Stroke, Vol 24, 2041-2044, Copyright © 1993 by American Heart Association
W Meng and DW Busija
BACKGROUND AND PURPOSE: Recent investigations indicated that degradation
fragments of angiotensins could be involved in the regulation of the
cerebral circulation and that their effects might be mediated by
prostaglandins. The present study was designed to examine the effect of
angiotensin-(1-7), a major endogenous heptapeptide fragment, on cerebral
arteriolar diameter and compare it with the octapeptide angiotensin II, and
further to determine whether prostaglandins mediate their effects. METHODS:
Newborn, anesthetized pigs were equipped with a closed cranial window, and
the diameter of one pial arteriole was measured using intravital
microscopy. RESULTS: Topical application of angiotensin-(1-7) (n = 9)
increased the diameter by 6.8 +/- 5.3% (mean +/- SEM), 10.4 +/- 5.2%, 14.3
+/- 5.9%, and 17.5 +/- 7.7% (P < .05) at 10(-7), 10(-6), 10(-5), and
10(-4) mol/L, respectively (baseline, 94 +/- 3 microns). Topical
application of angiotensin II (n = 8) increased the diameter by 9.6 +/-
7.0%, 9.6 +/- 7.6%, 11.3 +/- 8.4% (P < .05), and 5.5 +/- 7.9% at 10(-7),
10(-6), 10(- 5), and 10(-4) mol/L, respectively (baseline, 94 +/- 5
microns). After administration of indomethacin (5 mg/kg IV), which did not
significantly change the baseline arteriolar diameter, neither
angiotensin-(1-7) at 10(-4) mol/L nor angiotensin II at 10(-5) mol/L caused
significant vasodilation. CONCLUSIONS: The results indicate that
angiotensin-(1-7) is a modest dilator in the cerebral circulation, as is
angiotensin II, and that prostaglandins may mediate responses.
ARTICLES
Comparative effects of angiotensin-(1-7) and angiotensin II on piglet pial arterioles
Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157-1083.
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