Renin and Aldosterone Relationships in Manic Depressive Psychosis

1977 ◽  
Vol 131 (6) ◽  
pp. 575-581 ◽  
Author(s):  
R. P. Hullin ◽  
T. C. Jerram ◽  
M. R. Lee ◽  
M. J. Levell ◽  
S. P. Tyrer
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Primary Defect ◽  
Sodium Potassium ◽  
Manic Depressive Psychosis ◽  
Manic Depressive ◽  
Aldosterone Production ◽  
Depressive Patients

SUMMARY The paper describes a two-month period of study in four bipolar manic-depressive patients in a metabolic ward. Plasma renin activity, packed cell volume, plasma sodium and potassium were determined at intervals. Twenty-four-hour urinary sodium, potassium and creatinine were also estimated daily. Aldosterone production rate was measured on two occasions for each patient. Three of the patients showed at least one episode each of mania and depression during the study, while the fourth patient, who was receiving prophylactic lithium throughout, had one ten-day depressive episode but was otherwise normal.No obvious relationship between mood and plasma renin activity was observed, but the group showed a high resting renin activity, a blunted renin response to posture, and inappropriate aldosterone production rates for the renin activity found.It is postulated that a primary defect in the aldosterone-renin system may be present in bipolar manic-depressive psychosis.

VARIATIONS IN PLASMA RENIN ACTIVITY AND URINARY ALDOSTERONE EXCRETION IN NORMAL SUBJECTS AFTER SALT RESTRICTION AND ACUTE PITUITARY INHIBITION WITH 6-DEHYDRO-16-METHYLENE HYDROCORTISONE

1971 ◽  
Vol 67 (1) ◽  
pp. 159-173
Author(s):  
A. Peytremann ◽  
R. Veyrat ◽  
A. F. Muller
Keyword(s):  
Plasma Renin Activity ◽  
Salt Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Inhibitory Effect ◽  
Renin Activity ◽  
Sodium Balance ◽  
Experimental Conditions ◽  
Salt Restriction ◽  
Aldosterone Production

ABSTRACT Variations in plasma renin activity and urinary aldosterone excretion were studied in normal subjects submitted to salt restriction and simultaneous inhibition of ACTH production with a new synthetic steroid, 6-dehydro-16-methylene hydrocortisone (STC 407). At a dose of 10 mg t. i. d. this preparation exerts an inhibitory effect on the pituitary comparable to that of 2 mg of dexamethasone. In subjects maintained on a restricted salt intake, STC 407 does not delay the establishment of an equilibrium in sodium balance. The increases in endogenous aldosterone production and in plasma renin activity are also similar to those seen in the control subjects. A possible mineralocorticoid effect of STC 407 can be excluded. Under identical experimental conditions, the administration of dexamethasone yielded results comparable to those obtained with STC 407.

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.

EFFECT OF ADRENOCORTICOTROPHIC AND GROWTH HORMONES ON ALDOSTERONE PRODUCTION AND PLASMA RENIN ACTIVITY IN CHRONICALLY HYPOPHYSECTOMIZED SODIUM-DEFICIENT RATS

1970 ◽  
Vol 47 (2) ◽  
pp. 243-250 ◽  
Author(s):  
M. PALKOVITS ◽  
W. DE JONG ◽  
B. VAN DER WAL ◽  
D. DE WIED
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Normal Diet ◽  
Secretory Response ◽  
Renin Activity ◽  
Deficient Diet ◽  
Sodium Deficiency ◽  
Long Term Treatment ◽  
Aldosterone Production ◽  
Hypophysectomized Rats

SUMMARY Hypophysectomy abolishes the aldosterone secretory response to sodium deficiency in rats. Sodium deficiency causes a significant increase in plasma renin activity in chronically hypophysectomized rats which is of the same order as that found in intact animals. Long-term treatment with either adrenal maintenance doses of corticotrophin (ACTH) or with growth hormone (STH) did not affect the low rate of aldosterone production of hypophysectomized rats on a sodium-deficient diet. However, ACTH and STH given simultaneously restored the aldosterone secretory response to sodium deficiency in chronically hypophysectomized rats. The plasma renin activity of hypophysectomized rats on a sodium-deficient or a normal diet remained unaltered during treatment with either ACTH or STH or with the two hormones given simultaneously. This was also reflected in the systolic blood pressure of rats which, under the conditions used, did not change when the animals were sodium-deficient, or after hypophysectomy or hormone treatment. These results indicate that the effect of STH, in restoring the aldosterone secretory response to sodium deficiency in the presence of adrenal maintenance doses of ACTH in chronically hypophysectomized rats, is independent of changes in the renin-angiotensin system.

Effect of Chronic Low-Dose Arginine Vasopressin Infusion on Body Fluid Homoeostasis during Adaptation from a High-to a Low-Sodium Diet in Normal Man

1993 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
M. Sutters ◽  
D. J. S. Carmichael ◽  
S. L. Lightman ◽  
W. S. Peart
Keyword(s):  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Angiotensin I ◽  
Salt Restriction ◽  
Plasma Sodium Concentration ◽  
Plasma Arginine

1. A diuresis occurs within the first 36 h of salt restriction. A decline in plasma arginine vasopressin concentration may contribute to both the diuresis and antinatriuresis. 2. We have studied six normal human subjects during 36 h of dietary sodium restriction. In one study subjects received an intravenous infusion of D-glucose, and in the other an infusion of arginine vasopressin (6 fmol min−1 kg−1). 3. In the D-glucose phase plasma arginine vasopressin concentration fell (1.77 +034 to 1.02 +0.13 pg/ml), urine flow increased (67.9 +113 to 89.8 + 17.1 ml/h), haemoconcentration occurred (packed cell volume 40.8 +0.3 to 42.8 +03%, protein concentration 71.6 +03 to 74.5 + 0.6 g/l), plasma sodium concentration fell (140 +0.2 to 138 +0.2 mmol/l) and plasma renin activity increased (1600+153 to 3700 + 356 pg of angiotensin I h−1 ml−1). 4. In the arginine vasopressin phase plasma arginine vasopressin concentration remained constant (13 + 0.13 to 134 +0.11 pg/ml), the diuresis was reversed (65.7 +9.9 to 52.1 +8.9 ml/h), plasma sodium concentration fell further (139.8 +0.4 to 136.1 +0.4 mmol/l), the rise in plasma renin activity was reduced (arginine vasopressin 2552 + 292; D-glucose, 3700 + 356 pg of angiotensin I h−1 ml−1) and creatinine clearance was lower in the last 12 h of salt restriction (arginine vasopressin, 96.1 +6.9; D-glucose 116.5 + 6.8 ml/min). Renal sodium excretion was unaffected by arginine vasopressin infusion. 5. We conclude that the fall in plasma arginine vasopressin concentration during dietary salt restriction, whilst not affecting renal sodium excretion, may be important in the regulation of plasma sodium concentration, plasma renin activity and glomerular filtration.

Adenovirus-mediated human prostasin gene delivery is linked to increased aldosterone production and hypertension in rats

2003 ◽  
Vol 284 (4) ◽  
pp. R1031-R1036 ◽  
Author(s):  
Cindy Wang ◽  
Julie Chao ◽  
Lee Chao
Keyword(s):  
Blood Pressure ◽  
Gene Transfer ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Elevated Plasma ◽  
Aldosterone Production ◽  
Renal Kallikrein

Prostasin has been demonstrated to be an activator of epithelial sodium channels in cultured renal and bronchial epithelial cells. In this study, we evaluated the effects of adenovirus-mediated gene transfer of human prostasin on blood pressure regulation and sodium reabsorption in Wistar rats. Expression of human prostasin mRNA was identified in rat adrenal gland, liver, kidney, heart, lung, and aorta, and immunoreactive human prostasin was detected in the circulation and urine of rats receiving prostasin gene transfer. A single injection of adenovirus carrying the prostasin gene caused prolonged increases in blood pressure for 3–4 wk. Blood pressure increase was accompanied by elevated plasma aldosterone levels and reduced plasma renin activity. The increase in blood pressure and plasma aldosterone levels as well as the reduction of plasma renin activity correlated with the expression of human prostasin transgene. Elevated plasma aldosterone levels were detected at 3 days after gene transfer before the development of hypertension, indicating that stimulation of mineralocorticoid production is the primary target of prostasin. Prostasin gene transfer significantly reduced urinary K+ excretion but increased urinary Na+ and kallikrein excretion. Elevated renal kallikrein levels promote natriuresis, which may lead to sodium escape and prevent further increases of blood pressure after prostasin gene transfer. In summary, these results suggest that prostasin participates in blood pressure and electrolyte homeostasis by regulating the renin-angiotensin-aldosterone and kallikrein-kinin systems.

Glucocorticoid Inhibition of Mineralocorticoid Action in the Rat

1984 ◽  
Vol 67 (3) ◽  
pp. 329-335 ◽  
Author(s):  
C. J. Kenyon ◽  
N. A. Saccoccio ◽  
D. J. Morris
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Long Term Effects ◽  
Physiological Dose ◽  
Acute Changes ◽  
Adrenalectomized Rats

1. The mineralocorticoid activity of corticosterone based on acute changes in urinary Na+/K+ ratios in adrenalectomized rats was 1000 times less than that of aldosterone. However, corticosterone had only kaliuretic actions whereas aldosterone had both antinatriuretic and kaliuretic properties. Corticosterone inhibited the antinatriuretic actions of aldosterone. 2. Adrenalectomized rats infused continuously with a physiological dose of corticosterone (1 mg/day) were 5 times less sensitive to the antinatriuretic and 25 times less sensitive to the kaliuretic actions of aldosterone when administered acutely than were control adrenalectomized rats. 3. The long term effects of infusions of physiological doses of aldosterone and corticosterone were assessed in adrenalectomized rats maintained in metabolic cages. Aldosterone lowered plasma renin activity and reduced fluid (0.3% NaCl) intake; these effects were diminished when aldosterone and corticosterone were infused simultaneously. Plasma renin activity and fluid intake were correlated in long term infusion experiments. Both hormones had hypokalaemic effects but these were not additive. Corticosterone, but not aldosterone, increased systolic blood pressure and plasma sodium levels. 4. We conclude that glucocorticoid effects on water and electrolyte metabolism are different from those of mineralocorticoids, that glucocorticoids may antagonize mineralocorticoid effects and that interactions between mineralocorticoids and glucocorticoids may be important in long term blood pressure regulation.

Urinary Kallikrein and Plasma Renin during the Reversal of Renovascular Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 263s-266s
Author(s):  
O. P. Gulati ◽  
O. A. Carretero ◽  
T. Morino ◽  
N. B. Oza
Keyword(s):  
Plasma Renin Activity ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Renin Activity ◽  
Experimental Hypertension ◽  
Urinary Kallikrein ◽  
Sodium Potassium ◽  
Water Excretion

1. Urinary kallikrein, sodium, potassium and water excretion, and plasma renin activity were measured before and during the reversal of experimental hypertension produced by unclamping the renal artery in rats. 2. Kallikrein excretion decreased significantly after unclamping, suggesting that it does not play a significant role in the reversal of hypertension. 3. A decrease in plasma renin activity coupled with a slight increase of sodium excretion was observed, indicating that these might participate in the reversal of hypertension.

scholarly journals Plasma renin activity, serum aldosterone concentration and selected organ damage indices in essential arterial hypertension

2021 ◽  
Vol 17 (1) ◽  
pp. 9-18
Author(s):  
Tomasz Pizoń ◽  
Marek Rajzer ◽  
Wiktoria Wojciechowska ◽  
Tomasz Drożdż ◽  
Dorota Drożdż ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Arterial Hypertension ◽  
Plasma Renin ◽  
Organ Damage ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Damage Indices ◽  
Serum Aldosterone ◽  
Lower Egfr ◽  
Aldosterone To Renin Ratio

IntroductionThe aim of this study was to assess the relations between plasma renin activity (PRA), serum aldosterone concentration (ALDO) and selected asymptomatic organ damage (AOD) indices in mild primary arterial hypertension (AH).Material and MethodsWe measured PRA, ALDO, and selected AOD indices (carotid-femoral pulse wave velocity (cfPWV), central aortic pulse pressure (cPP), estimated glomerular filtration rate (eGFR)) in 122 patients with untreated AH.ResultsPatients with high PRA (≥ 0.65 ng/ml/h) were characterized by lower plasma sodium and aldosterone to renin ratio (ARR), higher ALDO, but a similar level of AOD indices compared to patients with low PRA. cfPWV (p = 0.04) and cPP (p = 0.019) increased with ARR, while eGFR decreased with ALDO (p = 0.008). Only eGFR was independently correlated with ALDO. In subjects with simultaneously high PRA and ARR values, we found significantly higher cfPWV (p = 0.02) and cPP (p = 0.04) and lower eGFR (p = 0.02) than in those with high PRA but low ARR values.ConclusionsAssessment of the influence of the renin-angiotensin-aldosterone system (RAAS) on AOD should include the relationship between renin and aldosterone. The PRA itself has no predictive value for AOD. More advanced arterial stiffness and renal impairment are associated with increased PRA and ARR. The RAAS activity might be useful in AOD prediction and hypertension severity assessment.

Sign in / Sign up

Export Citation Format

Share Document