Effect of Acute Hypercapnia on Alpha Atrial Natriuretic Peptide, Renin, Angiotensin II, Aldosterone, and Vasopressin Plasma Levels in Patients With COPD

CHEST Journal ◽  
1995 ◽  
Vol 107 (3) ◽  
pp. 780-786 ◽  
Author(s):  
François Chabot ◽  
Paul M. Mertes ◽  
Nicolas Delorme ◽  
Francine V. Schrijen ◽  
Claude G. Saunier ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Renin Angiotensin ◽  
Atrial Natriuretic

Diurnal change in plasma atrial natriuretic peptide concentrations

1987 ◽  
Vol 73 (5) ◽  
pp. 489-495 ◽  
Author(s):  
A. M. Richards ◽  
G. Tonolo ◽  
R. Fraser ◽  
J. J. Morton ◽  
B. J. Leckie ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Antidiuretic Hormone ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Diurnal Changes ◽  
Renin Angiotensin ◽  
Atrial Natriuretic

1. Diurnal changes in plasma concentrations of atrial natriuretic peptide (ANP), renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were investigated in seven normal volunteers studied under standardized conditions of dietary sodium, posture and physical activity. After completion of the diurnal study serial measurements of these variables were continued during, and on recovery from, a 2 day period of severe sodium depletion. 2. Clear diurnal variations in plasma concentrations of renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were observed. 3. Plasma ANP concentrations also varied significantly over 24 h. Values peaked about mid-day and a distinct trough in peptide concentrations occurred in the early evening. However, variations in plasma ANP values were of relatively small amplitude and not clearly independent of modest parallel shifts in sodium balance. 4. Changes in plasma ANP concentrations both within the diurnal study period and during sodium deprivation were closely and positively correlated with concomitant changes in cumulative sodium balance. 5. No simple parallel or reciprocal relationships between plasma concentrations of ANP, on the one hand, and concurrent plasma concentrations of other hormones or in the rate of urinary sodium excretion, on the other, were observed during the 25 h of the diurnal study.

Elevated angiotensin II and vasopressin in primary hyperparathyroidism. Angiotensin II infusion studies before and after removal of the parathyroid adenoma

1989 ◽  
Vol 120 (3) ◽  
pp. 362-368 ◽  
Author(s):  
B. Jespersen ◽  
E. B. Pedersen ◽  
P. Charles ◽  
H. Danielsen ◽  
H. Juhl
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Primary Hyperparathyroidism ◽  
Atrial Natriuretic Peptide ◽  
Creatinine Clearance ◽  
Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Plasma Levels ◽  
Before And After ◽  
Atrial Natriuretic

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.

Endogenous angiotensin II modulates the effect of atrial natriuretic peptide on extracellular fluid partition

1993 ◽  
Vol 264 (4) ◽  
pp. R676-R680
Author(s):  
J. P. Valentin ◽  
N. Nafrialdi ◽  
J. Ribstein ◽  
A. Mimran
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Renin Angiotensin System ◽  
Acute Administration ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Series Of Experiments ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) has been shown to promote a fluid shift from the intravascular toward the interstitial compartment and to interact with the renin-angiotensin system at the renal as well as the extrarenal level. In the present studies, the interaction between the renin-angiotensin system and the effects of ANP infusion (100 ng.kg-1 x min-1 for 45 min) on arterial pressure and hematocrit were assessed in bilaterally nephrectomized, anesthetized rats. In a first series of experiments, suppression of angiotensin II generation was achieved by chronic (10 days) treatment by the angiotensin-converting-enzyme inhibitor (ACEI) captopril in rats maintained on a low-sodium diet. ACEI pretreatment prevented the rise in hematocrit associated with ANP infusion (+2.1 +/- 0.1 vs. +5.8 +/- 0.2%, P < 0.05), without influencing the effect of ANP on arterial pressure. In ACEI-pretreated rats, acute administration of angiotensin II at a subpressor dose (2.5 ng.kg-1 x min-1) restored the ANP-induced increase in hematocrit. In a second series of experiments, acute blockade of the renin-angiotensin system was obtained by the ACEI enalaprilat or the nonpeptide angiotensin II receptor antagonist losartan (both 1 mg/kg i.v. bolus). In the presence of either enalaprilat or losartan, the ANP-induced increase in hematocrit was similarly prevented. These results indicate that the effect of ANP on vascular permeability is modulated by endogenous angiotensin II, possibly due to distinct influences of the two peptides at the level of pre- and postcapillary resistances.

Comparative Effects of Atrial Natriuretic Peptide and Brain Natriuretic Peptide on the Aldosterone and Pressor Responses to Angiotensin Ii in Man

1995 ◽  
Vol 88 (1) ◽  
pp. 81-86 ◽  
Author(s):  
Robert I. Cargill ◽  
Allan D. Struthers ◽  
Brian J. Lipworth
Keyword(s):  
Steady State ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Plasma Aldosterone ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Atrial Natriuretic

1. Atrial natriuretic peptide and brain natriuretic peptide have similar vasodilator and natriuretic properties, although little information is available regarding their relative effects as antagonists of the renin—angiotensin—aldosterone system. We have therefore compared how atrial natriuretic peptide and brain natriuretic peptide affect the systemic pressor and aldosterone responses to angiotensin II in eight male subjects. 2. Each subject was studied on three separate occasions, when they received a 60-min infusion of placebo, atrial natriuretic peptide (10 pmol min−1 kg−1) or brain natriuretic peptide (10 pmolmin−1 kg−1), with a concomitant infusion of angiotensin II (6 ng min−1 kg−1) given for the final 30 min of the infusion period. The change in haemodynamic parameters and plasma aldosterone induced by angiotensin II was measured. Plasma concentrations of atrial natriuretic peptide (182 ± 23 pmol/l) and brain natriuretic peptide (193 ± 25 pmol/l) achieved at steady-state during the infusion on each study day were not significantly different. 3. Increases in mean arterial pressure in response to angiotensin II were significantly lowered by concomitant infusion of atrial natriuretic peptide (21.0 ± 1.7 mmHg) and brain natriuretic peptide (20.1 ± 1.9 mmHg) compared with placebo (29.0 ± 4.1 mmHg). There were similar effects on systolic and diastolic blood pressure. Cardiac output was decreased on each study day to the same extent by angiotensin II infusion. Total systemic vascular resistance showed a non-significant trend towards an attenuated response to angiotensin II when atrial natriuretic peptide or brain natriuretic peptide was infused concomitantly in comparison with placebo. 4. Plasma aldosterone increased by 326 ± 49 pmol/l when angiotensin II was infused with placebo. Both atrial natriuretic peptide and brain natriuretic peptide significantly blunted this response, although the increase with atrial natriuretic peptide (19 ± 35 pmol/l) was significantly lower than the increase with brain natriuretic peptide (133 ± 19 pmol/l). 5. Atrial natriuretic peptide and brain natriuretic peptide were therefore equally effective in blunting the systemic pressor response to angiotensin II. It was apparent, however, in view of similar plasma concentrations at steady state, that on a molar basis atrial natriuretic peptide was a more potent inhibitor of angiotensin II-induced aldosterone secretion than brain natriuretic peptide. These results suggest a dissociation between the haemodynamic and hormonal effects of atrial natriuretic peptide and brain natriuretic peptide in terms of antagonism of the renin—angiotensin—aldosterone system.

Renal and Hormonal Effects of Chronic Inhibition of Neutral Endopeptidase (EC 3.4.24.11) in Normal Man

1993 ◽  
Vol 85 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Janice E. O'Connell ◽  
Alan G. Jardine ◽  
David L. Davies ◽  
James McQueen ◽  
John M. C. Connell
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Active Treatment ◽  
Cyclic Gmp ◽  
Plasma Levels ◽  
Neutral Endopeptidase ◽  
Active Therapy ◽  
Days Of Therapy ◽  
Atrial Natriuretic

1. Acute pharmacological inhibition of the enzyme neutral endopeptidase (EC 3.4.24.11), which cleaves the cardiac hormone atrial natriuretic peptide, raises endogenous levels of the hormone. Short-term administration of inhibitors causes natriuresis and diuresis in normal and hypertensive subjects; we report here the effects of an orally active neutral endopeptidase inhibitor (candoxatril, 200 mg) given twice daily for 10 days to normal salt-replete male subjects (n = 12) in a placebo-controlled cross-over study. 2. Candoxatril administration caused a transient natriuresis on day 1 of treatment, but this was not sustained, and cumulative sodium excretion at the end of the study was not altered by active therapy [1720 ± 40 versus 1734 ± 57 (placebo) mmol; means ± SEM]; exchangeable body sodium content was similarly unchanged. However, urinary cyclic GMP excretion was elevated throughout the active treatment phase when compared with placebo. 3. Although a change in plasma levels of atrial natriuretic peptide could not be demonstrated, platelet atrial natriuretic peptide binding sites were reduced by active treatment [23 ± 3 versus 39 ± 4 (placebo) fmol/109; P <0.001]. 4. Basal blood pressure and heart rate were not affected by candoxatril treatment. After 10 days of therapy subjects were given incremental infusions of angiotensin II (2, 4 and 8 ng min−1 kg−1) followed by phenylephrine. Although active therapy had not altered basal plasma concentrations of active renin and angiotensin II, levels of angiotensin II during infusion of the octapeptide were higher during the active phase. The diastolic pressor response to angiotensin II was increased during candoxatril treatment, although this is likely to reflect the higher plasma levels of angiotensin II during infusion of the octapeptide. In contrast, the systolic and diastolic pressor responses to phenylephrine were reduced by active treatment. 5. In conclusion, chronic candoxatril administration increases urinary cyclic GMP excretion without causing sustained natriuresis; evidence of atrial natriuretic peptide receptor down regulation was seen. There were no sustained hormonal or haemodynamic changes during therapy. The increased levels of angiotensin II during its infusion in the presence of candoxatril may reflect the role of neutral endopeptidase in clearing angiotensin II from the circulation.

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