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K+ plays a catalytic role in AHL Na+ reabsorption via Na+-K+-2Cl- cotransporter (NKCC2), recycling across luminal K+ channels, so that luminal K+ is not depleted. Based on models of the ascending Henle limb (AHL) epithelium, it has been hypothesized that NH4+ may also catalyze luminal Na+ uptake. This hypothesis requires that luminal NH4+ not be depleted, implying replenishment via either direct secretion of NH4+, or NH3 in parallel with a proton. In the present work, epithelial models of rat medullary and cortical AHL (Weinstein AM, Krahn TA. Am J Physiol Renal Physiol 298: F000-F000, 2009) are configured as tubules and examined in simulations of function in vitro and in vivo to assess the feasibility of a catalytic role for NH4+ in N+ reabsorption. Modulation of N+ transport is also examined by peritubular K+ concentration and by Bartter-type transport defects in NKCC2 (type 1), in luminal membrane K+ channels (type 2), and in peritubular Cl channels (type 3). It is found that a catalytic role for NH4+, which is significant in magnitude (relative to K+), is quantitatively realistic, in terms of uptake via NKCC2, and in terms of luminal membrane ammonia backflux. Simulation of a 90% NKCC2 defect is predicted to double distal N+ delivery; it is also predicted to increase distal acid delivery (principally as NH4+). With doubling of medullary K+, the model predicts a 30% increase in distal N+ delivery, but in this case there is a decrease in AHL acidification. This effect of peritubular on proton secretion appears to be akin to type 3 Bartter's pathophysiology, in which there is decreased peritubular HCO3- exit, cytosolic alkalinization, and a consequent decrease in luminal proton secretion by NHE3. One consequence of overlapping and redundant roles for K+ and NH4+, is a blunted impact of luminal membrane K+ permeability on overall N+ reabsorption, so that type 2 Bartter pathophysiology is not well captured by the model. [ABSTRACT FROM AUTHOR]

Renal dopamine and nitric oxide contribute to natriuresis during high-salt intake which maintains sodium and blood pressure homeostasis. We wanted to determine whether concurrent inhibition of these natriuretic factors increases blood pressure during high-sodium intake. Male Sprague-Dawley rats were divided into the following groups: 1) vehicle (V)-tap water, 2) NaCl-l% NaCI drinking water, 3)30 mM L-buthionine sulfoximine (BSO), an oxidant, 4) BSO plus NaCI, and 5) BSO plus NaCl with 1 mM tempol (antioxidant). Compared with V, NaCI intake for 10 days doubled sodium intake and increased urinary dopamine level but reduced urinary nitric oxide content. NaCI intake also reduced basal renal proximal tubular NaK-ATPase activity with no effect on blood pressure. However, NaCI intake in BSO-treated rats failed to reduce basal Na-K-ATPase activity despite higher urinary dopamine levels. Also, dopamine failed to inhibit proximal tubular Na-K-ATPase activity and these rats exhibited reduced urinary nitric oxide levels and high blood pressure. Tempol supplementation in NaCl plus BSO-treated rats reduced blood pressure. BSO treatment alone did not affect the urinary nitric oxide and dopamine levels or blood pressure. However, dopamine failed to inhibit proximal tubular Na-K-ATPase activity in BSO-treated rats. BSO treatment also increased basal protein kinase C activity, Dl receptor serine phosphorylation, and oxidative markers like malondialdehyde and 8-isoprostane. We suggest that NaCI-mediated reduction in nitric oxide does not increase blood pressure due to activation of Dl receptor signaling. Conversely, oxidative stress-provoked inhibition of Dl receptor signaling fails to elevate blood pressure due to presence of normal nitric oxide. However, simultaneously decreasing nitric oxide levels with NaCI and inhibiting Dl receptor signaling with BSO elevated blood pressure. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO), a neurotransmitter in the lower urinary tract, stimulates soluble guanylyl cyclase (sGC) and in turn cGMP-dependent protein kinase G (PKG) to modulate a number of downstream targets. NO donors reduce bladder hyperactivity in some pathological models but do not affect normal bladder activity in the adult rat. In this study, the NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP; 100 μM) decreased the amplitude and frequency of spontaneous and carbachol-enhanced contractions in neonatal rat bladder strips, which are intrinsically hyperactive. This effect was blocked by inhibition of sOC and mimicked by application of a membrane-permeable cGMP analog (8-bromo-cGMP, 100 μM). Inhibition of PKG prevented or reversed the inhibitory effects of 8-bromo-cGMP. A portion of the SNAP-mediated inhibition was also dependent upon PKG; however, a short-lasting, sGC-dependent inhibitory effect of SNAP was still present after PKG inhibition. Inhibition of NO synthase with L-NAME (100 μM) did not change the amplitude or frequency of contractions. However, inhibition of endogenous phosphodiesterase (PDE)-5 with zapnnast (25 μM) reduced the amplitude and frequency of phasic contractions and increased the magnitude of inhibition produced by maximal concentrations of SNAP, suggesting that endogenous PDEs are constitutively active and regulate cGMP production. These results suggest that the NO-cGMP-PKG pathway may be involved in inhibitory control of the neonatal rat bladder. [ABSTRACT FROM AUTHOR]

Effects of aldosterone receptor (AR) blockade with eplerenone (epl) on renal Na+ excretion, arterial blood pressure, intra-adrenal and renal ANG II, and plasma aldosterone levels during ANG Il-dependent hypertension were evaluated. Rats from one cohort (n = 10/group) 1) control, 2) control + epl (25 mg/day), 3) ANG II (60 ng/min), and 4) ANG 11 + epl were maintained in metabolic cages for 28 days for daily urine collections. Systolic blood pressure (SBP) was measured weekly by tail-cuff. In a second cohort (n = 12/group), daily SBP was measured by telemetry (n = 6 rats/group) I) control, 2) ANG 11, and 3) ANG II + epl. A diet containing epl (0.1%) was provided after 1 wk of ANG II infusion. Direct monitoring of BP by telemetry showed that epl delayed the onset of the increase in SBP by 2 days and slightly reduced SBP (186 ± 6 vs. 177 ± 8 mmHg). EpI transiently increased Na+ excretion within 24 h of treatment in both normo- and hypertensive rats; however, balance was reestablished within 5 days suggesting that alternative mechanisms for conserving Na+ are activated. Cortical α-epithelial Na+ channel content (α-ENaC) was not altered after 21 days of epl treatment. EpI exacerbated the ANG lI-mediated increases in intrarenal ANG 11(226 ± 16 vs. 365 ± 38 fmol/g) and further increased intra-adrenal ANG 11(3.9 ± 0.3 vs. 8.2 ± 0.9 fmol/mg) and aldosterone (255 ± 55 vs. 710 ± 87 pmol/mg) content. Exacerbation of intrarenal ANG II levels likely contributes to the maintenance of α-ENaC protein content and thus Na+ reabsorption, which helps explain the ineffectiveness of AR blockade in reducing SBP in ANG Il-infused models of hypertension. [ABSTRACT FROM AUTHOR]

The purpose of the present studies was to determine the effects of high-dose aldosterone and dDAVP treatment on renal aquaporin-2 (AQP2) regulation and urinary concentration. Rats were treated for 6 days with either vehicle (CON: n = 8), dDAVP (0.5 ng/h, dDAVP, n = 10), aldosterone (Aldo, 150 µg/day, n = 10) or combined dDAVP and aldosterone treatment (dDAVP+Aldo, a = 10) and had free access to water with a fixed food intake. Aldosterone treatment induced hypokalemia, decreased urine osmolality, and increased the urine volume and water intake in ALDO compared with CON and dDAVP+Aldo compared with dDAVP. Immunohistochemistry and semiquantitative laser confocal microscopy revealed a distinct increase in basolateral domain AQP2 labeling in cortical collecting duct (CCD) principal cells and a reduction in apical domain labeling in Aldo compared with CON rats. Given the presence of hypokalemia in aldosterone-treated rats, we studied dietary-induced hypokalemia in rats, which also reduced apical AQP2 expression in the CCD but did not induce any increase in basolateral AQP2 expression in the CCD as observed with aldosterone treatment. The aldosterone-induced basolateral AQP2 expression in the CCD was thus independent of hypokalemia but was dependent on the presence of sodium and aldosterone. This redistribution was clearly blocked by mineralocorticoid receptor blockade. The increased basolateral expression of AQP2 induced by aldosterone may play a significant role in water metabolism in conditions with increased sodium reabsorption in the CCD. [ABSTRACT FROM AUTHOR]

Myelomeningocele (MMC) is the most common cause of neurogenic bladder dysfunction (NBD). We recently developed a novel retinoic acid (RA)-induced MMC model in fetal rats. The objective of this study was to use this model to assess functional and structural characteristics of the detrusor muscle in MMC-associated NBD. Time-dated pregnant Sprague-Dawley rats were gavage fed 60 mg/kg RA dissolved in olive oil or olive oil alone [embryonic day 10 (E10)]. Bladder specimens from olive oil-exposed fetuses (OIL; n = 71), MMC (n = 79), and RA-exposed-no MMC (RA, n = 62) were randomly assigned for functional and histopathological evaluation and protein analysis. Contractility responses to field and agonist-mediated stimulation (KCI and bethanecol) were analyzed. The expression patterns of a-smooth muscle actin, myosin, desmin, vimentin, and collagen III and I were analyzed by immunohistochemistry and Western blotting. Spatial and temporal distribution of nerve fibers within the detrusor muscle was monitored by neurotubulin-β-III throughout gestation. Neither OIL, MMC, nor RA detrusor responded to field stimulation. MMC bladder strips showed a significant decrease in contractility after KCI and bethanechol stimulation compared with OIL and RA bladders. Bladder detrusor morphology and expression patterns of smooth muscle markers were similar between groups. Detrusor muscles in OIL and RA fetuses were densely innervated, possessing abundant intramural ganglia and nerve trunks that branch to supply smooth muscle bundles. In MMC bladders, neurotubulin-β-III-positive nerve fibers were markedly decreased with advancing gestational age and were almost completely absent at term (E22). We conclude that the biomechanical properties of fetal rat MMC bladders are analogous to that seen in humans with MMC-associated NBD. Decreased nerve density indicates loss of peripheral neural innervation throughout gestation. The early observation of decreased innervation and decreased contractility in the absence of morphologic abnormalities in muscle structure or extracellular matrix supports a pathophysiological hypothesis that denervation is the primary insult preceding the observed alterations in bladder muscle structure and function. [ABSTRACT FROM AUTHOR]

Recent studies show nitric oxide (NO) deficiency is both a cause and consequence of chronic kidney disease (CKD). Reduced renal neuronal NO synthase (nNOS) abundance and activity parallel development of CKD with different models in the Sprague-Dawley (SD) rats, whereas Wistar Furth (WF) rats are protected against CKD and show preserved renal NO production. In this study, we compared renal NO in response to DOCA/salt-induced injury between the WF and SD. Studies were conducted on sham WF (n = 6) and SD (n = 6) and uninephrectized (UNX)+75 mg DOCA+1% NaCl (WF n = 9; SD n = 10) rats followed for 5 wk. Kidneys were harvested for Western blot, NOS activity, and histology. Other measurements included creatinine clearance and 24-h total NO production and urinary protein excretion. Absolute values of kidney weight were lower in WF than SD rats that showed similar percent increases with UNX+DOCA/NaCI. Proteinuria and decreased creatinine clearance were present in the SD but not the WF rats following UNX+DOCA/NaCl. Glomerular injury was mild in the WF compared with SD rats that showed many globally damaged glomeruli. Although renal nNOS abundance was decreased in both strains (higher baseline in WF), soluble NOS activity was maintained in the WF but significantly reduced in the SD rats. Renal endothelial NOS abundance and membrane NOS activity were unaffected by treatment. In summary, WF rats showed resistance to UNX+DOCA/NaCl-induced CKD with maintained renal NO production despite mild reduction in nNOS abundance. Further studies are needed to evaluate how WF rats maintain renal NO production despite similar changes in abundance as the vulnerable SD strain. [ABSTRACT FROM AUTHOR]

A low nephron endowment may be associated with hypertension. Nephrogenesis is the process that leads to the formation of nephrons until week 36 of gestation in humans and may be inhibited by many factors like intrauterine growth restriction and premature birth. To study the consequences of a low glomerular number, animal models have been developed. We describe a model of postnatal food restriction in the rat in which litter size is increased to 20 pups, which leads to growth restriction. In the rat, active nephrogenesis continues until postnatal day 8, which coincides with the growth restriction in our model. Design-based stereological methods were used to estimate glomerular number and volume. Our results show an ~25% lower glomerular number in rats after postnatal food restriction (30,800 glomeruli/ kidney) compared with control rats (39,600 glomeruli/kidney, P < 0.001). Mean glomerular volume was increased by 35% in the growth-restricted rats (P = 0.006). There was a significant negative correlation between glomerular volume and glomerular number (r = -0.76, P < 0.001). We conclude that postnatal food restriction in the rat leads to a low nephron endowment with compensatory enlargement. It is therefore a suitable model to study the effect of intrauterine growth restriction or prematurity on kidney development and the consequences of a reduced glomerular number in later life. [ABSTRACT FROM AUTHOR]

Dysregulation of kidney nitric oxide synthase (NOS) I may alter renal hemodynamics in diabetes. Four types of studies were performed in anesthetized 1- to 2-wk-streptozotocin diabetic rats. 1) Glomerular filtration rate (GFR) was measured before and during NOS I blockade. Subsequent addition of nonspecific NOS blocker tested for residual NO from other isoforms. Acute systemic NOS I blockade reduced GFR only in diabetics. Nonspecific NOS blockade had no additional effect on NOS I-blocked diabetics. 2) Renal blood flow (RBF) was monitored for evidence that tubuloglomerular feedback (TGF) resets during 1 h of continuous activation with benzolamide. NOS I blockade was added to test for the role of NOS I in TGF resetting. During 1 h of TGF activation in controls, RBF initially declined and then returned to baseline. In diabetic and NOS I-blocked rats, RBF declined and remained low. 3) The ability of NOS I blockade to increase the homeostatic efficiency of TGF in diabetes was tested by micropuncture in free-flowing nephrons. The addition of NOS I blocker to the tubular fluid increased TGF efficiency in control and diabetic rats. 4) The influence of distal salt delivery on local NOS I activity was tested by micropuncture. Henle's loop was perfused at varying rates with NOS I blocker while single-nephron GFR (SNGFR) from the late proximal tubule was measured. In controls, NOS I blockade mainly reduced SNGFR when flow through Henle's loop was high. In diabetics, NOS I blockade reduced SNGFR independently of flow through Henle's loop. In conclusion, normally, salt delivered to the macula densa (MD) exerts immediate control over MD NOS I activity. In diabetes, there is ongoing overactivity of NOS I that is not regulated by MD salt. [ABSTRACT FROM AUTHOR]

Recent studies have demonstrated that a novel anion exchanger, pendrin, is expressed in the apical domain of type B intercalated cells in the mammalian collecting duct. The purpose of this study was l) to determine the expression and distribution of pendrin along the collecting duct and connecting tubule of mouse and rat kidney and establish whether pendrin is expressed in the nonA-non-B intercalated cells and 2) to determine the intracellular localization of pendrin in the different populations of intercalated cells by immunoelectron microscopy. A peptide-derived affinity-purified antibody was generated that specifically recognized pendrin in immunoblots of rat and mouse kidney. Immunohistochemistry and confocal laser scanning microscopy demonstrated the presence of pendrin in apical domains of all type B intercalated cells in mouse and rat connecting tubule and collecting duct. In addition, strong pendrin immunostaining was observed in non-A-non-B intercalated cells. There was no labeling of type A intercalated cells. Immunoelectron microscopy demonstrated that pendrin was located in the apical plasma membrane and intracellular vesicles of both type B intercalated cells and non-A-non-B cells; the latter was identifled by the presence of H[sup +]-ATPase in the apical plasma membrahe. The results of this study demonstrate that both pendrin and H[sup +]-ATPase are expressed in the apical plasma membrane of non-A-non-B intercalated cells, suggesting that these cells are capable of both HCO[sup -, sub 3] and proton secretion. Furthermore, the presence of pendrin in both the apical plasma membrane and the apical intracellular vesicles of type B and non-A-non-B intercalated cells suggests that HCO[sup -, sub 3] secretion may be regulated by trafficking of pendrin between the two membrane compartments. [ABSTRACT FROM AUTHOR]

To test the role of epithelial Na channels in the day-to-day regulation of renal Na excretion, rats were infused via osmotic minipumps with the Na channel blocker amiloride at rates that achieved drug concentrations of 2-5 µM in the lumen of the distal nephron. Daily Na excretion rates were unchanged, although amiloride-treated animals tended to excrete more Na in the afternoon and less in the late evening than controls. When the rats were given a low-Na diet, Na excretion rates were elevated in the amiloride-treated group within 4 h and remained higher than controls for at least 48 h. Adrenalectomized animals responded similarly to the low-Na diet. In contrast, rats infused with polythiazide at rates designed to inhibit NaCl transport in the distal tubule were able to conserve Na as well as did the controls. Injection of aldosterone (2 µg/100 g body wt) decreased Na excretion in control animals after a 1-h delay. This effect was largely abolished in amiloridetreated rats. On the basis of quantitative analysis of the results, we conclude that activation of amiloride-sensitive channels by mineralocorticoids accounts for 50-80% of the immediate natriuretic response of the kidney to a reduction in Na intake. Furthermore, the channels are necessary to achieve minimal rates of Na excretion during more chronic Na deprivation. [ABSTRACT FROM AUTHOR]

Presents information on a study which localized the sodium/hydrogen exchanger (NHE) isoform NHE4 along the rat nephron. Experimental procedures; Immunofluorescence localization of NHE4 along the rat nephron; Transport properties of NHE4 in native membrane preparations.

Deals with a study which evaluated the relative abundances of renal sodium transporters in lean and obese Zucker rats at two and four months of age by semiquantitative immunoblotting. Methods of the study; How obese Zucker rats had increased blood pressure and responded abnormally to a saline challenge; Normal basic renal function of obese rats.

Presents information on a study that proposed a numerical model that simulates acid-base transport in rat distal tubule. Methodology of the study; Results and discussion on the study.

Presents a study which investigated the localization of cAMP-coupled prostaglandin E[sub 2] EP2 and EP4 receptor expression in rat kidneys. Role of PGE[sub 2] receptors in urine concentration and renal blood flow; Methodology; Results.

Presents a study which evaluated the localization of epithelial sodium channel (ENaC) subunit messenger RNA and protein in the principal cells of a rat kidney. Presence of ENaC in the organs of the body; Immunocytochemistry and immunoelectron microscopy of the kidneys; Immunoblotting of homogenates from the kidney.

Presents a study which examined the baseline blood pressure and renal function in different levels of blood urea nitrogen in rats. Details on urea; Methodology; Results; Conclusions.

Presents a study which determined the intrinsic capacities of inner medullary collecting ducts (IMCD) in absorbing the secreting solutes and fluid in an isotonic medium using an in vitro method in rat kidneys. Discussion on renal sodium chloride excretion; Methodology; Effects of serum proteins on fluid secretion; Studies to evaluate cellular mechanisms of solute and fluid secretion in IMCD.

Features a study which described elevated histochemical signals for nitric oxide synthase-1 and cyclooxygenase-2 in the juxtaglomerular apparatus and adjacent limb of the kidney of fawn-hooded hypertensive rats. Levels of renin immunoreactivity and renin ribonucleic acid expression in afferent arterioles; Methodology; Results and discussion.

Features a study which examined the role of inflammation in the development of renal interstitial fibrosis in Zucker obese rats that rapidly presented kidney lesions in the absence of hypertension and hyperglycemia. Quantification of type I and III collagens; Methodology; Results and discussion.

Presents a study which investigated the renal distribution of pendrin, an apical chlorine/hydroxide/bicarbonate exchanger in rat kidney cortex, and its function. Experimental procedures; Results; Discussion.

Presents information on a study which examined the mechanisms of chlorine transport in rat lymphocytes under a variety of conditions. Methods used; Results; Discussion.

Presents a study on the localization and characterization of an additional urea transporter isoform in the inner medullary collecting duct in rats. Materials and methods used; Results; Discussion.

Presents a study which determined the contribution of cytoskeleton elements in the control of sodium/hydrogen exchanger 3 activity present in the luminal membrane of rat kidney cortical tubules under basal conditions. Materials and methods used; Results; Discussion.

Presents a study which determined the effect of early diabetes on components of the glomerular renin-angiotensin system and on the expression of kidney AT [sub 2] receptors in rats. Methods used; Results; Discussion.

Presents information on a study which evaluated the effects of increasing the viscosity in peritubular capillary perfusates on proximal convoluted tubule acidification in rat kidney. Methods used; Results; Discussion.

Presents information on a study which examined the effect of dietary potassium intake on the apical potassium channels in the medullary thick ascending limb of rat kidneys. Methods used; Results; Discussion.

Presents information on a study which investigated the renal handling of water in rats with decompensated liver cirrhosis. Methodology; Results; Discussion.

Presents information on a study which assessed the presence, signal transduction and actions of E-prostanoid receptor subtypes in preglomerular arterioles of Sprague-Dawley rat kidneys. Methods; Results; Discussion.

Focuses on a study which determined whether male rats are more sensitive to the hypertensive and proteinuric effects of chronic nitric oxide synthase inhibition than female rats. Materials and methods; Results; Discussion.

Presents a study which examined whether chronic lithium treatment affects the expression of whole kidney aquaporin levels or of major renal sodium transporters. Association of the changes in the abundance of aquaporin and sodium transporters with alterations in urinary concentration and urinary sodium excretion in lithium-treated rats; Methodology; Results and discussion.

Presents a study which measured the L-kynurenine and quinolinic acid concentrations in serum and cerebrospinal fluid in renal-insufficient rats. Methodology; Results; Discussion.

Presents a study which examined the hydroxyeicosatetraenoic acid release in response to angiotensin II from preglomerular microvessels of rats. Materials and methodology; Results; Discussion.

Presents information on a study which examined the effects of ...-monomethyl-L-arginine methyl ester on fluid and hydrocarbonic acid transport in wild-type mice. Details on the proximal tubule transport in neuronal nitric oxide synthase-knockout mice; Methodology; Results; Discussion.

Presents a study which determined the involvement of renal aquaporin-2 in the pathogenesis of impaired water excretion in rats with experimental model of glucocorticoid deficiency. Methodology; Results; Discussion.

Presents a study which examined the chaotic behavior of renal sympathetic nerve activity in normal rats before and after sinoaortic and cardiac baroreceptor denervation and in rats with congestive heart failure. Methodology; Results; Discussion.

Focuses on a study which determined the effect of increased arterial pressure in the distribution or activity of sodium transporters in spontaneously hypertensive rat (SHR) and the development of chronic hypertension in SHR. Experimental procedures; Results; Discussion.

Discusses a study which investigated total renal blood flow and medullary blood flow autoregulatory behavior and pressure-natriuresis in angiotensin II-infused hypertensive rats. Methods; Results; Discussion.

Discusses a study which determined the role of prostaglandins E in alpha-mediated inhibition of permeability, sodium, and urea transport in the rat inner medullary collecting duct. Materials and methods; Results; Discussion.

Presents a study which estimated the clearances for FITC-Ficoll and albumin in rat kidneys by inhibiting the tubular activity. Effect of temperature to the tubular activity; Methodology; Summary of recorded parameters at eight degrees centigrade; Results of the two-pore analysis.

Presents a study which developed a mathematical model of the outer medullary collecting duct of the rat consisting of intercalated cells and a paracellular pathway. Parameters of the model; Discussion.

Presents a study which investigated the effects of vasopressin on abundances of the epithelial sodium channel in rat kidney by quantitative immunoblotting. Methodology; Results of the study; Discussion of the results.

Presents information on a study which examined the hypothesis that there is conditional failure of renal autoregulation in Brown Norway rats. Methods; Results of the study; Discussion.

Presents a study which determined whether glomerular pressure increased with aging in spontaneously hypertensive rats and might account for eventual appearance of glomerular sclerosis and renal failure in older rats. Methods used; Results and discussion.

Presents a study which examined the ontogeny of the arachidonic acid metabolic pathways regulating proximal convoluted tubular sodium-potassium-ATPase activity in infant and adult rats. Materials and methods used; Results and discussion.

Provides information on a study which examined the expression of transforming growth factor-beta type II signaling receptor protein and mRNA levels in the diabetic mouse kidney. Role of high ambient glucose in the regulation of the growth factor in cultured mesangial cells; Research design and methods; Results and discussion.

Provides information on a study which investigated the effect of the 1-34 and 3-34 parathyroid hormone peptides on the distribution of renal type IIa Na-Pi cotransporter in rat kidneys. Materials and methods used; Results and discussion.

Provides information on a study which demonstrated that in rats with 5/6 nephrectomy, renal cortical and inner medullary neuronal NOS expression is downregulated, associated with decreased urinary excretion of nitric oxide products. Materials and methods used; Results and discussion.

Presents information on a study which reported cloning and localization of a rat homolog of the mouse sulfonylurea receptor 2B, RT-PCR. Methods; Results of the study; Discussion.

Deals with a study that characterized glomerular and preglomerular vascular ANG II receptors and protein kinase C isoforms in streptozotocin-induced diabetic rats after treatment with low or high doses of insulin, or a low dose of insulin with captoril, an ACE inhibitor. Materials and methods; Results of the study; Discussion.