Natriuretic Hormone: A Contribution to the Development of a Hypothesis

Physiology ◽  
1991 ◽  
Vol 6 (3) ◽  
pp. 114-118
Author(s):  
B Lichardus

For two decades before the discovery of atrial natriuretic peptide and the recent announcement of the isolation of endogenous ouabain, the experimental background for the hypothesis of the existence of a natriuretic hormone, mostly furnished by a few laboratories, kept this challenge alive.

1991 ◽  
Vol 261 (2) ◽  
pp. E177-E182 ◽  
Author(s):  
D. G. Gardner ◽  
E. D. Newman ◽  
K. K. Nakamura ◽  
K. P. Nguyen

Endothelin (ET) effected a dose-dependent increment in atrial natriuretic peptide (ANP) secretion and ANP mRNA accumulation in neonatal rat atrial and ventricular cardiocytes but had no effect on the processing of the ANP prohormone to the mature ANP product. The secretagogue effect was not limited by cell density. Both basal and ET-dependent secretory activity were abrogated by the calmodulin antagonist calmidazolium but were unaffected by meclophenamate or pertussis toxin. The magnitude of the ET-dependent increment in ANP secretion was amplified by culturing the cells in a dynamically pulsating (vs. static) environment, implying an interaction between mechanical and agonist-mediated secretory stimuli in this system. ET also promoted immunoreactive ANP release from primary cultures of fetal rat hypothalamic cultures, suggesting that this regulatory function may be generally employed in ANP gene-expressing cells. These findings demonstrate that ET has parallel effects on ANP synthesis and secretion and support a role for this peptide in the regulation of local and circulating levels of the natriuretic hormone.


1987 ◽  
Vol 72 (3) ◽  
pp. 305-312 ◽  
Author(s):  
J. V. Anderson ◽  
J. Donckier ◽  
N. N. Payne ◽  
J. Beacham ◽  
J. D. H. Slater ◽  
...  

1. The administration of exogenous atrial natriuretic peptide (ANP) causes a natriuresis and diuresis in man, but this has, to date, only been demonstrated at plasma ANP concentrations within the high pathological or pharmacological ranges. Evidence that ANP acts physiologically requires the demonstration of a natriuretic effect when it is infused to recreate plasma concentrations similar to those observed after physiological stimuli. 2. We infused human α-ANP (1–28) at a calculated rate of 1.2 pmol min−1 kg−1 for 3 h into seven water-loaded normal subjects, achieving plasma ANP concentrations within the upper part of the physiological range. The subjects' resting plasma ANP concentration increased from 3.8 ± 1.5 to 20.9 ± 1.9 pmol/l. 3. The infusion of ANP caused a 60% increase of mean urinary sodium excretion from 111 ± 18 to 182 ± 30 μmol/min (P < 0.001) and a 28% increase of mean water excretion from 10.8 ± 0.8 to 13.8 ± 1.6 ml/min (P < 0.01). 4. The infusion suppressed mean plasma renin activity from 1.55 ± 0.10 to 1.17 ± 0.06 pmol of ANG I h−1 ml−1 (P < 0.001). Mean plasma aldosterone concentration (242 ± 16 basally and 215 ± 15 pmol/l at the end of ANP infusion) did not change significantly. Pulse rate and blood pressure were unchanged throughout the study. 5. No significant change in any of the variables mentioned above occurred during the infusion of the vehicle alone on a separate study day. 6. The demonstration that recreation of plasma concentrations of ANP within the physiological range by intravenous infusion induces a natriuresis provides new evidence supporting the role of ANP as a natriuretic hormone.


PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0260131
Author(s):  
Gulay Tegin ◽  
Yonglin Gao ◽  
John M. Hamlyn ◽  
Barbara J. Clark ◽  
Rif S. El-Mallakh

Background Endogenous ouabain (EO) and atrial natriuretic peptide (ANP) are important in regulation of sodium and fluid balance. There is indirect evidence that ANP may be involved in the regulation of endogenous cardenolides. Methods H295R are human adrenocortical cells known to release EO. Cells were treated with ANP at physiologic concentrations or vehicle (0.1% DMSO), with or without guanylyl cyclase inhibitor 1,2,4 oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). Cyclic guanosine monophosphate (cGMP), the intracellular second messenger of ANP, was measured by a chemiluminescent immunoassay and EO was measured by radioimmunoassay of C18 extracted samples. Results EO secretion is inhibited by ANP treatment, with the most prolonged inhibition (90 min vs ≤ 60 min) occurring at physiologic ANP concentrations (50 pg/mL). Inhibition of guanylyl cyclase with ODQ, also reduces EO secretion. The inhibitory effects on EO release in response to cotreatment with ANP and ODQ appeared to be additive. Conclusions ANP inhibits basal EO secretion, and it is unlikely that this is mediated through ANP-A or ANP-B receptors (the most common natriuretic peptide receptors) or their cGMP second messenger; the underlying mechanisms involved are not revealed in the current studies. The role of ANP in the control of EO synthesis and secretion in vivo requires further investigation.


1986 ◽  
Vol 71 (3) ◽  
pp. 319-322 ◽  
Author(s):  
J. V. Anderson ◽  
N. D. Millar ◽  
J. P. O'Hare ◽  
J. C. MacKenzie ◽  
R. J. M. Corrall ◽  
...  

1. Thermoneutral water immersion produces a physiological increase of thoracic blood volume, raises central venous pressure and increases urinary sodium excretion by a hitherto ill-understood mechanism. We have investigated whether this enhanced sodium excretion could be mediated by the recently discovered natriuretic factor, atrial natriuretic peptide (ANP). 2. During water immersion there was a highly significant (P < 0.001) twofold increase of the mean plasma ANP concentration and a doubling of the mean urinary sodium excretion. Both were unchanged during the control experiments. 3. These results are consistent with the hypotheses (a) that ANP is released into plasma in response to central blood volume expansion and (b) that it functions as a natriuretic hormone in normal man under physiological conditions.


2001 ◽  
Vol 120 (5) ◽  
pp. A682-A682
Author(s):  
W GOWERJR ◽  
G CARTER ◽  
C LANDON ◽  
W GOWERIII ◽  
J DIETZ ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document