Isolated Krebs-perfused rabbit-mesentery blood vessels release a prostaglandin E-like substance (PGE) when treated with angiotensin II, angiotensin I, arachidonic acid, or bradykinin. The specific competitive antagonist [Sar1,Ile8]angiotensin II, was found to inhibit angiotensin II-induced PGE release. The angiotensin antagonist did not block PGE release by bradykinin, whereas indomethacin blocked PGE release induced by all agonists. SQ-20881, the converting-enzyme and bradykininase inhibitor, decreased the PGE release by angiotensin I, enhanced the release by bradykinin, and did not affect release by angiotensin II. Pressor and depressor responses were obtained in mesenteric preparations constricted by epinephrine to a pressure of 60 mmHg. Angiotensin II induced an initial increase in mesenteric vascular resistance followed by a depressor response below basal pressure. The pressor responses were enhanced by indomethacin and the depressor responses were eliminated. Bolus injections of both bradykinin and arachidonic acid produced decreases in perfusion pressure, but indomethacin completely inhibited only the arachidonic acid-induced responses while only diminishing bradykinin-induced responses. The ability of angiotensin to increase mesenteric vascular resistance and to release PGE which decrease vascular resistance is discussed.

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The effect of angiotensin on the action of tyramine was studied in isolated rabbit left atria paced by point and field stimulation to more clearly define the interaction of angiotensin with the sympathetic nervous system. Administration of angiotensin resulted in similar increases in contractility in both point- and field-stimulated atria. In point-stimulated preparations only the muscle is stimulated to contract, whereas in field-stimulated preparations both nerve and muscle are stimulated. 1-Sar-8-Ala-angiotensin II completely blocked the direct inotropic effect of angiotensin in a molar dose ratio of 3:1 in both point- and field-stimulated preparations. However, angiotensin (0.05-10 ng/ml) potentiated the inotropic effect of tyramine in field-stimulated atria only. This facilitatory effect was not inhibited by 1-Sar-8-Ala-angiotensin II at a molar dose ratio of 3:1; indeed, a ratio of 500:1 was necessary for complete blockade of this angiotensin-induced potentiation. This antagonist in odses of 0.1-1000 ng/ml was without contractile effect in any preparation, regardless of whether tyramine was present. The data suggest the presence of (1) a presynaptic angiotensin receptor that, in the presence of sympathetic nerve stimulation, modulates the release of norepinephrine and (2) a second angiotensin receptor in cardiac tissue that directly influences myocardial contractility.

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