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 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was undertaken to investigate the effect of a continuous calcium infusion on the plasma levels of aldosterone, renin activity, and cortisol in six anephric and four nonnephrectomized patients on regular hemodialysis. In both groups, a significant increase in whole blood ionized calcium (b-Ca2+) was demonstrated. A significant increase in plasma aldosterone (PAC) was noted in the nonnephrectomized patients, in whom the rise in PAC correlated with the increase in b-Ca2+. However, in the anephric patients only a smaller and insignificant increase in PAC was found. No significant changes were demonstrated in plasma cortisol or renin activity, nor in potassium or sodium concentrations in either group. It is concluded that ionized calcium influences the plasma levels of aldosterone in uremic patients on regular hemodialysis.
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PMID:Calcium-dependent aldosterone secretion in anephric and nonnephrectomized patients on regular hemodialysis. 23 32

The circadian rhythm of plasma aldosterone (PAC) and cortisol concentration (PCC), and renin activity (PRA) was measured in five steroid and five non-steroid treated kidney transplanted patients--all with denervated kidney grafts--and compared with four normal controls and two steroid-treated patients with non-renal disease and thus normal renal innervation. The non-steroid treated patients had a normal circadian thythm of PAC and PCC, but without variation of PRA, suggesting that denervation of the kidneys has no influence on the circadian rhythm of PAC. In both steroid treated groups the PAC showed an inverse diurnal variation--now correlating to the diurnal variation in PRA. The inverse circadian rhythm of PAC in patients with suppressed ACTH secretion remains unexplained, but is in accordance with the nocturnal peak of sodium and water excretion in steroid treated patients.
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PMID:Circadian rhythm of plasma aldosterone and plasma renin activity in steroid and non-steroid treated kidney transplanted patients. 33 62

The present investigation was carried out on 17 male patients, 2 of whom nephrectomized, affected by terminal renal failure on regular 4 h dialysis three times a week. Plasma prolactin (PRL), aldosterone (PA) and renin activity (PRA) were determined by radioimmunoassay before, and after the 1st, 2nd and 3rd h of hemodialysis. High levels of PRL were found in 9 nonnephrectomized patients; during the 1st and 2nd h of dialysis means values of PRL showed a slight tendency to increase, whilst during the 3rd h values decreased to predialysis concentrations. In one case a fall in PRL levels immediately after nephrectomy was observed but in another patient who came to our attention after surgery, PRL was significantly increased with values higher than those usually found in nonnephrectomized patients. PRA was elevated in 10 patients and showed no significant modifications during hemodialysis. PAC was high in 8 patients and decreased significantly during hemodialysis. A drop in sodium and potassium levels and a decrease in body weight during dialysis were also observed. These results suggest that in uremia the high levels of PRL are not consequent to hydroelectrolyte disorders or to a condition of hyperaldosteronism, since these parameters present a different pattern during hemodialysis.
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PMID:Prolactinemia during hemodialysis: lack of correlation with sodium, potassium and renin-aldosterone system. 90 75

Previous studies have demonstrated a renal Na+ conservation during repeated days of exercise in the heat. The present study was intended to describe the role of plasma aldosterone (PAC) in reducing urine Na+ losses during and after 60 min of exercise (60% VO2max) in a warm environment (30 degrees C, 50-53% relative humidity). Additional measurements were made of plasma renin activity (PRA) in an effort to demonstrate the relationship between PRA and PAC. This study shows that a single bout of exercise can significantly reduce urine Na+, Cl-, and H20 excretions for up to 48 hours. Both PRA and PAC were significantly elevated during and immediately after exercise and returned to the pre-exercise level within 6-12 hours of recovery. Subsequently, ingestion of 180 mEq of Na+ each day with ad libitum water intake results in an increased NaCl storage and an expansion of the extracellular volume.
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PMID:Exercise induced sodium conservation: changes in plasma renin and aldosterone. 101 55

Cardiovascular parameters, hematocrit (Ht), plasma electrolytes, renin activity (PRA) and aldosterone concentration (PAC) were measured in 12 normal human subjects (6 males and 6 females) eating an ad lib diet. At 8 AM, volunteers assumed the following postural changes: 1 hour supine, then 2 hours upright and finally 1 hour supine. Orthostatism induced the following changes: heart rate, systolic and diastolic blood pressure increased immediately; Ht rose significantly at the 5th min in males but not in females; Plasma sodium showed no variations but potassium increased after 30 min; PRA rose significantly at the 5th min and, after 120 min of orthostatism, was found to be 3 times greater than its value after recumbency; and PAC increased significantly at the 15th min and exhibited a plateau 4.5 times its basal values after 90 min of upright posture. When subjects returned to the supine position all the parameters, except PAC decreased. During active orthostatism, a significant correlation was found between PAC and plasma potassium, but correlation was closer between PAC and PRA and between PAC and PRA + potassium. It can be concluded that the renin-angiotensin system is a more potent stimulus for aldosterone secretion than plasma potassium in normal man assuming postural changes. The results presented here can be applied to the development of a short posture test in non-hospitalized patients.
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PMID:A kinetic study of plasma renin and aldosterone during changes of posture in man. 124 91

The aim of the present study is to explore whether the renal and cardiovascular response to clonidine in type II diabetic patients is different from that in control subjects, and to clarify the role of central alpha 2-receptor in the regulation of cardiovascular response and sodium handling in type II diabetes mellitus (DM). Thirty-five diabetic inpatients aged 30-71 years (54.1 +/- 9.7) and ten control subjects (N) were enrolled in this study after their fasting plasma glucose had been improved. To evaluate the peripheral sympathetic nerve activity, 24-hour urinary catecholamine was measured, and pulse rate (PR) responses to a 30-second standing test was determined. On another day, blood pressure (BP), PR, plasma norepinephrine (PNE), cyclic AMP (p-cAMP), renin activity (PRA), aldosterone (PAC) and growth hormone (p-GH) were measured at 0, 30, 60, 90, 120, 150, 180 minutes following the oral administration of clonidine (150 micrograms). Type II DM were classified as DM with hyper-response (DM-HR, n = 12) when their PR decreased after clonidine more than that of N, and if not, they were classified as DM with normal response (DM-NR, n = 23). Urinary catecholamine excretions in type II DM were within the normal range. BP, PNE and p-cAMP were markedly decreased with clonidine in similar fashion in DM-NR, DM-HR and N. The percent changes of PNE were correlated positively with the changes of p-cAMP in both N and DM-NR (r = 0.660 and 0.449, respectively), but not in DM-HR. No significant difference in the changes of p-GH (delta p-GH) and integral of GH (the area under the curve) following clonidine administration was observed in the three groups. The decrease in PR was correlated with neither delta p-GH (N: r = 0.082, DM-NR: r = -0.400, DM-HR: r = 0.242) or integral of GH (N: r = 0.191, DM-NR: r = 0.382, DM-HR: r = 0.162). The fractional excretion of sodium (FENa) decreased in N (p < 0.01), increased in DM-NR (p < 0.05) and did not change in DM-HR. The changes of FENa were not correlated with those of PRA and PAC.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Altered responses of heart rate, renal sodium handling and plasma growth hormone to clonidine in type II diabetic patients]. 133 89

A placebo-controlled, double-blind crossover study was undertaken in 10 normal subjects to examine the effects of arotinolol (10 mg bid), a nonselective beta blocker with alpha-blocking activity, on exercise capacity and hormone levels during exercise after a 2-week treatment period. Maximal oxygen uptake (VO2 max) and blood lactic acid concentration (LA) were measured during progressive exercise testing. An exercise intensity equivalent to 4 mmol/l of LA was used for the constant workload exercise test. Humoral factors were measured after 20 minutes of constant workload exercise. The administration of arotinolol significantly decreased systolic blood pressure and heart rate at rest and during exercise, but diastolic blood pressure did not change. No significant difference was found between arotinolol and placebo with regard to VO2 max and maximal workload. Plasma renin activity (PRA), aldosterone (PAC), and norepinephrine (NE) levels at rest and during exercise did not differ between the two treatments. In contrast, plasma epinephrine (EN) levels at rest and during exercise were significantly greater with arotinolol. Atrial natriuretic peptide (ANP) at rest did not differ between the two treatments. However, exercise caused a significant increase in ANP after arotinolol treatment. These findings suggest that arotinolol decreases blood pressure and heart rate without affecting exercise capacity.
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PMID:Effects of arotinolol on exercise capacity and humoral factors during exercise in normal subjects. 138 11

The relationship between plasma renin (PRC) and aldosterone (PAC) concentrations was determined in 83 normal third trimester pregnant women (P), 50 women with pregnancy-induced hypertension (PIH), and 80 age-matched nonpregnant women not taking oral contraceptives (NP). Normal pregnant women had a slightly higher 24-h urine sodium: creatinine ratio than the other groups (P less than .001) (NP: 10 +/- 4 v P: 15 +/- 8 v PIH: 12 +/- 7; mean +/- SD). Both PRC and PAC were higher in normal pregnant women as was the ratio PAC:PRC [normal pregnant 195 (158 to 337) v nonpregnant 130 (101 to 209), median (interquartile range); P less than .001]. This was accompanied by a slightly reduced slope (sensitivity) of the logPRC-logPAC relationship in normal pregnant women (P less than .05). Women with PIH had reduced PRC and PAC compared with normal pregnant women but a two-fold greater increase in PAC:PRC ratio [PIH 411 (277 to 598) v normal pregnancy 195 (158 to 337), P less than .001], with a rise in the slope (sensitivity) of the logPRC-logPAC relationship in women with PIH (P less than .001). Thus there is proportionately greater aldosterone release in the third trimester of normal pregnancy than in nonpregnant women. This preferential increase in aldosterone may be due to altered adrenal sensitivity to angiotensin II or may reflect enhanced nonangiotensin stimulation of aldosterone during pregnancy. Women with PIH have reduced PRC and PAC but relatively greater stimulation of aldosterone than normal pregnant women, possibly due to enhanced sensitivity of the adrenal glands to angiotensin II.
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PMID:Renin-aldosterone relationships in pregnancy-induced hypertension. 152 61

The study was undertaken to clarify the role of atrial natriuretic polypeptide (ANP) in essential hypertension (EH). Plasma levels of alpha-human ANP (alpha hANP) were measured in 13 normal subjects, 25 patients with EH, 5 patients with primary aldosteronism (PA), 3 patients with renovascular hypertension (RVH) and 3 patients with pheochromocytoma (PC). Plasma level of alpha hANP (normal: 38.1 +/- 20.5pg/ml) was high in all hypertensive subjects. Synthetic alpha hANP was intravenously administrated to these subjects as follows: first a dose of 0.01 microgram/kg/min for 30 minutes, second a dose of 0.03 microgram/kg/min for 30 minutes, and then in normal subjects and EH 0.03 microgram/kg/min with a dose of 6.5 micrograms/kg/min of metoclopramide (MC) for 30 minutes. After the infusion of 0.01 microgram/kg/min alpha hANP, arterial blood pressure was significantly depressed in EH, RVH and PA, but not in PC. Marked diuretic and natriuretic responses were observed with increase in creatinine clearance and fractional sodium excretion in EH, RVH and PA, but not in PC. Sodium clearance/lithium clearance was slightly increased after infusion of 0.03 microgram/kg/min of alpha hANP in hypertensive subjects. Plasma renin activity did not change in low and normal renin EH and PA after infusion of either dose of alpha hANP, but was suppressed after 0.03 microgram/kg/min of alpha hANP in normal subjects and high renin EH, RVH and PC. Plasma aldosterone concentration was suppressed after either dose of alpha hANP in normal subjects and in EH, RVH and PC, but not in PA. Plasma cGMP concentration and urinary cGMP excretion were decreased after either dose of alpha hANP in both normal and hypertensive subjects. Furthermore, the decrease of PAC by alpha hANP was normalized by MC in normal subjects and EH. The rise in plasma cGMP by alpha hANP was suppressed by MC in both normal subjects and EH, but no changes were observed in arterial blood pressure and natriuretic response. These results suggest that alpha hANP secretion increases with elevation of blood pressure in EH, improving increase of circulatory blood volume, and alpha hANP may play a role in elevating blood pressure in EH. Moreover, it is considered that ANP increases sodium and water excretion through its effect on both renal glomeruli and distal tubules in EH. Hypotensive and natriuretic effects of ANP in EH may be concerned with dopaminergic activity which are probably related to the production of cGMP in the vascular wall and inhibition of the excretion of aldosterone in the adrenal cortex.
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PMID:[The significance of atrial natriuretic polypeptide in the cause of essential hypertension]. 165 13

The effect of xipamide on plasma alpha-atrial natriuretic peptide and the renin-aldosterone-kallikrein system have been studied in 12 healthy men, using a double-blind cross-over design. After a run-in period on placebo of 1 week, the subjects were treated with either placebo (n = 6) or xipamide 20 mg once daily (n = 6) for 16 weeks and were then switched to the alternative medication for another 16 weeks. The plasma concentration of alpha-atrial natriuretic peptide fell after 1 week of xipamide administration and increased during prolonged xipamide administration but remained reduced. The changes in plasma alpha-ANP observed after 1 week of xipamide were negatively correlated with the changes in hematocrit and hemoglobin. Plasma renin activity (PRA), aldosterone concentration (PAC), and urinary excretion of aldosterone and kallikrein increased after 1 week of xipamide administration, levelled off during the second and fourth weeks, but remained elevated during further prolonged xipamide administration for 16 weeks. The xipamide-induced changes in PRA and PAC were positively correlated with the changes in the hematocrit and hemoglobin. The changes in plasma renin, aldosterone, and alpha-atrial natriuretic peptide during xipamide administration may be related to diuretic-induced volume contraction.
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PMID:Hormonal effects of the diuretic xipamide in healthy men. 183 91


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