Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1985;7:775-782

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Snajdar, R. M.
Right arrow Articles by Rapp, J. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Snajdar, R. M.
Right arrow Articles by Rapp, J. P.

Hypertension, Vol 7, 775-782, Copyright © 1985 by American Heart Association


ARTICLES

Atrial natriuretic factor in Dahl rats. Atrial content and renal and aortic responses

RM Snajdar and JP Rapp

Inbred Dahl salt-sensitive rats had a higher content of atrial natriuretic factor by bioassay in their atria than did inbred Dahl salt- resistant rats. This finding was true both in young 1- to 2-month-old rats, when blood pressure differences between strains were small, and in 7-month-old rats, when blood pressure differences were marked. Atria from salt-sensitive rats had more atrial natriuretic factor than did atria from salt-resistant rats when the rats were fed either low (0.3% NaCl) or high (8% NaCl) salt diet, but a high salt diet suppressed the atrial content of atrial natriuretic factor equally in both strains. In young, prehypertensive salt-sensitive rats, intravenous injections of atrial natriuretic factor caused significantly less natriuresis and diuresis than in salt-resistant rats (p less than 0.05). As the rats aged and salt-sensitive rats became markedly hypertensive, the strain responses to atrial natriuretic factor were reversed, that is, the salt- sensitive rats became more sensitive to atrial natriuretic factor than did the salt-resistant rats. Aortic vascular smooth muscle response to contraction with KCl was equally inhibited in both strains by atrial extracts or atriopeptin II. Thus, the salt-sensitive rat renal hyporesponsiveness to atrial natriuretic factor was not associated with a generalized hyporesponsiveness of vascular tissue to atrial natriuretic factor. It is argued that salt-sensitive rats could have two defects relating to atrial natriuretic factor, one involving hyporesponsive kidneys and another involving decreased release of atrial natriuretic factor from the atria.