title: Effects of angiotensin II on canine and porcine coronary epicardial and resistance arteries.
abstract: Coronary resistance arteriolar diameter importantly regulates myocardial blood flow, and is influenced by circulating neurohumoral agents. Angiotensin II (A-II) is a circulating polypeptide that is chronically elevated in heart failure and serves as a potent peripheral vasoconstrictor agent. However, its effects on isolated coronary resistance arterioles is relatively unknown. We compared the vasomotor effects of A-II on coronary epicardial and resistance arterioles in vitro from both the canine and porcine heart in order to determine the effects of A-II in different vascular beds and species. Epicardial rings were studied under isometric recording conditions, while resistance arterioles (50-150 microns) were studied in vitro using a video imaging system to record diameter. A-II, whether applied to passively distended or preconstricted porcine resistance arterioles, did not cause vasoconstriction when applied as a bolus or as cumulative doses. In preconstricted canine resistance arterioles, A-II elicited dose-dependent vasodilation (EC50 = 0.2 nM). In passively distended canine arterioles, high concentrations of A-II (0.1 microM) applied as a bolus elicited transient vasoconstriction in 28% of the vessels studied. In large epicardial rings, A-II was a weak vasoconstrictor, with greater potency in canine arteries compared to porcine arteries. In canine arteries, vasoconstriction to A-II was augmented after incubation with indomethacin. In contrast to the findings in canine arteries, the A-II vasoconstrictor response in porcine coronary arteries was decreased after incubation with indomethacin or removal of the endothelium. Thus, A-II elicits the release of a vasodilator prostanoid in epicardial canine coronary arteries and a vasoconstrictor prostanoid in porcine vessels which modulate the vasomotor action of A-II.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine College of Medicine, Columbia, MO.
authors.forename: P R
authors.initials: PR
authors.lastname: Myers
authors.forename: L C
authors.initials: LC
authors.lastname: Katwa
authors.forename: M
authors.initials: M
authors.lastname: Tanner
authors.forename: C
authors.initials: C
authors.lastname: Morrow
authors.forename: E
authors.initials: E
authors.lastname: Guarda
authors.forename: J L
authors.initials: JL
authors.lastname: Parker
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects* / Q000378:metabolism; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000378:metabolism; D005260:Female; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011945:Receptors, Angiotensin / Q000378:metabolism; D013552:Swine; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D011945:Receptors, Angiotensin; D000804:Angiotensin II; D007213:Indomethacin