Open AccessRole of Autonomic Nervous System and Vasoactive Hormones in the Release of Atrial Natriuretic Peptides in Conscious Rats
Author(s) -
Markus Haass,
Zofia ZukowskaGrojec,
Irwin J. Kopin,
Nadav Zamir
Publication year - 1987
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-198710000-00007
Subject(s) - vasopressin , propranolol , endocrinology , medicine , phentolamine , angiotensin ii , plasma renin activity , renin–angiotensin system , basal (medicine) , atrial natriuretic peptide , prazosin , chemistry , saralasin , blood pressure , antagonist , receptor , insulin
Atrial natriuretic peptides (ANPs) have been implicated in volume homeostasis and blood pressure regulation; however, little is known about factors regulating the release of ANPs. We therefore examined the roles of the sympathetic and parasympathetic nervous systems, the renin-angiotensin system, and vasopressin in the release of ANPs, under basal conditions and after acute blood volume expansion or acute salt loading in conscious rats. Plasma concentrations of immunoreactive ANPs (ir-ANPs) were measured by specific radioimmunoassay. Both acute blood volume expansion and acute salt loading increased basal plasma levels of ir-ANPs (90.4 +/- 5.2 pg/ml) four- to fivefold within 2 min. Basal and stimulated plasma levels of ir-ANPs were unaltered by pretreatment with methylatropine or with propranolol or by ganglionic blockade with hexamethonium. Total adrenergic blockade (combined treatment with yohimbine, prazosin, and propranolol) had no effect on basal or salt loading-stimulated plasma levels of ir-ANPs and slightly attenuated blood volume expansion-induced release of ANPs. Ganglionic blockade with chlorisondamine tripled basal plasma concentrations of ir-ANPs but had no effect on stimulation-induced release of ANPs. Acute blockade of the renin-angiotensin system with captopril or infusion of saralasin or pretreatment with a vasopressin pressor antagonist had no effect on basal or stimulated release of ANPs. Following intravenous bolus injections of graded doses of l-norepinephrine, angiotensin II, and vasopressin, mean arterial pressure and plasma levels of ir-ANPs increased in a dose-dependent manner. In conclusion, plasma concentrations of ir-ANPs can be acutely elevated by several physiological stimuli: volume expansion; salt loading; and pressor hormones.(ABSTRACT TRUNCATED AT 250 WORDS)