CATECHOLAMINES, RENIN AND ALDOSTERONE IN POSTURAL HYPOTENSION

1969 ◽  
Vol 62 (3) ◽  
pp. 399-410 ◽  
Author(s):  
H. Hedeland ◽  
J.-F. Dymling ◽  
B. Hökfelt
Keyword(s):  
Plasma Renin Activity ◽  
Potassium Chloride ◽  
Healthy Subjects ◽  
Postural Hypotension ◽  
Plasma Renin ◽  
The Other ◽  
Renin Activity ◽  
Deficient Diet ◽  
Urinary Catecholamines ◽  
Salt Restriction

ABSTRACT The interrelation between catecholamines, renin and aldosterone has been studied in two patients with postural hypotension. Under basal conditions both patients presented subnormal values for urinary catecholamines and plasma renin activity. Urinary aldosterone was subnormal in one of the patients and normal in the other. Attempts to increase catecholamine production using insulin induced hypoglycaemia were ineffective in both patients. Tilting was performed in one of the patients but this did not change the urinary catecholamines whereas the plasma renin levels increased in relation to the degree of tilting in a manner known to occur in healthy subjects. In both patients the infusion of noradrenaline was accompanied by an increase in plasma renin activity. On a sodium deficient diet both patients conserved sodium at the renal level, although the response seemed delayed in one of them. During equilibration the urinary catecholamines did not increase whereas the plasma renin and urinary aldosterone values rose in both patients; again the response seemed delayed in one patient. Potassium chloride was administered orally to one of the patients and resulted in an increased urinary output of catecholamines and aldosterone. Our results indicate that baro- and/or osmoreceptor mechanisms can stimulate the production of renin and aldosterone adequately in response to salt restriction and tilting even in the presence of severe sympathetic insufficiency.

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.

Hypertension in Dahl salt-sensitive rats: biochemical and immunohistochemical studies

1992 ◽  
Vol 83 (1) ◽  
pp. 13-22 ◽  
Author(s):  
J. Bouhnik ◽  
J. P. Richoux ◽  
H. Huang ◽  
F. Savoie ◽  
T. Baussant ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
High Salt ◽  
Renin Activity ◽  
Deficient Diet ◽  
High Salt Diet ◽  
Salt Diet ◽  
Plasma Angiotensin

1. The renin-angiotensin and kinin-kallikrein systems of Dahl salt-sensitive and salt-resistant rats fed diets with different salt contents were analysed using biochemical and immunocytochemical techniques. 2. Blood pressure increased by 45% in salt-sensitive rats only, after 4 weeks on a high-salt diet. The plasma renin activity and plasma angiotensin II concentration remained at the same levels in salt-sensitive rats on the high-salt diet as on the normal salt diet, whereas the plasma renin activity and plasma angiotensin II concentration of salt-resistant rats fed the high-salt diet were lower. The plasma renin activity and the plasma angiotensin II concentration were elevated in both salt-resistant and salt-sensitive rats fed the salt-deficient diet but were much more elevated in salt-resistant than in salt-sensitive rats. 3. The kidney immunocytochemical data paralleled the data on plasma parameters. Salt-sensitive rats had fewer renin positive juxtaglomerular apparatuses than salt-resistant rats on the normal diet, and the increase on the sodium-deficient diet was also smaller in salt-sensitive rats. Salt-sensitive rats fed the high-salt diet and the standard diet had almost no angiotensin II immunoreactivity compared with the salt-resistant rats on the same diets. 4. The total renal kallikrein content of salt-sensitive rats was lower than that of salt-resistant rats on all three diets, as was the amount of kallikrein excreted in the urine on the standard and the high-salt diets. The differences resulted from a reduction in active kallikrein. The increase in kallikrein in salt-sensitive and salt-resistant rats on the salt-deficient diet was not significantly different. 5. There were similar changes in immunopositive kallikrein in the kidneys of salt-sensitive and salt-resistant rats with diet, with a large increase in kallikrein biosynthesis on the low-salt diet. The plasma concentration of high-molecular-mass kininogen was not significantly different in salt-sensitive and salt-resistant rats, but there was a significant increase in T-kininogen in salt-sensitive rats fed the high-salt diet. 6. In conclusion, the absence of decreases in the plasma renin activity and the plasma angiotensin II concentration in salt-sensitive rats fed the high-salt diet might partially explain the increase in blood pressure.

THE EFFECT OF INSULIN INDUCED HYPOGLYCAEMIA ON PLASMA RENIN ACTIVITY AND URINARY CATECHOLAMINES BEFORE AND FOLLOWING CLONIDINE (CATAPRESAN®) IN MAN

1972 ◽  
Vol 71 (2) ◽  
pp. 321-330 ◽  
Author(s):  
H. Hedeland ◽  
J.-F. Dymling ◽  
B. Hökfelt
Keyword(s):  
Plasma Renin Activity ◽  
Urinary Excretion ◽  
Adrenal Medulla ◽  
Sympathetic Nerve ◽  
Plasma Renin ◽  
Renin Activity ◽  
Nerve Endings ◽  
Urinary Catecholamines ◽  
A Minor ◽  
Noradrenaline And Adrenaline

ABSTRACT The present study was concerned with the relation of catecholamine production and plasma renin activity. The catecholamine production was measured as the urinary excretion of noradrenaline and adrenaline. Thirteen subjects were studied under basal conditions and also following insulin induced hypoglycaemia both before and during treatment with the imidazoline derivate clonidine. Before clonidine, hypoglycaemia produced a marked increase in catecholamine production and an elevation of plasma renin activity. These parameters were significantly correlated. Treatment with clonidine markedly suppressed noradrenaline production and plasma renin activity. Adrenaline production showed a minor decrease. During clonidine treatment insulin induced pronounced hypoglycaemia. In spite of this the increase in adrenaline production and plasma renin activity was less marked as compared to that before clonidine. There was no longer any significant correlation between catecholamine production and plasma renin activity. Our results indicate that sympathetic amines liberated from the adrenal medulla and/or the sympathetic nerve endings can stimulate renin production.

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.

The Effect of Mental Stress on Catecholamines, their Metabolites and Plasma Renin Activity in Patients with Essential Hypertension and in Healthy Subjects

1979 ◽  
Vol 57 (s5) ◽  
pp. 229s-231s ◽  
Author(s):  
W. Januszewicz ◽  
M. Sznajderman ◽  
B. Wocial ◽  
T. Feltynowski ◽  
T. Klonowicz
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Urinary Excretion ◽  
Mental Stress ◽  
Healthy Subjects ◽  
Plasma Renin ◽  
Renin Activity ◽  
Vanillylmandelic Acid ◽  
Before And After ◽  
Noradrenaline And Adrenaline

1. Ten patients with essential hypertension and ten healthy men were submitted to mental stress consisting of Kraepelin's arithmetic test combined with noise. Concentrations of plasma and urine catecholamines and of their metabolites as well as plasma renin activity before and after the test were studied. 2. In both groups a significant increase of noradrenaline and adrenaline in blood and noradrenaline in urine was observed. The urinary excretion of dopamine fell significantly in both groups after stress. 3. After mental stress a significant increase in urinary excretion of 3-methoxy-4-hydroxyphenylglycol was observed in both groups. The excretion of vanillylmandelic acid decreased significantly only in healthy subjects. 4. The plasma renin activity rose significantly in both groups but the increase was more pronounced in healthy subjects.

PLASMA RENIN ACTIVITY IN PANHYPOPITUITARISM

1972 ◽  
Vol 69 (3) ◽  
pp. 531-541 ◽  
Author(s):  
M. Murakami ◽  
R. Takeda ◽  
S. Morimoto ◽  
K. Hirasawa ◽  
K. Uchida ◽  
...  
Keyword(s):  
Serum Level ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Normal Subjects ◽  
The Other ◽  
Renin Activity ◽  
Sodium Restriction ◽  
Normal Limits ◽  
Furosemide Administration ◽  
Very High

ABSTRACT The response of plasma renin activity (PRA) to sodium restriction, furosemide and ACTH administration were studied in six patients with panhypopituitarism of various causes and in a patient with Addison's disease. In all the patients with panhypopituitarism, the basal levels of PRA were within normal limits and the responses of PRA and sodium homoeostasis to sodium restriction and furosemide administration were not significantly different from those of normal subjects. On the other hand, in an Addisonian patient the basal level of PRA was very high and this was further increased with a decrease in the serum level of sodium and an increase in the serum level of potassium after one day of sodium restriction. The administration of 1 mg of synthetic β1–24 ACTH every 12 hours for 2 days caused an increased plasma 11-OHCS and urinary 17-OHCS. with a decrease of sodium and an increase of potassium loss in the urine but failed to change PRA in patients with panhypopituitarism. In the Addisonian patient, ACTH did not influence the levels of plasma 11-OHCS, urinary 17-OHCS, PRA as well as serum and urinary electrolytes. From these results it is suggested that ACTH does not directly act on renin secretion and that PRA can adequately respond to various stimuli such as sodium restriction and furosemide administration in a condition of ACTH deficiency.

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.

scholarly journals SUN-189 A Case of Delayed Hypoaldosteronism Following Unilateral Adrenalectomy for Primary Aldosteronism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Julie Schommer ◽  
Amal A Shibli-Rahhal
Keyword(s):  
Adrenal Gland ◽  
Plasma Renin Activity ◽  
Potassium Chloride ◽  
Primary Aldosteronism ◽  
Plasma Renin ◽  
Renin Activity ◽  
Endocrine Society ◽  
Unilateral Adrenalectomy ◽  
One Year ◽  
Aldosterone To Renin Ratio

Abstract BACKGROUND: Hypoaldosteronism occurs in 6–30% of patients following unilateral adrenalectomy for primary aldosteronism. The Endocrine Society guidelines recommend discontinuing potassium supplementation and spironolactone postoperatively with repeat renin and aldosterone after surgery to monitor for cure. Clinical Case: A 69-year-old male with a 15-year history of hypertension on amlodipine 10 mg daily, atenolol 100 mg daily, terazosin 5 mg daily, valsartan 160 mg daily, spironolactone 50 mg three times daily, with longstanding hypokalemia on potassium chloride 20 mEq four times daily presented with an ischemic stroke and persistent hypertension (BP 182/79). Following discontinuation of spironolactone, evaluation revealed aldosterone concentration of 214 ng/dL (normal 4.0 - 31) and plasma renin activity of 0.1 ng/mL/hr (normal 0.5 - 4.0), giving an aldosterone-to-renin ratio of 2,140. CT of the abdomen showed a 3 cm right adrenal mass. He underwent uncomplicated right adrenalectomy for primary aldosteronism. Postoperative potassium was 3.4 mEq/L (normal 3.5–5.0) and hypertension persisted, so he was discharged on potassium chloride 10 mEq, losartan 100 mg daily, amlodipine 10 mg daily, and labetalol 200 mg twice daily. Two weeks later potassium level was 5.1 mEq/L and potassium chloride supplement was discontinued. Six months postoperatively, potassium was 5.7 mEq/L with well-controlled blood pressure, so losartan was discontinued. Labs over the subsequent several weeks showed persistent hyperkalemia up to 6.2 mEq/L and new hyponatremia to 128 mEq/L (normal 134 - 150). Repeat plasma renin activity was 0.51 ng/mL/hr and aldosterone concentration <1.0 ng/dL. Morning cortisol concentration was 18.3 ug/dL (normal 6.7 - 22.6) and ACTH 38 pg/mL (normal 6.0 - 50 pg/mL). He was diagnosed with postsurgical hypoaldosteronism. Potassium stabilized at 5.1 mEq/L and sodium stabilized at 134 mEq/L, so he was monitored without treatment for hypoaldosteronism. One year postoperatively his labs showed: potassium 5.1 mEq/L, sodium 135 mEq/L, renin 1.0 ng/mL/hr, and aldosterone 5.7 ng/dL. Conclusion: This patient had primary aldosteronism leading to suppression of aldosterone secretion from the contralateral healthy adrenal gland. This resulted in postoperative hypoaldosteronism once the affected adrenal gland was resected. This case demonstrates the need for continued monitoring of potassium, sodium, renin, and aldosterone following unilateral adrenalectomy for primary aldosteronism, especially in the setting of postoperative angiotensin receptor blocker use or other medications which can affect the renin-angiotensin-aldosterone system.

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