ON THE ROLE OF DIGOXIN-LIKE SUBSTANCES, ANP, AND AVP IN NATRIURESIS INDUCED BY HYPERTONIC SALINE INFUSION IN DOGS

Citation
B. Lichardus et al., ON THE ROLE OF DIGOXIN-LIKE SUBSTANCES, ANP, AND AVP IN NATRIURESIS INDUCED BY HYPERTONIC SALINE INFUSION IN DOGS, Journal of cardiovascular pharmacology, 22, 1993, pp. 190000082-190000083
Citations number
4
Categorie Soggetti
Cardiac & Cardiovascular System","Respiratory System","Pharmacology & Pharmacy
ISSN journal
01602446
Volume
22
Year of publication
1993
Supplement
2
Pages
190000082 - 190000083
Database
ISI
SICI code
0160-2446(1993)22:<190000082:OTRODS>2.0.ZU;2-6
Abstract
The increase of sodium concentration in cerebrospinal fluid or in plas ma triggers the osmoregulatory mechanism, namely, the enhancement of r enal free-water reabsorption and natriuresis. The increase of free-wat er reabsorption has been recognized for many years as a consequence of the osmotically released vasopressin (AVP). However, the control of r enal sodium excretion in the mechanism of osmoregulation has not been clarified. It has been suggested to be, at least in part, of hormonal nature, implying the decreased release of aldosterone and the increase d release of atrial natriuretic peptide (ANP), digoxin-like substances (DLIS), and AVP. Neither of these factors, however, has been unequivo cally linked to the mechanism of immediate natriuresis caused by an ac ute increase in cerebrospinal fluid or plasma sodium concentration. It was reconfirmed in our present experiments in anesthetized dogs that aldosterone, ANP, and DLIS could hardly play a role in the immediate n atriuresis after the i.v. infusion of hypertonic saline (20% NaCl solu tion infused in 20 min in an amount that was 0.13% of body weight). Ho wever, the role of AVP in this type of natriuresis seems more promisin g as a V1/V2 receptor antagonist applied i.v. before the hypertonic sa line loading completely prevented the increase of renal sodium excreti on. Natriuresis after the isotonic saline load was not impaired by the same antagonist of vasopressin receptors.