scholarly journals Role of atrial natriuretic factor, cyclic GMP and the renin–aldosterone system in acute volume regulation of healthy human subjects

1988 ◽  
Vol 18 (4) ◽  
pp. 425-429 ◽  
Author(s):  
A. L. GERBES ◽  
R. M. ARENDT ◽  
R. GERZER ◽  
W. SCHNIZER ◽  
D. JÜNGST ◽  
...  
1987 ◽  
Vol 294 (3) ◽  
pp. 139-143 ◽  
Author(s):  
Ferid Murad ◽  
Dale C. Lehman ◽  
Brian M. Bennett ◽  
C. Molina ◽  
Scott A. Waldman

1995 ◽  
Vol 146 (3) ◽  
pp. 373-380 ◽  
Author(s):  
D L Vesely ◽  
S Chiou ◽  
M A Douglass ◽  
M T McCormick ◽  
G Rodriguez-Paz ◽  
...  

Abstract The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1–30 (long acting natriuretic peptide), 31–67 (vessel dilator) and 79–98 (kaliuretic peptide) as well as 99–126 (atrial natriuretic factor (ANF)) of the 126 amino acid ANF prohormone inhibit aldosterone secretion. Thirty healthy human subjects were studied following infusion of 100 ng/kg body weight/min for 60 min of each of the respective peptides. Kaliuretic peptide decreased plasma aldosterone concentration by the greatest amount (6-fold) and plasma aldosterone was still significantly decreased (P<0·001) three hours after stopping the infusion. In contrast, within 30 min of cessation of the ANF infusion, plasma aldosterone levels had returned to pre-infusion values. Long acting natriuretic peptide also significantly (P<0·01) decreased plasma aldosterone levels which remained significantly (P<0·001) decreased 3 h after cessation of infusion. Vessel dilator did not decrease plasma aldosterone levels. Kaliuretic peptide, ANF and long acting natriuretic peptide also decreased (P<0·01) urinary aldosterone concentrations. None of these peptides changed the plasma potassium concentration. We conclude that two new peptide hormones (long acting natriuretic peptide and kaliuretic peptide) inhibit aldosterone secretion. The length of time that aldosterone secretion is inhibited following kaliuretic peptide and long acting natriuretic peptide infusion is significantly longer (P<0·001) than following ANF infusion. Journal of Endocrinology (1995) 146, 373–380


2009 ◽  
Vol 3 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Tsuneo Ogawa ◽  
Monica Forero ◽  
Patrick G. Burgon ◽  
Mercedes L. Kuroski de Bold ◽  
Tina Georgalis ◽  
...  

1986 ◽  
Vol 251 (5) ◽  
pp. R1000-R1004
Author(s):  
K. Miki ◽  
G. Hajduczok ◽  
M. R. Klocke ◽  
J. A. Krasney ◽  
S. K. Hong ◽  
...  

The potential role of atrial natriuretic factor (ANF) in the renal response to head-out water immersion (WI) was studied. Five female mongrel dogs, trained to stand for 100 min in air followed by 100 min of thermoneutral WI at 37 degrees C or 200 min in air (timed control, TC), were chronically instrumented with arterial and venous catheters. The animals were hydrated with a volume of 0.45% NaCl solution equivalent to 2% of their body weight. Prehydration levels of arterial ANF were 243 +/- 15 (SE), and venous ANF levels were 211 +/- 21 pg/ml. WI resulted in an increase in urine flow from 0.7 +/- 0.1 ml/min to a peak flow of 2.2 +/- 0.3 ml/min (P less than 0.05). On immersion, plasma venous and arterial ANF levels increased significantly by 29 and 21% from the preimmersion values of 183 +/- 14 and 222 +/- 20 pg/ml, respectively. The arterial-venous difference for plasma ANF was maintained at 35 +/- 14 pg/ml (P less than 0.05) during WI; therefore venous sampling may suffice as a measure of circulating ANF levels. Sodium excretion increased linearly during WI to a peak value of 228 +/- 32 mu eq/min from a base line of 52 +/- 12 mu eq/min (P less than 0.05). These data indicate that peripheral tissues extract ANF and that WI is a physiological stimulus for the release of ANF. However, the time course and magnitude of the changes in plasma ANF and urine sodium excretion during WI are not comparable, and other mechanisms are likely responsible for the WI natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)


Hypertension ◽  
1988 ◽  
Vol 12 (3) ◽  
pp. 274-278 ◽  
Author(s):  
F J Salazar ◽  
R Bolterman ◽  
M J Fiksen-Olsen ◽  
T Quesada ◽  
J C Romero

1987 ◽  
Vol 65 (8) ◽  
pp. 1706-1711 ◽  
Author(s):  
C. I. Johnston ◽  
L. F. Arnolda ◽  
K. Tsunoda ◽  
P. A. Phillips ◽  
G. P. Hodsman

Congestive cardiac failure causes activation of various neurohumoral responses that increase total peripheral resistance and promote salt and water retention. These effects increase blood pressure and organ perfusion in the short term, but ultimately cause further cardiac decompensation by increasing ventricular afterload and cardiac work. The role of the renin–angiotensin–aldosterone system and the catecholamines is partially understood, and blockade of these systems as a treatment of heart failure is now established. The role of vasopressin in heart failure is more controversial, but there is now compelling evidence that vasopressin may have important vasoconstrictor actions in addition to its fluid retaining properties. Atrial natriuretic factor is a newly described cardiac hormone released from the atrium. Atrial natriuretic factor causes natriuresis, diuresis, vasodilatation, suppression of thirst, and suppression of both renin and aldosterone. These actions largely counteract the effects of the renin–angiotensin system and vasopressin. Plasma atrial natriuretic factor has been reported to be markedly elevated in human and experimental heart failure, and may act to limit the neurohumoral response to reduced cardiac output. This review summarizes our understanding of the vasoactive hormones and reports experimental evidence supporting a pathophysiological role for vasopressin and atrial natriuretic factor in congestive cardiac failure.


Sign in / Sign up

Export Citation Format

Share Document