scholarly journals Plasma Levels of .ALPHA.-Atrial Natriuretic Peptide, Renin Activity, Angiotensin II and Aldosterone in Patients Undergoing Cardiac Surgery.

1992 ◽  
Vol 12 (1) ◽  
pp. 44-51
Author(s):  
Kazuyoshi AOYAMA ◽  
Takeyoshi SATA ◽  
Akio SHIGEMATSU
CHEST Journal ◽  
1995 ◽  
Vol 107 (3) ◽  
pp. 780-786 ◽  
Author(s):  
François Chabot ◽  
Paul M. Mertes ◽  
Nicolas Delorme ◽  
Francine V. Schrijen ◽  
Claude G. Saunier ◽  
...  

1987 ◽  
Vol 72 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Lynn Chartier ◽  
Ernesto L. Schiffrin

1. Previous studies have shown that atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone by isolated adrenal glomerulosa cells stimulated by angiotensin II, adrenocorticotropic hormone and potassium in vitro. We have also demonstrated that this inhibitory effect of ANP on plasma aldosterone induced by angiotensin II and adrenocorticotropic hormone can be reproduced in vivo in conscious unrestrained rats. In this study, we have investigated the effect of an intravenous infusion of ANP on plasma aldosterone in conscious unrestrained sodium-depleted rats. 2. During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. ANP infused intravenously at a dose which increased the plasma concentration of the peptide three- to five-fold, produced a significant decrement in the concentration of aldosterone in plasma after an infusion period of 120 min. There was no significant effect of ANP on plasma renin activity and plasma corticosterone concentration. 3. Since the increase in plasma aldosterone levels in sodium-depleted rats is mainly dependent on the activation of the renin–angiotensin system, we conclude that ANP may modulate the effect of endogenous as well as exogenous angiotensin II on plasma aldosterone secretion.


1989 ◽  
Vol 120 (3) ◽  
pp. 362-368 ◽  
Author(s):  
B. Jespersen ◽  
E. B. Pedersen ◽  
P. Charles ◽  
H. Danielsen ◽  
H. Juhl

Abstract. In order to evaluate the role of calcium metabolism in blood pressure regulation, 15 patients with primary hyperparathyroidism and 9 healthy control subjects were studied before and during angiotensin II infusion. The patients were re-investigated 2–5 months after removal of the parathyroid adenoma. Blood pressure, plasma levels of angiotensin II, aldosterone, arginine vasopressin, and atrial natriuretic peptide, and creatinine clearance were determined. Blood pressure and the blood pressure response to angiotensin II infusion were both the same before and after the operation. Angiotensin II and arginine vasopressin during basal conditions were significantly higher before than after the operation (angiotensin II: 17 (median) to 10 pmol/l, P < 0.02; arginine vasopressin: 2.9 to 1.9 pmol/l, P < 0.01), whereas aldosterone, atrial natriuretic peptide, and creatinine clearance were unchanged. During angiotensin II infusion, aldosterone, arginine vasopressin, and atrial natriuretic peptide increased to approximately the same levels before and after the operation. Blood pressure was not correlated to any of the hormones measured. Thus, patients with primary hyperparathyroidism have elevated plasma levels of angiotensin II and arginine vasopressin which may be compensatory phenomena counteracting volume depletion owing to a decreased renal concentrating ability induced by hypercalcemia, and owing to PTH-induced inhibition of renal sodium reabsorption.


2000 ◽  
Vol 99 (5) ◽  
pp. 461-466 ◽  
Author(s):  
Massimo CUGNO ◽  
Piergiuseppe AGOSTONI ◽  
Hans R. BRUNNER ◽  
Marco GARDINALI ◽  
Angelo AGOSTONI ◽  
...  

Induction of congestive heart failure by high-frequency pacing has been reported to increase plasma levels of immunoreactive kinins in dogs. In the present study, we evaluated plasma bradykinin levels in human heart failure. Utilizing a recently developed method, we specifically measured plasma levels of bradykinin-(1–9) nonapeptide in 21 patients with chronic congestive heart failure [New York Heart Association (NYHA) stages III and IV). At the same time, we measured plasma atrial natriuretic peptide levels and plasma renin activity, and, as a marker of inflammation, plasma levels of tumour necrosis factor. In addition, 18 healthy subjects matched for gender and age served as normal controls. Plasma bradykinin concentrations were not higher in patients with chronic congestive heart failure (median 2.1 fmol/ml) than in healthy subjects (2.6 fmol/ml). In contrast, plasma atrial natriuretic peptide levels were clearly higher (patients, 63 fmol/ml; controls, 24 fmol/ml; P < 0.0001), despite diuretic treatment and in the presence of high plasma renin activity (patients, 13.0 ng·h-1·ml-1; controls, 0.3 ng·h-1·ml-1; P < 0.0001). Tumour necrosis factor was elevated in heart failure patients in NYHA class IV only (27 pg/ml, compared with 21 pg/ml in controls; P = 0.013). Bradykinin, atrial natriuretic peptide and plasma renin activity levels were not correlated with the severity of the disease, as assessed by NYHA classification. These results indicate that a rather selective cytokine activation, without concomitant stimulation of the kallikrein–kinin system, occurs in human chronic congestive heart failure.


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