LH than canvasbacks (F = 35.9, P less than 0.001). Both species responded to LHRH with a twofold increase in circulating LH. These data indicate that seasonal variations in reproduction shown by the two species in captivity may be associated with differences in LHRH-sensitive pools of LH.

Immature chickens and ducks were maintained on synthetic diets containing normal (0.4%), low (0.018%), or high (1.9%) sodium for 8 days, with freshwater available ad libitum. Food intake was similar in both species regardless of the diet but weight gain was depressed in birds fed the low-sodium diet. In both species the circulating aldosterone concentration was increased within 24 hr of dietary sodium depletion, although maximal levels were not attained until after 5 days. The magnitude of adrenocorticotrophin (ACTH)-induced aldosterone secretion was also increased in sodium-deprived chickens and ducks. The basal aldosterone level was slightly suppressed by excess dietary sodium, which blunted the aldosterone response to exogenous ACTH. The transfer of chickens and ducks from low- to high-sodium regimes reduced the aldosterone levels (within 24 hr) to those in their respective controls. The transfer of birds from high- to low-sodium diets resulted in a prompt increase in the aldosterone concentration, although of reduced magnitude when compared with control birds transferred to low sodium. In both species alterations in the dietary sodium content had no effect on basal or ACTH-induced corticosterone secretion. The plasma prolactin levels in chickens were also unrelated to their sodium status. These results suggest that homeostatic adaptations in electrolyte balance during sodium depletion or excess are principally mediated by alterations in aldosterone secretion.

Serum levels of prolactin were determined in nonbreeding male and female canvasbacks (Aythya valisineria) from mid-April to late June to evaluate the temporal changes occurring during spring. During this time interval, serum prolactin levels increased 1.5- to 2-fold in both males and nonlaying females (P less than 0.01). Serum prolactin levels of males and females exposed to natural lighting and temperature at Delta, Manitoba (50 degrees 11'N, 98 degrees 19'W), steadily increased from mid-April when the daylength was 14 hr light and peaked in mid-June when daylength was 16.25 hr light. Administration of exogenous estradiol via slow-release subdermally implanted capsules in females with intact reproductive systems had a marginal effect on reducing the seasonal increase in prolactin. Exogenous testosterone in similar slow-release capsules implanted subdermally in males had no influence on circulating prolactin levels.

Adrenergic mechanisms for the pressor actions of blood-borne L-norepinephrine (NE) and fowl angiotensin II (ANG II) were studied in barbiturate-anesthetized adult ducks (Anas platyrhynchos). NE (1.5-6.0 nmol X kg-1) or ANG II (0.4-1.6 nmol X kg-1) injected iv caused dose-dependent increases in mean arterial pressure (Pa) and pulse pressure (Pp) but slowed cardiac frequency (fH); higher doses of ANG II increased Pa, Pp, and fH X beta-Adrenergic blockade by propranolol lowered baseline Pa, completely blocked cardiovascular responses to isoproterenol, augmented the bradycardic effect of NE, and inhibited the stimulation of Pp by ANG II. However, the tachycardiac effect of high-dose ANG II persisted during beta-blockade. alpha-Adrenergic blockade following iv prazosin completely blocked the pressor effect of methoxamine, diminished the pressure response to NE, and decreased Pa sensitivity to ANG II injections. Combined alpha- and beta-adrenergic blockade decreased both the sensitivity and the maximal Pa response to ANG II. We conclude that (i) beta-adrenergic mechanisms predominate in the maintenance of resting Pa, (ii) NE increases Pa principally by alpha-adrenergic action while beta-adrenergic stimulation buffers the consequent bradycardia, and (iii) although the positive chronotropic effect of high doses of ANG II probably is not mediated by catecholamines, low doses of ANG II elevate Pa and Pp by alpha- and beta-adrenergic mechanisms.

The effects of [1-24]ACTH, [5-Val]angiotensin II, and potassium (K+) on the secretion of corticosterone and aldosterone by tissue slices from the subcapsular (SCZ) and inner (IZ) zones of the duck adrenal gland were determined using incubation and superfusion systems. Both methods demonstrated that the release of corticosterone and aldosterone from IZ and SCZ cells was dependent on the ACTH dose concentration. The IZ cells produced more corticosterone than the SCZ cells in response to stimulation with 1-1000 ng ACTH/ml. The dose response by aldosterone from the cells of the SCZ and the IZ were comparable, but the proportion of aldosterone per total amount of steroid released was greater by cells of the SCZ (11.3%), than by cells of the IZ (3.6%). Elevating the K+ concentration in the incubation medium from 4.0 to 6.5 and 11.2 mM did not directly stimulate corticosteroid release or potentiate the stimulatory effect of ACTH. Superfusion with 10(-12) to 10(-5) M AII stimulated the release of aldosterone from the SCZ cells but had no detectable effect on the IZ and failed to stimulate corticosterone release from either the SCZ or IZ cells. The results presented here demonstrate that in the bird stimulation for the release of corticosterone and aldosterone are different. Methodology for superfusion of adrenal tissue and for the direct radioimmunoassay of aldosterone and corticosterone in the superfusate are described.

Salt-adapted Pekin ducks were observed during a 2-week period following adrenalectomy so as to test the hypothesis that NaCl secretion by the nasal salt glands depends on adrenocortical steroids. Three days after adrenalectomy the total inputs of fluid and Na+ during a 90-min iv infusion of 1000 mOsm/kg NaCl were 77 and 80% respectively, of those in the sham-operated controls; 7 days after adrenalectomy they were 88 and 90%. Two weeks after adrenalectomy, cardiovascular function had deteriorated slightly and the total outputs of fluid and Na+ had fallen to 65 and 64%, respectively, of the control outputs. The onset of cardiovascular deterioration was delayed by feeding the ducks 0.9% NaCl drinking water ad libitum for 1 month before, and 2 weeks after, adrenalectomy. Adaptive hypertrophy of the nasal salt glands was not steroid-dependent since there was no measurable decrease in the weight of the glands during a 2-week period following adrenalectomy.

Though birds lack the pars intermedia of the hypophysis, their pituitary glands do secrete MSH. This hormone and ACTH are elaborated in special cells of the pars distalis called corticomelanotrops. The present study was designed to ascertain whether the release of MSH in aves is under either stimulatory or inhibitory hypothalamic control. Extracts of median eminence were injected in ducks and plasma MSH was observed to rise after the injections: on the other hand, when pituitaries were ectopically grafted, significant changes in the levels of circulating MSH were not detected. Twenty days after grafting, the transplants were extirpated and incubated in media containing median eminence extracts. The extracts stimulated the release of MSH not only from grafts but also from pieces of normotopic glands. The grafts showed cells which contained ACTH but not MSH; however, they contained small amounts of MSH, detectable by RIA. The administration of ergocryptine brought about the inhibition of MSH secretion in vivo, and it is suggested that this drug acted on hypothalamic structures rather than directly on the corticomelanotrops. On the basis of the preceding results, it is concluded for the first time that in ducks the release of MSH has stimulatory control from the hypothalamus, contrarily to that occurring in almost all the animals so far investigated.