Control of plasma aldosterone in diabetic patients with hyporeninemic hypoaldosteronism

Summary In three patients with diabetes and hyporeninemic hypoaldosteronism changes in renin activity, plasma aldosterone and cortisol were examined under various conditions: orthostasis and intravenous furosemide, infusion of synthetic 1–24 ACTH on two consecutive days and diurnal variations in basal hormone fluctuations.Each patient showed unmeasurably low renin activity unresponsive to orthostasis and intravenous furosemide while plasma aldosterone was below normal range.Under ACTH-infusion only marked increases in aldosterone were observed in one patient whereas cortisol responded normally in all diabetics tested.Analysis of diurnal night day fluctuations (20.00–8.00) in plasma aldosterone and cortisol revealed a close and statistically significant relationship between both hormones in each of the three patients (p<0.05–<0.001). Variations in plasma aldosterone thus were mediated through changes in endogenous pituitary ACTH. Compared with normal controls however, diurnal aldosterone curves were set at a lower level.Our results demonstrate that a reduced sensitivity of the adrenal gland to ACTH is not responsible for the observed subnormal plasma aldosterone levels in these patients. Therefore, the lack of circulating angiotensin II seems to be the causative reason of hypoaldosteronism.The exact mechanism of undetectable renin activity in these patients remains unknown.     

Reduced aldosterone and sodium excretion in endurance-trained athletes before and during immersion

Summary Aldosterone excretion (AE) and plasma renin activity (PRA) were measured in eight untrained (UT) and eight endurance-trained (TR) male subjects before and during 4 h head-out immersion to study the mechanism of reduced renal sodium excretion in athletes. AE was significantly lower before immersion, and decreased less during immersion, in TR than in UT. Fractional sodium excretion, too, was lower and increased less during immersion in TR than in UT. PRA decreased in the water bath in all subjects (p<0.001) with no significant difference between the groups. During immersion, plasma sodium concentration oscillated whereas potassium concentration showed a temporary rise in TR (p<0.001). The attenuated response of AE in TR may be due partly to this increase of plasma potassium concentration. The generally reduced aldosterone release in TR might be caused by a training induced adaptation of the adrenals to corticotropin. The lowered renal sodium excretion of TR in spite of the decreased AE suggests an intensified aldosterone effect in these subjects, diminishing the salt loss during exercise. A preliminary report was presented at the 45th meeting of the German Physiological Society [Pflügers Arch.359 (Suppl.),R. 138 (1975)] Supported by the Minister für Wissenschaft und Forschung des Landes Nordrhein-Westfalen, Grant No. 06/0604/685 11     

Plasma AVP,neurophysin, renin activity,and aldosterone during submaximal exercise performed until exhaustion in trained and untrained men

Summary The effect of intense muscular work (80% of maximal oxygen uptake) on responses of plasma hormones involved in electrolyte and water balance were measured in 14 male subjects. They were divided into three groups according to their maximal oxygen uptake and the duration of exercise performed until exhaustion: well trained subjects (group I), trained subjects (group II), and untrained subjects (group III).Pulmonary gas exchange, heart rate, rectal and skin temperature, and weight loss were measured as well as hematocrit and plasma and urine sodium and potassium concentrations.Rectal temperature increased significantly in all subjects after exhaustion. The variation of hematocrit was smallest and the weight loss greatest in the well-trained subjects. Plasma aldosterone, renin activity (PRA), vasopressin (AVP), and neurophysin (Np) displayed highly significant increases after exercise in all three groups: PRA was increased 4.5 times (p<0.01), aldosterone 13 times (p<0.05), Np 2.6 times (p<0.05), and AVP 4.8 times (p<0.05). Nevertheless, there was no correlation between the changes in PRA and those in plasma aldosterone, nor between aldosterone and plasma sodium or potassium.At the urinary level, the only striking observation was that free water clearance tends to become positive after exercise. Our results provide evidence that this kind of exercise produces a highly significant increase in plasma levels of the hormones involved in electrolyte and water balance. They also indicate that it is among the well-trained subjects that sweat loss is highest though the hematocrit increase is the smallest; this suggests that water is shifted more efficiently from the extravascular compartment.     

Captopril before and after spironolactone therapy in primary aldosteronism

Summary In three patients with primary aldosteronism, the acute effect of a single dose of captopril on the elevated mean arterial blood pressure (MAP) was studied before and after 4 weeks of treatment with spironolactone. Before spironolactone therapy, captopril did not cause any drop in MAP. Four weeks later, after an oral daily dose of 400 mg spironolactone, MAP was still elevated in all three patients, though electrolyte abnormalities were fully corrected. Since plasma renin activity (PRA) was increased to values above the normal range, the acute effect of captopril on MAP was tested again. A single dose of 25 mg captopril then caused a fall in MAP to normal. These data reveal the conversion from a renin-independent to a renindependent kind of hypertension after spironolactone therapy in three patients with primary aldosteronism syndrome. This might be of pathogenetic and therapeutic interest.Abbreviations CT Computed tomography - MAP Mean arterial pressure - PA Plasma aldosterone - PRA Plasma renin activity     

Plasma vasopressin,renin activity,and aldosterone responses to maximal exercise in active college females

Summary The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · hr⁻¹ 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4±0.6 ngAI · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · ml⁻¹, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

静脉注射速尿激发试验对腺瘤型原发性醛固酮增多症患者的影响

目的比较顽固性高血压(高血压)患者与原发性醛固酮增多症(原醛)患者大剂量速尿静脉注射激发试验对血浆醛固酮/肾素比值(ARR)的影响。方法20例顽固性高血压患者和19例原醛患者入选,在清晨平卧时抽取空腹血后静脉快速注射速尿40mg,注射后10、30min各抽血一次查血浆醛固酮(ALD)及肾素(PRA)水平,并计算出ARR。结果顽固性高血压患者的平均空腹血浆ALD(127.5±13.62)pg/ml,PRA为(4.2±0.96)ng/ml/h,ARR为8.1±1.3,静脉注射速尿40mg以后10、30min患者的血浆PRA迅速升高,高峰在10min时,分别为(5.81±1.12),(95.56±1.21)ng/ml/h,P值均小于0.05,有统计学意义。PRA的上升幅度大于ALD的上升幅度,ARR反而有所下降,(6.02±1.2;6.5±1.58)。原醛组的平均空腹ALD165.75±18.56;PRA2.16±0.4;ARR26.61±9.16。ARR明显高于顽固性高血压组,P<0.01。静脉注射速尿后PRA上升不明显,ARR变化不大。两组比较P<0.05。结论顽固性高血压患者ARR比值明显大于原醛患者。静脉快速注射速尿可快速激发顽固性高血压患者的PRA的增加,PRA以10min时最为明显,但原醛患者PRA及ARR增加均不明显。ALD两组均有持续上升趋势。     

Rapid increase of mineralocorticoids after furosemide in low-renin essential hypertension: Evidence for 18-hydroxycorticosterone to be a better marker than aldosterone

Summary The response of plasma renin activity (PRA), plasma aldosterone, 18-hydroxycorticoster-one (18-OH-B), 18-hydroxydeoxycorticosterone (18-OH-DOC) and corticosterone to furosemide were compared in 20 normal control subjects, 16 patients with normal-renin essential hypertension (NREH) and 12 patients with low-renin essential hypertension (LREH). Analyses were performed before medication, and 15 min (supine) and 120 min (active orthostasis) after IV administration of 40 mg furosemide. In normotensive subjects PRA increased 15 min after administration of furosemide from 0.8±0.4 ng AI/ml·h (SD) to 3.4±1.4 (P<0.01), plasma aldosterone from 109±28 pg/ml to 139±40 (P<0.01) and 18-OH-B from 199±90 to 279±85 (P<0.01). In patients with NREH, PRA increased significantly less (P<0.01) and no significant increase of plasma aldosterone or 18-OH-B was found. PRA of patients with LREH (0.2±0.1 ng AI/ml·h) remained practically unchanged 15 min after furosemide administration, but in contrast to NREH aldosterone increased from 111±37 to 160±66 (P<0.05) and 18-OH-B from 162±101 to 261±71 pg/ml (P<0.01). The relative increase of plasma 18-OH-B was significantly greater in patients with LREH than in patients with NREH. The plasma levels of aldosterone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P<0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P<0.01) only at 120 min after furosemide administration combined with active orthostasis. In summary, our results support the concept that sensitivity of the mineralocorticoid-producing cells is enhanced in patients with LREH. Postfurosemide 18-OH-B seems to be a better marker of this phenomenon than aldosterone.Presented in part at the Kongress der Deutschen Gesellschaft für Innere Medizin, Wiesbaden, 1981     

The effect of estriol succinate therapy on plasma renin activity and urinary aldosterone in postmenopausal women

The effects of estriol succinate (Synapause^®, 2 mg daily) ¹ on the renin-aldosterone system and blood pressure (RR) were studied in 14 postmenopausal women after bilateral oophorectomy. Plasma renin activity (PRA) and daily urinary aldosterone excretion (dU-Ald) were determined 1 mth after the operation and before estrogen treatment, at the end of 2 mth therapy, and, for the third time, 2 mth after the termination of treatment with the drug. No changes in PRA, dU-Ald or RR were found in normotensive women, or in 3 women with hypertension in this group.Another group of 11 postmenopausal women was investigated after long-term estriol succinate therrpy, which had lasted for 5–8 yr after oophorectomy. PRA, dU-Ald and RR were measured during treatment and 2 mth after terminating the therapy. No changes were found either in hormone or RR levels. This group also included 5 women with hypertension. Between the groups there were no differences in the mean levels of PRA or dU-Ald.The results suggest that estriol succinate is devoid of general harmful effects on the renin-aldosterone system during postmenopausal therapy for climacteric symptoms.     

Plasma vasopressin,neurophysin, renin and aldosterone during a 4-day head-down bed rest with and without exercise

Summary The purpose of this study was to investigate the main renal and hormonal responses to head-down bed rest, which is curently considered a reliable experimental model for the simulation of weightlessness. Urinary output and electrolytes, plasma renin activity (PRA), aldosterone (PA), antidiuretic hormone (ADH) and immunoreactive neurophysin-I (Np) were measured in eight adult volunteers submitted to a 4-day head-down bed rest (–6) after a 24-h control period in the horizontal position (day 0). Four of the eight subjects were submitted to two 1-h periods of controlled muscular exercise (50% ) from day 1 to day 4. Throughout the head-down bed rest period, urinary output remained stable, although lower than in the control period (day 0), but the urinary Na/K ratio decreased. Plasma electrolytes and osmolality, and creatinine clearance remained unchanged. There was no significant difference between exercising and non-exercising subjects. At the hormonal level, PRA and PA increased during the head-down bed rest. This increase was more pronounced in the group with exercise. At the end of the tilt period, PRA and PA were about 3 times higher than on day 1. No significant changes could be observed for ADH and Np. It is concluded that a 4-day head-down bed rest results in no apparent changes in neurohypophyseal secretory activity, and in a progressive secondary hyperaldosteronism.Presented in part at the 35^th Congress of the International Astronautical Federation, Lausanne, October 1984     

Ageing and circadian rhythm of plasma renin and aldosterone

Five men and 8 women, 60–69 yr of age, and 4 men and 5 women, 17–37 yr of age, volunteered for this exploration of possible age-related changes in circadian-rhythm (CR) characteristics of radio-immunoassayable plasma renin (PRA) and aldosterone (PA). Blood was drawn at 06.00, 08.00, 12.00, 18.00, 20.00 and 24.00 from recumbent subjects on a habitual sodium intake of 120–140 mEq/ 24 h. Time-qualified data of PRA and PA, fitted by a 24-h cosine curve, were summarized by a population mean-cosinor method. Circadian characteristics were compared by a multivariate analysis using Hotelling's t² test.Rhythmometry reveals in the elderly women a lower mesor (P < 0.001) and amplitude (P = 0.036) of the CR in PRA and a higher mesor and amplitude (P = 0.021 and P = 0.020, respectively) of the PA-CR. The PRA acrophase is delayed (P < 0.001) in the elderly women (04.40 vs. 08.04) while the timing of the PA acrophase is similar in the age groups of women compared (05.52 vs. 05.20). These differences found in women were not observed in the smaller groups of men. The seventh decade of life may be characterized by an internal circadian desynchronization between the major components of the renin-angiotensin-aldosterone system. A sex-dependent amplification of the extent of circadian variation in aldosterone may precede a decrease in the circadian amplitude occurring during the eighth decade of life, as a sign of the adrenopause in women.     

Renin-hyporesponsiveness in essential hypertension dissociation between plasma renin and catecholamines or aldosterone following furosemide

Summary The influences of sequential stimulation with upright posture and sodium depletion by intravenous furosemide on blood levels of norepinephrine, epinephrine, dopamine, renin and aldosterone was studied in 26 normal subjects and 45 patients with borderline (N=20) or established (N=25) essential hypertension. Basal 24-h urinary sodium, norepinephrine and epinephrine excretion rates and basal (supine) plasma catecholamine, renin and aldosterone levels and the body sodium-volume state were comparable between the three groups. Assumption of the upright posture for 10 to 60 min caused significant increases in plasma norepinephrine (P<0.001), epinephrine (P<0.001) or dopamine (P<0.05) levels. Upright plasma catecholamine concentrations were similar in normal and hypertensive subjects and they were not modified further by furosemide. In contrast upright posture as well as furosemide induced each a successive significant (P<0.02) increase in plasma renin and aldosterone levels. Furosemide-stimulated renin was significantly (P<0.05) lower in patients with established hypertension than in normal or borderline hypertensive subjects; however, plasma aldosterone levels were comparable. These findings suggest that renin release induced by furosemide is not mediated by increased adrenergic activity. Consequently, renin-hyporesponsiveness in established hypertension cannot be explained by decreased sympathetic activity. In contrast to the altered renin regulation, aldosterone-responsiveness to upright posture or furosemide as well as adrenergic activity under these conditions appear to be usually normal in borderline or established hypertension.Supported by the Swiss National Science Foundation     

Serial measurements of plasma renin activity,aldosterone and cortisol during percutaneous transluminal angiaplasty of the renal artery in man

Fifteen patients (eight men, seven women) with hypertension and renal artery stenosis underwent dilation of the stenosis by percutaneous transluminal renal angioplasty (PTRA). During and shortly after this treatment the effects on the renin-angio-tensin-aldosterone system and blood pressure were studied. Plasma renin activity (PRA) was measured in peripheral blood and in renal venous blood during the PTRA. PRA increased in peripheral blood during PTRA as a result of an immediate significant rise in renal venous plasma renin activity by 132 ± 134% (P < 0.01) on the dilated side. PRA in the contralateral renal vein was close to that in peripheral blood. Within 10 min after PTRA i:here was a significant increase in serum aldosterone from 439 ± 343 to 774 ± 635 pmol l-¹ (P < 0.025), while serum cortisol remained unchanged. The aldosterone increase was most probably mediated by angiotensin II. Systolic and diastolic blood pressures were unchanged during PTRA in spite of renin and aldosterone increases, suggesting that antihypertensive factors counteract the pressor effects of a physiologically relevant increase in PRA.     

Effect of ageing on circadian rhythms of plasma renin and aldosterone in mesor-hypertensive women

This study investigated the changes in circadian rhythms of plasma renin activity (PRA) and plasma aldosterone (PA) which occur in essential mesor-hypertensive women, increasing in age. Systemic blood samples were taken throughout a 12 h period from both mesor-hypertensive women and clinically healthy women (control). The women in each group were either post-menopausal or had normal menstrual cycles. A cosinor method of temporal series was the analysis employed to compute the properties of PRA and PA circadian rhythms.The clearest effect of ageing, recorded in essential mesor-hypertensive women, is a decrease in circadian mesor of PRA cycle (P = 0.002). The age-related changes in clinically healthy women appear to be more extensive and involve a decrease for both mesor (P < 0.001) and amplitude (P = 0.007) of PRA circadian rhythm. These disparities are convincing evidence for a non-physiological decline of the RAAS rhythmic function in the aged essential mesor-hypertensive women. The lack of an age-associated decrease in circadian PRA amplitude merits a pathophysiological and clinical investigation because it is a possible risk factor for post-menopausal, essential mesor-hypertensive women.     

Salivary electrolytes in digitalis-treated patients with and without raised aldosterone excretion

Summary Salivary electrolytes (sodium, potassium, calcium) were measured in 10 digitalis-treated patients receiving spironolactone. Two of them could be identified as digitalis-intoxicated. The results showed good correlation with digoxin concentration in serum irrespective of whether aldosterone excretion was increased or not. This leads to the suggestion that the salivary electrolyte changes effected by digitalis treatment are independent from secondary aldosteronism and spironolactone therapy.     

Association of spironolactone treatment and arterial stiffness and cardiovascular disease in hypertensive patients

IntroductionThe aim of the current study was to evaluate the association of spironolactone and arterial stiffness and composite cardiovascular disease (CVD, including coronary heart disease, congestive heart failure and ischemic stroke) in hypertensive patients.Material and methodsBaseline data were collected and arterial stiffness was presented by carotid-femoral pulse wave velocity (cf-PWV) using applanation tonometry. Serum levels of fasting plasma glucose, total cholesterol, C-reactive protein and creatinine were measured using an automatic biochemistry analyzer. Plasma aldosterone concentration and plasma renin activity were determined by radioimmunoassay. The associations of spironolactone and arterial stiffness and composite CVD were evaluated.ResultsCompared to patients without spironolactone (n = 274), those with spironolactone (n = 170) were older and more likely to have diabetes and chronic heart failure. No differences in antihypertensive medications used were observed except for spironolactone. Mean number of antihypertensive medications used was significantly higher in the spironolactone group (2.6 ±0.8 vs. 2.2 ±0.6). Compared to patients without spironolactone, those with spironolactone had significantly lower cf-PWV (9.4 ±1.8 vs. 10.1 ±2.2 m/s). After adjustment for covariates, spironolactone was still associated with 10% lower risk of arterial stiffness, with a 95% confidence interval (CI) of 0.85–0.97. In patients without arterial stiffness, after adjustment for covariates, no significant association of spironolactone and composite CVD was observed. However, in patients with increased arterial stiffness, after adjustment for covariates, spironolactone was still independently associated with 11% lower risk of composite CVD (95% CI: 0.83–0.97).ConclusionsSpironolactone treatment is independently associated with lower cf-PWV and lower prevalence of composite CVD in patients with increased arterial stiffness.     

An early effect of acute plasma volume expansion in humans on serum erythropoietin concentration

The effect of acute plasma volume change in humans on serum erythropoietin [EPO]_s, plasma active renin [REN] and plasma aldosterone [ALDO] concentrations was examined. Plasma volume (PV) expansion was induced by intravenous infusion of 150 ml (30g) of plasma albumin and 500 ml of physiological saline. The [EPO]_s decreased by 14.3% (corrected values for PV expansion) and remained decreased for 5 h. The [REN] was decreased by more than 25% during the day of the experiment and [ALDO] by more than 60%. Only a weak positive correlation was found between [EPO]_s and [REN] (r = 0.35;P < 0.05) but a lack of correlation between changes in PV and [EPO]_s as well as between [EPO]_s and [ALDO] was seen. We postulated that in healthy men an acute PV expansion by 10% to 17.5% would not appear to promote stimulation of EPO synthesis for at least 11 h. Since a weak positive correlation was observed between [EPO]_s and [REN] and a lack of correlation between [EPO]_s and [ALDO], it would seem that there is no direct link between [REN] and [ALDO] and erythropoietin synthesis in healthy subjects.A preliminary report on the topic was presented at the 33rd German National Congress on Sportsmedicine, Padeborn, Germany     

Effect of spironolactone on hypertrophy of left ventricular myocardium in Wistar rats with experimental uremia

Chronic renal failure was modeled in rats by partial nephrectomy. Blood pressure, heart rate, concentrations of aldosterone, urea, creatinine, electrolytes, and protein, index of hypertrophy of visceral organs, and 24-h diuresis were evaluated. In rats treated with spironolactone, the index of myocardial hypertrophy did not considerably differ from that in sham-operated animals, whereas in untreated rats the test parameters considerably differ from the control. We concluded that the blockade of aldosterone receptors with spironolactone produced a cardioprotective effect in Wistar rats with subtotal nephrectomy. __________ Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 145, No. 6, pp. 659–662, June, 2008     

Effects of angiotensin II on arterial pressure,renin and aldosterone during exercise

Summary To evaluate the effect of isotonic exercise on the response to angiotensin II, angiotensin II in saline solution was infused intravenously (7.5 ng · kg⁻¹ · min⁻¹) in seven normal sodium replete male volunteers before, during and after a graded uninterrupted exercise test on the bicycle ergometer until exhaustion. The subjects performed a similar exercise test on another day under randomized conditions when saline solution only was infused. At rest in recumbency angiotensin II infusion increased plasma angiotensin II from 17 to 162 pg · ml⁻¹ (P<0.001). When the tests with and without angiotensin II are compared, the difference in plasma angiotensin II throughout the experiment ranged from 86 to 145 pg · ml⁻¹. The difference in mean intra-arterial pressure averaged 17 mmHg at recumbent rest, 12 mmHg in the sitting position, 9 mmHg at 10% of peak work rate and declined progressively throughout the exercise test to become non-significant at the higher levels of activity. Plasma renin activity rose with increasing levels of activity but angiotensin II significantly reduced the increase. Plasma aldosterone, only measured at rest and at peak exercise, was higher during angiotensin II infusion; the difference in plasma aldosterone was significant at rest, but not at peak exercise. In conclusion, the exercise-induced elevation of angiotensin II does not appear to be an important factor in the increase of blood pressure. It is suggested that the vasodilating mechanisms in the working muscles and the vasoconstricting mechanisms in the non-working vascular beds are powerful and dominant during isotonic exercise and attenuate the opposing or additive vasoconstrictor effects of angiotensin II. The negative feedback effect of angiotensin II on renal renin secretion, however, is not inhibited by exercise.     

Evidence for a subgroup of essential hypertensives with non-suppressible excretion of aldosterone during sodium loading

Summary In patients with grade I and II essential hypertension studied during sodium loading (Na⁺ excretion above 175 meq·d^–1) we found a bimodal behaviour of aldosterone excretion and could distinguish two groups of patients: In the major part of essential hypertensives sodium loading led to a suppression of aldosterone excretion below 6 µg·d^–1, which is the highest control value during sodium loading, with an average of 2.7±1.4 (SD) µg·d^–1. Aldosterone excretion in a second group of patients was not suppressible below 6 µg·d^–1 despite forced sodium loading; it resulted in an average value of 10.0±3.0 (SD) µg·d^–1. During sodium deprivation or free sodium intake, aldosterone excretion in the first group of patients followed exactly the behaviour of normotensive controls, while in the second group of essential hypertensives the correlation of aldosterone excretion and log. Na excretion or log. Na⁺/K⁺ ratio in 24 h urine (r=–0.59) was far below the control value ofr=–0.87. Serum potassium concentration during sodium loading was significantly (p<0.001) lower (3.81±0.44 meq·l^–1) in the essential hypertensives with non-suppressible aldosterone excretion compared to those with suppressible aldosterone excretion (4.26±0.37 meq·l^–1). The blood pressure response to treatment with 200 mg spironolactone·d^–1 was better (p<0.05) in patients with non-suppressible aldosterone excretion compared to the essential hypertensives with normal aldosterone regulation. The plasma renin activity of both groups of patients was not significantly different, however, a tendency prevailed towards lower PRA-values in the patient group with non-suppressible aldosterone excretion during sodium loading.With the technical help of Mrs. R. Schendschilorz and Mrs. G. Suckau