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.