title: Pharmacologic inhomogeneity between the reactivity of intramural coronary arteries and arterioles.
abstract: We hypothesized that because of their size, anatomic location, and hemodynamic function, coronary arteries and arterioles would respond differently to vasoactive substances. Intramural arteries (281.7 +/- 23.1 microm) and arterioles (77.3 +/- 6.6 microm) of the left anterior descending coronary of rats were isolated and cannulated. Spontaneous tone was lower in arteries than in arterioles (81.1 +/- 5.7 vs. 53.0 +/- 3.9% of passive diameter, p < 0.05 at 60 mm Hg intraluminal pressure). Arterial tone was adjusted by the thromboxane receptor agonist U46619 (5 x 10(-8) M ) to reach an active tone close to that of arterioles. Bradykinin elicited dilations in both types of vessels. Acetylcholine (10(-6) - 10(-5) M ) dilated arteries (by 42.6 +/- 11.5 microm) but constricted arterioles (by 16.4 +/- 9.3 microm). Sodium nitroprusside and adenosine elicited significantly greater dilations in arterioles than in arteries (by 7.9 and 11.9%, respectively, p < 0.05), whereas dilations to norepinephrine were similar. Inhibition of nitric oxide synthesis caused a significantly smaller constriction in arteries (10.2 +/- 3.31%) than in arterioles (31.6 +/- 6.9%) and completely blocked bradykinin-and acetylcholine-induced dilations, whereas it did not affect dilations to sodium nitroprusside, adenosine, and norepinephrine. Compared with arteries, arterioles have a greater spontaneous tone and enhanced nitric oxide modulation of basal tone and exhibit greater responsiveness to nitric oxide and adenosine. In addition, nitric oxide synthase is activated differently by pharmacologic stimuli in these segments. The qualitative and quantitative differences among vasoactive responses of coronary arteries and arterioles demonstrated in this study suggest segment-specific roles for endothelial and metabolic factors in regulation of coronary vascular resistance.
authors.affiliation: Institute of Human Physiology, Semmelweis University, Budapest, Hungary.
authors.forename: M
authors.initials: M
authors.lastname: Szekeres
authors.forename: L
authors.initials: L
authors.lastname: Dézsi
authors.forename: G L
authors.initials: GL
authors.lastname: Nádasy
authors.forename: G
authors.initials: G
authors.lastname: Kaley
authors.forename: A
authors.initials: A
authors.lastname: Koller
mesh_terms: D000818:Animals; D001160:Arterioles / Q000187:drug effects* / Q000502:physiology; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology; D009569:Nitric Oxide / Q000819:agonists / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000502:physiology; D019335:Nitroarginine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D019335:Nitroarginine; D009569:Nitric Oxide