Angiotensin II induces endothelium-dependent vasodilation of rat cerebral arterioles

• Published in: The American journal of physiology Vol. 258; no. 6 Pt 2; p. H1840
• Main Authors: Haberl, R L, Anneser, F, Villringer, A, Einhäupl, K M
• Format: Journal Article
• Language: English
• Published: United States 01.06.1990
• Subjects: Angiotensin II - pharmacology; Animals; Arterioles - drug effects; Cerebral Arteries - drug effects; Cerebral Arteries - physiology; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiology; Fluorescein; Fluoresceins - pharmacology; Indomethacin - pharmacology; Light; Male; Methylene Blue - pharmacology; Pia Mater - blood supply; Rats; Rats, Inbred Strains; Vasodilation - drug effects; Vasodilation - radiation effects
• ISSN: 0002-9513
• DOI: 10.1152/ajpheart.1990.258.6.H1840

We evaluated the response of cerebral arterioles to angiotensin II (ANG II) in anesthetized rats equipped with a closed cranial window. Topical application of 10(-10)-10(-5) M ANG II induced dose-dependent arteriolar vasodilation. Maximum vasodilation of 24 +/- 2.2% (+/- SE) was attained at a concentration of 10(-6) M ANG II. The dilation in response to ANG II was blocked by 3 micrograms/ml indomethacin, a cyclooxygenase inhibitor, and was reversed to minimal vasoconstriction by 10(-5) M methylene blue, a substance that has been reported to eliminate endothelium-dependent vasodilation. Coapplication of indomethacin with methylene blue reduced the arteriolar response to ANG II to a similar extent as the application of indomethacin alone. Indomethacin or methylene blue did not inhibit the vasodilation induced by 10(-5) M adenosine, which is not endothelium and cyclooxygenase dependent. Mercury light illumination of the pial vessels after intravenous injection of fluorescein dye, a technique that has been used by others to functionally damage endothelial cells, reversed ANG II (10(-6) M)-induced vasodilation into a -14.2 +/- 2.3% constriction while not affecting the response to adenosine. Our data suggest that ANG II produces vasodilator responses of rat cerebral arterioles by the release of a factor that is derived from the endothelium and may be generated through a cyclooxygenase-dependent mechanism.