AJP - Regulatory, Integrative and Comparative Physiology, Vol 264, Issue 5 903-R911, Copyright © 1993 by American Physiological Society

ARTICLES

Angiotensin II-induced endothelium-dependent relaxation of fowl aorta

K. Hasegawa, H. Nishimura and M. C. Khosla
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.

In the domestic fowl, angiotensin II (ANG II) decreases blood pressure in vivo and causes endothelium-dependent relaxation of aortic smooth muscles in vitro. To characterize ANG II-induced vasorelaxation, we compared endothelium-dependent vasodilatory effects of [Asp1,Val5]-ANG II (fowl ANG II) and acetylcholine (ACh) with the endothelium-independent vasorelaxing effect of sodium nitroprusside (SNP) on isometric tension of fowl aortic rings. Hemoglobin (Hb), gossypol, and N omega-nitro-L-arginine methyl ester (L-NAME), inhibitors for endothelium-derived relaxing factor (EDRF) in mammalian blood vessels, partially inhibited vasorelaxation induced by ANG II and ACh in fowl. Hb also markedly attenuated SNP-induced vasorelaxation, but not 8-bromoguanosine 3',5'-cyclic monophosphate-induced relaxation. 3,4,5-Trimethoxybenzoic acid 8-(diethylamino)octyl ester hydrochloride (TMB-8) or the removal of Ca2+ from the bathing medium attenuated the ACh-induced relaxation but did not significantly reduce vasorelaxation induced by ANG II or SNP. In the zero Ca2+ medium, aortic rings showed tachyphylaxis to ACh, while ANG II caused tachyphylaxis regardless of the presence or absence of external Ca2+. Furthermore, pretreatment of the ring with a high dose of ACh abolished the vasorelaxation response to ANG II, suggesting that ACh and ANG II may share a common Ca2+ pool. Calmidazolium, a calmodulin antagonist, abolished the vasorelaxation induced by ANG II and ACh but not that by SNP. Comparison of the vasodilatory effects of several ANG II analogues on fowl aortic rings showed an approximate potency order of [Asp1,Val5]-ANG II = [Asp1,Ile5]-ANG II > [Asn1,Ile5]-ANG II = [Sar1,Ile5]-ANG II > [Val5]-ANG III.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				C. A. Ruiz-Feria, Y. Yang, and H. Nishimura Do incremental increases in blood pressure elicit neointimal plaques through endothelial injury? Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2004; 287(6): R1486 - R1493. [Abstract] [Full Text] [PDF]

				H. Nishimura, Y. Yang, C. Hubert, J.-M. Gasc, K. Ruijtenbeek, J. De Mey, H. A. J. S. Boudier, and P. Corvol Maturation-dependent changes of angiotensin receptor expression in fowl Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2003; 285(1): R231 - R242. [Abstract] [Full Text] [PDF]

				K. Ruijtenbeek, C. G. A. Kessels, E. Villamor, C. E. Blanco, and J. G. R. De Mey Direct effects of acute hypoxia on the reactivity of peripheral arteries of the chicken embryo Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2002; 283(2): R331 - R338. [Abstract] [Full Text] [PDF]

				L. A. Martinez-Lemus, R. K. Hester, E. J. Becker, J. S. Jeffrey, and T. W. Odom Pulmonary artery endothelium-dependent vasodilation is impaired in a chicken model of pulmonary hypertension Am J Physiol Regulatory Integrative Comp Physiol, July 1, 1999; 277(1): R190 - R197. [Abstract] [Full Text] [PDF]

				N. HILL-KAPTURCZAK, M. H. KAPTURCZAK, E. R. BLOCK, J. M. PATEL, T. MALINSKI, K. M. MADSEN, and C. C. TISHER Angiotensin II-Stimulated Nitric Oxide Release from Porcine Pulmonary Endothelium Is Mediated by Angiotensin IV J. Am. Soc. Nephrol., March 1, 1999; 10(3): 481 - 491. [Abstract] [Full Text]

				N. Seyedi, X. Xu, A. Nasjletti, and T. H. Hintze Coronary Kinin Generation Mediates Nitric Oxide Release After Angiotensin Receptor Stimulation Hypertension, July 1, 1995; 26(1): 164 - 170. [Abstract] [Full Text]