Search

Background: Most treated hypertensive patients do not achieve adequate blood pressure (BP) control. Initiating therapy with two drugs has been suggested when BP is >20/10 mm Hg above goal. To ensure patients' compliance, such treatment needs to be well tolerated and must not compromise health-related quality of life (HRQL). The primary objective of this study was to compare the effects on HRQL of initiating treatment with felodipine + metoprolol (F+M) fixed combination tablets, or enalapril (E), or placebo (P)., Methods: A total of 947 patients of both sexes with primary hypertension (diastolic BP 95 to 110 mm Hg), aged 20 to 70 years, participated in this randomized, double-blind, parallel group, 12-week, multicenter trial. Treatment was initiated with F+M 5 + 50 mg, or E 10 mg, or P. Doses were doubled after 4 or 8 weeks if diastolic BP was >90 mm Hg. The HRQL was measured at baseline and at the last visit using two validated questionnaires: the Psychological General Well-being Index (PGWB) and the Subjective Symptom Assessment Profile (SSA-P). Office BP was measured at trough, that is, 24 h after the previous dose., Results: The HRQL was high at baseline and generally well maintained during the study. For example, the mean (SD) PGWB total score was 104 (16) at baseline and 105 (16) at 12 weeks in all three treatment groups. The BP reductions after F+M (18/14 mm Hg) and E (12/9 mm Hg) were significantly greater than after P (7/7 mm Hg), and the reduction after F+M was significantly greater than after E., Conclusions: The HRQL is maintained in the presence of substantial BP reduction during antihypertensive treatment with F+M fixed combination tablets.

Background: There are numerous data indicating a significant role of the sympathoadrenal system and the reninangiotensin- aldosterone system in the regulation of blood pressure and the pathogenesis of essential hypertension. However, the genetic background of essential hypertension remains unclear., Aim: To determine the effects of genetic factors on selected indicators of the activity of the sympathoadrenal system and the renin-angiotensin-aldosterone system in twins., Methods: We studied 39 monozygotic twin pairs (age 33+/-7 years) and 37 same-gender dizygotic twin pairs (age 36+/-7 years). We measured blood and urine adrenaline (A), noradrenaline (NA), dopamine (DA) and aldosterone (ALD) levels, as well as plasma renin activity (PRA) and serum angiotensin-converting enzyme (ACE) activity. Parameters of the genetic models for age- and gender-adjusted data were estimated by model fitting and path analysis technique using LISREL 8., Results: The effects of genetic factors on the variability of blood and urine catecholamine levels were 69% and 65% for A, 42% and 76% for NA, and 58% and 40% for DA, respectively. We also found shared environmental components for blood NA (28%) and urine DA (17%). Genetic factors accounted for 36% of the variability of PRA and 80% of the variability of ACE. ALD levels were related only to environmental factors (including a shared environmental component, estimated at 25%, for urine ALD)., Conclusions: We found significant effects of genetic factors on the activity of the sympathoadrenal system, as indicated by blood and urine catecholamine levels. We also found the effect of genetic factors on PRA and ACE, but not on aldosterone levels.

In recent years there has been a growing interest in rare forms of secondary hypertension. Data from these studies enlarge our knowledge of hypertension pathophysiology and make possible establishing new possibilities of hypertension treatment. Primary reninism, Liddle's syndrome and neurovascular contact has been presented in the article. The pathogenesis, clinical symptoms and treatment of these rare forms of hypertension is discussed in this article.

The aim of the present study was to assess the efficacy and tolerability of a calcium antagonist/beta-blocker fixed combination tablet used as first-line antihypertesnive therapy in comparison with an angiotensin converting enzyme inhibitor and placebo. Patients with uncomplicated essential hypertension (diastolic blood pressure between 95 and 110 mm Hg at the end of a 4-week run-in period) were randomly allocated to a double-blind, 12-week treatment with either a combination tablet of felodipine and metoprolol (Logimax), 5/50 mg daily (n = 321), enalapril, 10 mg daily (n = 321), or placebo (n = 304), with the possibility of doubling the dose after 4 or 8 weeks of treatment if needed (diastolic blood pressure remaining >90 mm Hg). The combined felodipine-metoprolol treatment controlled blood pressure (diastolic < or =90 mm Hg 24 h after dose) in 72% of patients after 12 weeks, as compared with 49% for enalapril and 30% for placebo. A dose adjustment was required in 38% of patients receiving the combination, in 63% of patients allocated to placebo, and 61% of enalapril-treated patients. The overall incidence of adverse events was 54.5% during felodipine-metoprolol treatment; the corresponding values for enalapril and placebo were 51.7% and 47.4%, respectively. Withdrawal of treatment due to adverse events occurred in 18 patients treated with the combination, in 10 patients on enalapril, and 12 patients on placebo. No significant change in patients' well-being was observed in either of the three study groups. These results show that a fixed combination tablet of felodipine and metoprolol allows to normalize blood pressure in a substantially larger fraction of patients than enalapril given alone. This improved efficacy is obtained without impairing the tolerability. The fixed-dose combination of felodipine and metoprolol, therefore, may become a valuable option to initiate antihypertensive treatment.

The aim of this study was to evaluate the effect of renal artery stenosis (RAS) correction in hypertensive patients on 24 h SBP, 24 h DBP, creatinine clearance (GFR), urinary albumin excretion (UAE) and LV morphology and mass (LVMI). A total of 61 hypertensive patients with RAS undergoing PTRA and/or surgical treatment entered the prospective study. The final analysis was done in 44 patients (age range 45.8 +/- 16.2 years) with RAS (atherosclerosis (ASC) 31 patients, fibromuscular dysplasia (FMD) 12 patients, arteritis 1 patient) who underwent PTRA (34 patients) or surgical treatment (10 patients) and presented no Doppler signs of restenosis (or a new stenosis) during 1-year observation. The pre-interventional assessment repeated after 6 and 12 months included ABPM, GFR, UAE and echocardiography. The results were analysed in the combined group (CG) and in according aetiology. 24 h SBP and 24 h DBP decreased in all groups 6 months post-intervention and did not change further. Cure of HT was observed in 35% and 29% of ASC patients at 6 and 12 months respectively; and in 58% of FMD patients. Failure rate at 12 months was 48% in ASC against 25% in FMD. The mean GFR in CG was higher 12 months after intervention. The increase in GFR was noted in 45% of patients, the decrease in 25% of patients at 12 months. Normal values of UAE were found in 71% of patients, pre- and post-intervention alike. Mean LVMI and number of patients with LVH in CG decreased already during the initial 6 months post-intervention and did not change further. In conclusion, correction of RAS leads to cure of or improved control of hypertension in the majority of the patients with FMD, but in the ASC group in about half of cases no BP cure or improvement was seen. The renal function was improved or stable in two-thirds of patients after revascularization. Successful renal revascularization was followed by regression of LVH, which was evident within 6 months post-intervention.

This paper discusses the most significant aspects of secondary hypertension in older patients against the background of a rising proportion of elderly in the hypertensive population. Renal artery stenosis and pheochromocytoma are singled out as those causes of secondary hypertension which appear to be related to older age. The available data relevant to epidemiology of these conditions and age-dependent clinical characteristics are reviewed. Preservation of renal function in the elderly with renal artery stenosis is underlined as an important goal of therapy with revascularising techniques. It is proposed that screening for renal artery stenosis and pheochromocytoma may be equally important in the elderly as in the younger hypertensive patient.

Objective: To assess the effect of 1-year treatment with rilmenidine, an oxazoline compound that exerts its antihypertensive effects through binding to imidazoline receptors in the brainstem, on left ventricular hypertrophy (LVH) secondary to essential, mild-to-moderate hypertension [supine diastolic blood pressure (DBP)95-115 mmHg]., Methods: We performed a double-blind, randomized, controlled (versus slow-release nifedipine) trial. Adjustment of treatment took place every month (M) between inclusion (MO) and an evaluation after 6 months (M6), then during M9 and after 1 year (M12) to achieve supine DBP values < or = 90 mmHg. Patients were dropped from our study if they had DBP> 95mmHg during two consecutive visits or DBP>115 mmHg on one occasion. The daily dosage of rilmenidine was 1 mg, and could be increased to 2 mg/day. The daily dosage of slow-release nifedipine was started from the beginning at the maximum dosage of 40 mg/day, so that there was no true adjustment of treatment despite the allocation of patients to a different unit in the case of DBP> 95 mmHg. The primary criterion was the change in left ventricular mass index (LVMI, g/m2), assessed by echocardiography, between MO and M12 for patients who completed the trial., Results: After a 1-month placebo run-in period, 76 patients were selected and 73 were included (35 treated with rilmenidine and 38 treated with nifedipine). Fifteen patients withdrew from the study and two completed the study with a major deviation from protocol, leaving 56 patients (24 treated with rilmenidine and 32 treated with nifedipine) for a per-protocol analysis. Baseline demographic characteristics and history of arterial hypertension for the rilmenidine and nifedipine groups were similar, for included patients and for those taken into account for the per-protocol analysis. Between MO and M12, DBP in members of the per-protocol population was adequately controlled for those in the rilmenidine group (102.7+/-4.6 versus 88.5+/-7.1 mmHg, respectively) and for those in the nifedipine group (102.7+/-5.1 versus 85.6+/-79 mmHg, respectively). During MO, LVMI of patients in the rilmenidine group (176.9+/-41.3 g/m2) was slightly higher than that of patients in the nifedipine group (172.6+/-35.1 g/m2). During M12, LVMI was observed to have decreased both for patients in the rilmenidine group (to 154.8+/-40.2 g/m2, a decrease of 22.1+/-23.3 g/m2, P< 0.001) and for those in the nifedipine group (to 145.6+/-36.4 g/m2, a decrease of 26.9+/-29.5 g/m2, P< 0.001) but the difference between these two groups was not significant (P= 0.5)., Conclusion: One-year treatment with a daily dosage of 1 or 2 mg rilmenidine achieves a significant reduction of left ventricular mass, which is not statistically different than that occurring with a daily dosage of 40 mg of slow-release nifedipine.

Hemorrheological and humoral abnormalities and excessive platelet activity can predict the development of cardiovascular complications in patients with essential hypertension. A study was conducted to assess the influence of gender on these factors and the interrelations between changes in hemorrheology and the sympatho-adrenal system in 54 patients (18 women, 36 men) with essential hypertension (aged 39.6 +/- 9.7 years) and 25 healthy volunteers (10 women, 15 men; aged 36.0 +/- 7.2 years). A decrease in erythrocyte deformability (p < 0.01) was found in the hypertensive men compared with the hypertensive women. Hematocrit (p < 0.01), blood viscosity at the shear rates of 0.3 s-1 (p < 0.01) and 6 s-1 (p < 0.01), plasma viscosity (p < 0.01), erythrocyte aggregation (p < 0.01), and neuropeptide Y (p < 0.02) concentrations were higher in the hypertensive men than in the hypertensive women. A positive correlation between blood fibrinogen and serotonin was found in the pooled hypertensive group and in the hypertensive men (p < 0.01) and between blood viscosity (shear rate 6 s-1) and neuropeptide Y in the pooled hypertensive group (p < 0.01). Neuropeptide Y correlated with filtration time of 1 mL blood in the hypertensive men (p < 0.05) and in the pooled normotensive group (p < 0.01) and with beta-thromboglobulin in the hypertensive women (p < 0.001). A positive correlation was also found in the hypertensive men between erythrocyte and platelet aggregation (p < 0.01) and between beta-thromboglobulin and adrenaline (p < 0.01). Hemorrheological and humoral abnormalities are more pronounced in men than in women with essential hypertension and may contribute to the increased incidence of cardiovascular events in men.

The paper reviews the main lines of research pertaining to modern understanding of pathogenesis of essential hypertension. Attention is focused on the role of sympathetic activity, including the neuropeptide Y, as well as on those of atrial natriuretic peptide, endothelins and nitric oxide. The concept of endothelial dysfunction is discussed as a possible factor contributing to the development of hypertension, but also as its sequel. Finally, hyperinsulinemia and insulin resistance are viewed within a scope of interrelated factors of possible pathogenetic significance in essential hypertension. Genetic studies are singled out as the most promising line of further research.

Pheochromocytoma is a unique type of hypertension caused by excessive production of catecholamines by the chromaffin tumor. Pheochromocytoma, a potentially life-threatening disease, is a rare cause of hypertension. The incidence varies from 0.1 to 0.8% of hypertensive population. The author's experience is based on 138 patients treated in one institution from 1956 to 1995. Hormonal activity of pheochromocytoma varies considerably, influencing the pattern, of blood pressure and the clinical symptoms. It is emphasized that different other humoral mechanisms may play a role in the pathophysiology of this type of endocrine hypertension. Biochemical tests and non-invasive localizing methods are essential for the definite diagnosis of pheochromocytoma. A great progress has been made in this respect during the last three decades. Surgical removal of the tumor is the only definite therapy with low morbidity and mortality.

Neuropeptide-Y (NPY) is a peptide proposed to modulate the effect of the sympathetic nervous system on blood pressure control and contribute to the development of essential hypertension. To assess the possible influence of gender on its role, we evaluated plasma NPY, noradrenaline (NA) and adrenaline (A) concentrations in men and women with essential hypertension. No difference in NPY concentration was found between genders, but NPY concentration was elevated in both hypertensive men and women. NA levels were similar in all investigated hyper- and normotensives, while A was increased only in hypertensive men. These results suggest various patterns of sympatho-adrenal activity in gender subgroups of patients with essential hypertension.

Neuropeptide Y (NPY) is a vasoconstrictor sympathetic cotransmitter and a modulator of adrenergic function whose role in hypertension is yet unknown. We studied the co-release of NPY and noradrenaline (NA) in patients with essential hypertension (13 females, 11 males, age 42 +/- 13 years) by measuring plasma levels of NPY-immunoreactivity (-ir, radioimmunoassay) and NA (radioenzymatic method) following administration of clonidine (CL 300 micrograms, p.o.). At rest, only NPY-ir levels significantly correlated with diastolic blood pressure (DBP, r = 0.42, p < 0.05). Three hours after CL, there were a decrease in mean arterial pressure and plasma NA (by 31 +/- 14 mmHG, p < 0.05 and 92 +/- 10 pg/ml, p < 0.01) but no change in NPY-ir levels. Patients were subsequently subdivided into groups with high (> or = 90 mmHg) or normal DBP (< or = 89 mmHg) and with or without elevated plasma NA levels (above or below 414 pg/ml, a normotensive mean +1 standard deviation). In hypertensives, but not in those with normal DBP, plasma NPY-ir correlated not only with DBP but also with systolic and mean blood pressure (r = 0.53 and r = 0.60, respectively) at rest. Hypertensives with "high" NA had significantly lower resting plasma NPY-ir levels than those with "low" NA (7.1 +/- 3.6 vs 14.7 +/- 6.0 fmol/ml, p < 0.05). In the former group, CL evoked the greatest fall in plasma NA, and also decreased NPY-ir levels by 50% (p < 0.05). Thus, patients with essential hypertension were found to display differential patterns of changes in sympathetic cotransmitters to clonidine. NPY may contribute to the increased blood pressure in hypertensives and together with NA, mediate hypotensive action of clonidine but only in the hyperadrenergic subgroup of hypertensives.

Background: Endothelin-1 (ET-1) may play an important role in the development and maintenance of hypertensive states. In patients with essential hypertension, ET-1 plasma concentration increases or remains unchanged. The aim of the present study was to investigate ET-1 plasma concentration in patients with mild-to-moderate essential hypertension and its interrelationship with catecholamines, neuropeptide Y and atrial natriuretic peptide (ANP)., Methods: The study included 37 patients (mean age 38.2 +/- 1.6 years) with mild-to-moderate essential hypertension. The control group consisted of 21 healthy volunteers (mean age 35.6 +/- 1.4 years). ET-1, neuropeptide Y and ANP were determined by radioimmunoassay methods and catecholamine plasma concentration was determined radioenzymatically., Results: Our study shows that plasma ET-1 and neuropeptide Y levels are elevated in patients with essential hypertension compared with a control group. No correlation was found in either of the groups between plasma ET-1 level and plasma neuropeptide Y, catecholamine or ANP concentrations., Conclusion: Our results suggest that ET-1 is relevant in the development and maintenance of elevated blood pressure.

Ketanserin, a serotonin-2-receptor antagonist, was administered to 16 patients with mild to moderate essential hypertension in randomized single-blind placebo controlled study. After 2 weeks of placebo administration ketanserin 60 mg daily was given for 3 weeks. In 7 patients the normalization of blood pressure was obtained and they were given the same daily dose of ketanserin for another 3 weeks. In the remaining 9 patients the dose of ketanserin was increased to 120 mg daily for the same period; in one additional case blood pressure decreased to normal. In the whole group the decrease of diastolic pressure was statistically significant comparing to placebo period. Ketanserin therapy did not influence serum free serotonin concentration, but the hypotensive effect was greater in patients with lower serotonin blood levels. Serum aldosterone concentration decreased in the initial period of treatment; the decrease was more pronounced in patients who responded to therapy. In this subgroup of patients diastolic blood pressure correlated positively with plasma renin activity. Ketanserin lowered serum adrenaline concentration, particularly in patients with good response to therapy. There was also decrease of total cholesterol concentration without any significant changes in HDL--cholesterol fraction. The authors conclude that oral chronic ketanserin treatment is an effective therapy in essential hypertension and that its effectiveness is greater in patients with lower serum serotonin levels. The hypotensive effect of the drug may be connected with lower sympathetic activity and with changes in renin-angiotensin-aldosterone system. Ketanserin is well tolerated and exerts beneficial effect on lipid metabolism.

We evaluated the effect of captopril treatment on left ventricular mass (LVM) and function in sustained mild-to-moderate primary hypertension. In 16 men aged 34.5 +/- 6.4 yrs. M-mode echo and pulsed wave Doppler recordings were obtained prior to and after 2 months captopril treatment (50-150 mg daily). No significant changes in heart rate, systolic blood pressure, ejection fraction, fractional shortening, cardiac output, LVM and Doppler-derived indices of mitral inflow were observed. Diastolic blood pressure measured during examination fell from 102.2 +/- 13.3 to 90.3 +/- 9 mmHg (p less than 0.026). No consistent correlations between catecholamines and indexes of left ventricular function were found. Two-month captopril therapy in mild-to-moderate hypertension results in diastolic blood pressure lowering with no effect on LVM or left ventricular function.

89 patients were operated upon for pheochromocytoma. 61 patients (37 women and 24 men) were available for follow-up. Mean age at operation was 39 +/- 12.3 yrs. Before operation paroxysmal and sustained hypertension were observed in 34 (55.7%) and 27 (44.3%) patients, respectively. Postoperatively permanent normalization of blood pressure was achieved in 38 cases (62.3%). All patients were divided into four groups. Group I with increased urine excretion of noradrenaline (NA) and adrenaline (A) consisted of 19 (31.1%) patients. Group II (increased NA excretion) included 27 (44.3%) patients. Group III comprised 3 (4.9%) cases with elevated A excretion. 12 (19.7%) patients with normal urinary excretion of catecholamines and increased excretion of methoxycatecholamines were alloted to group IV. Permanent normalization of blood pressure predominantly was observed in group IV--91.6%, whilst in group I, II and III this hypotensive effect was noted in 57.9%, 51.8% and 2/3, respectively. Permanent normalization of blood pressure can be mainly expected in patients with pheochromocytoma in whom catecholamines are rapidly inactivated within the tumor.

Concentration of free serotonin, adrenaline, noradrenaline, aldosterone and plasma renin activity have been assayed in blood of 18 patients with the primary arterial hypertension (WHO stage I) and in 10 healthy volunteers. It was found that blood free serotonin and noradrenaline are increased in hypertensive patient. No difference in adrenaline and aldosterone levels and plasma renin activity was seen. No significant correlation between free serotonin and assayed hormones was noted.

In the face known antihypertensive action of small dopamine (DA) concentrations, serum free and conjugated dopamine levels were determined during orthostatic impulse. It was also estimated, whether correlation between blood pressure changes and serum dopamine concentration existed under those conditions. 9 patients with borderline hypertension, 8 with fixed hypertension and 5 healthy volunteers (control group) underwent the 10 minute passive tilt up test. It caused significant decrease of free DA concentration in healthy men as well as in those with borderline hypertension and conjugated DA level in both groups of patients with primary hypertension. Blood pressure increased only in patients with borderline hypertension. Most expressed changes in dopamine concentration were also observed in those patients and they only had increased serum DBH activity. Blood pressure changes inversely correlated with changes of serum free and/or conjugated DA levels in the control group and in patients with primary hypertension. Authors stated basing on this study results, that serum DA level lowering caused by the orthostatic impulse can be one of phenomenons enable adaptation for a vertical position.

Serotonin appears to play an important part in the pathogenesis of essential hypertension. Various studies have shown, that the metabolism of serotonin may be disturbed in some pathological conditions for example in hypertension. It concerns also the changed mechanisms of uptake and release of serotonin. The certain blood vessels may become more hypersensitive to the vasoconstrictor effects of serotonin in patients with hypertension than in normal subjects. During chronic treatment with ketanserin, S2-serotonergic antagonist, blood pressure is reduced in spontaneously hypertensive rats and in humans. This fact can also indicate indirectly, that that serotonin plays a part in the pathogenesis of essential hypertension. The aim of the study was to determine the concentration of free serotonin (S) in the blood of 15 patients with sustained essential hypertension in the mean age 32.8 +/- 1.8, of 23 patients with borderline essential hypertension in the mean age 29.0 +/- 3.0 and of 10 normal subjects in the mean age 31.1 +/- 1.7 years. Plasma free serotonin was determined by fluorometric method. All patients and controls were investigated at the hospital. They were on normosodium diet, without drugs for last two weeks. The fasting blood samples were collected in the supine position. Free serotonin blood concentration was significantly higher in hypertensive group than in normal subjects. The important difference of serotonin blood concentration between two groups of hypertensive patients was noticed. It was significantly higher in group of patients with sustained hypertension, than in group with borderline hypertension (p less than 0.05). Our results are similar to the observations of other authors.(ABSTRACT TRUNCATED AT 250 WORDS)

The study included 30 patients with borderline essential hypertension (HPT) (21 with a positive family history of hypertension, mean age 24.6 years, 9 with a negative family history, mean age 27.2 years) and 10 normotensive controls (mean age 27.5 years). In all of them 24-hour urinary noradrenaline (NA) and adrenaline (A) excretion was assayed. Blood levels of NA, A and dopamine, the prostacycline metabolite 6-keto-PGF1 alpha, beta-thromboglobulin, cholesterol, triglycerides and HDL cholesterol were measured, LDL cholesterol was calculated according to the Friedewald equation. Besides, lecithin cholesterol acyltransferase activity was assayed. Patients with HPT and a positive family history had elevated sympathetic and platelet activity and diminished 6-keto-PGF1 alpha blood levels. Their HDL cholesterol level was significantly lower than that of healthy controls. In patients with HPT and a positive family history of HPT the atherogenic index (total cholesterol to HDL cholesterol ratio) was highest, but did not differ significantly from that in other groups. The assessment of the examined humoral factors indicates that patients with borderline HPT with genetic predisposition to high blood pressure have a humoral profile different from that of patients without genetic predisposition. These findings suggest the importance of genetic factors in the development of essential HPT.

The arterial pressure, the pulse frequency, the concentration of arterial natriuretic peptide (ANP), the aldosterone++ concentration and the plasma renin activity were determined in patients with primary hypertension after administration of furosemide in conditions of active assuming of erect position. The ANP concentration was lowered in that conditions both in the patients and in healthy subjects.

1. Urinary excretion of dopa, catecholamines and their metabolites (vanillylmandelic acid, methoxycatecholamines, 3-methoxy-4-hydroxyphenylglycol and homovanillic acid) were studied in eighty patients with essential hypertension and in twenty-five healthy control subjects. 2. Increased urinary excretion of catecholamines, dopa and catecholamine metabolites was found in a proportion of cases. 3. The relationship between urinary excretion of catecholamine metabolites and the excretion of dopa and noradrenaline was studied. 4. In view of the suggested significance of 3-methoxy-4-hydroxyphenylglycol as an index of brain catecholamine metabolism, particular attention was paid to urinary excretion of this metabolite in the subjects under study.

The metabolism of 3H-catecholamines after i.p. injection of 3H-tyrosine was studied in the heart and adrenals of spontaneously hypertensive (SHR) and normotensive Wistar (NCR) rats at rest and following running stress. In the heart of 8-week-old NCR a sharp stress-induced increase of the levels of 3H-A and 3H-DA with an elevation of the levels of their metabolites was observed. In contrast, there was no stress-related change in the levels of 3H-NA, 3H-A and 3H-VMA in the hearts of young SHR, while the 3H-DA level, though increased after stress, remained still lower than in the age-matched NCR. In the phase of established hypertension (24 weeks) lower levels of 3H-NA and 3H-A in the heart already present at rest, as compared with NCR, remained lower after stress but the elevation of the level of their metabolites 3H-VMA and 3H-MA, was similar in both strains. In the adrenals of 8-week-old SHR the basal 3H-A level was already higher than in NCR. Stress provoked a marked decrease of adrenal 3H-A accompanied by increased formation of 3H-MA and an increase in the levels of 3H-NA and 3H-DA, more pronounced in SHR than NCR. In the phase of advanced hypertension a further elevation of 3H-A and 3H-MA and an increase of basal 3H-DA level in the adrenals were found at rest. The decreased levels of 3H-catecholamines in the heart of stressed young and non-stressed older SHR may indicate an increase in their rate of release and/or their impaired synthesis. An increased basal level of 3H-A in the adrenals of SHR concomitant with the development of hypertension, may reflect an increased synthesis and/or decreased release, as evidenced by the proportionally lower increase of its extraneuronal metabolite 3H-MA. The adrenal response to stress, more intense in SHR than in NCR, may be considered as due to enhanced release of 3H-A from the gland.

Plasma atrial natriuretic factor (ANF) and catecholamine concentrations were determined in 11 untreated patients with uncomplicated essential hypertension and seven normotensive subjects during graded submaximal exercise on a treadmill (loads: I 40%, II 60%, III 80% of maximal oxygen consumption). No significant differences in plasma ANF and catecholamine concentrations were found between the hypertensive and the normotensive subjects. The results do not support the presence of significant differences in the release of ANF and catecholamines during dynamic exercise between patients with uncomplicated essential hypertension and normotensive subjects.