Hypertension, Vol 7, 867-872, Copyright © 1985 by American Heart Association
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.
ARTICLES
In vivo influence of prostaglandin I2 on systemic and renal circulation in the rat
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