Demonstration of different contractile mechanisms for angiotensin II and des-Asp1-angiotensin II in rabbit aortic strips.

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Abstract
Evidence of selective inhibition, differences in dose-response relationships, and cross-tachyphylaxis studies suggest that separate receptors and/or mechanisms may be involved in responses to angiotensin (Ang), [Sar1]Ang II and Ang III (= des-Asp1-Ang II). The extracellular Ca2+ requirment for contractile responses induced by angiotensin peptides and norepinephrine was determined in rabbit aortic strips. Responses to K+ and [Sar1]Ang II were attenuated markedly by treatment with SKF-525A [.beta.-diethylaminoethyl diphenylpropyl acetate hydrochloride], verapamil or Ca2+-free buffer. The response to Ang II was not impaired by verapamil, was blocked partially by SKF-525A and was reduced markedly in Ca2+-free medium. Norepinephrine- and Ang III-induced contractions were not dependent on extracellular Ca2+. K+, Ang II and [Sar1]Ang II required extracellular Ca2+ to induce contraction of the rabbit aorta. Ang III may have a mechanism of action that differs from that of [Sar1]Ang II and Ang II.