Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1985;7:867-872

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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yoshioka, T.
Right arrow Articles by Ichikawa, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yoshioka, T.
Right arrow Articles by Ichikawa, I.

Hypertension, Vol 7, 867-872, Copyright © 1985 by American Heart Association


ARTICLES

In vivo influence of prostaglandin I2 on systemic and renal circulation in the rat

T Yoshioka, A Yared, H Miyazawa and I Ichikawa

The effect of prostaglandin I2 and two other vasodilator agents, acetylcholine and sodium nitroprusside, on systemic and renal circulation was studied in 29 adult euvolemic Sprague-Dawley rats. Intra-aortic infusion of prostaglandin I2 (3.6 micrograms/kg/hr; n = 6 rats) produced significant vasodilation (p less than 0.05), as indicated by an average reduction in total peripheral vascular resistance of 24.8 +/- 2.0%, while renal vascular resistance remained essentially unchanged. Essentially identical findings were obtained in a separate group of six rats pretreated with intravenous administration of saralasin (0.5 mg/kg/hr). In contrast, in another group of six rats pretreated with saralasin, intraaortic infusion of acetylcholine (0.35 mg/kg/hr), which caused a reduction in total peripheral vascular resistance (21.4 +/- 3.8%) comparable to that induced by prostaglandin I2, produced a significant fall in renal vascular resistance (average, 27.7 +/- 5.0%) and, hence, an increase in renal blood flow (average, 26.2 +/- 2.9%). The effect of sodium nitroprusside (0.4 mg/kg/hr i.v.) was intermediate between those of prostaglandin I2 and acetylcholine: both renal vascular resistance and total peripheral vascular resistance fell mildly. These results indicate that prostaglandin I2, given in a dose sufficient to cause systemic vasodilation, fails to induce any discernible renal vasodilative response and that this absence of renal vasodilation by prostaglandin I2 in vivo is not due, as previously postulated, to the highly efficient offsetting influence of intrarenal angiotensin II release.


This article has been cited by other articles:


Home page
Exp PhysiolHome page
B. Badzynska and J. Sadowski
Opposed effects of prostaglandin E2 on perfusion of rat renal cortex and medulla: interactions with the renin-angiotensin system
Exp Physiol, December 1, 2008; 93(12): 1292 - 1302.
[Abstract] [Full Text] [PDF]