title: Beating myocardium counteracts myogenic tone of coronary microvessels: involvement of ATP-sensitive potassium channels.
abstract: Myogenic tone is intrinsic to vascular tissue and plays an important role in determining basal coronary resistance. However, the effect of the beating heart on myogenic tone is unknown. We investigated the effects of myocardium-derived vasoactive factors on the myogenic tone of coronary microvessels in the resting condition and during increased metabolism. Pressurized isolated coronary vessels (detector vessel, DV) of rabbits (n = 33, maximal inner diameter 201 +/- 8 microm) were gently placed on beating hearts of anesthetized dogs and observed with an intravital microscope equipped with a floating objective. To shut off the myocardium-derived vasoactive signals, we placed plastic film between DV and the heart. The intravascular pressure was changed from 120 to 60 cmH(2)O, and pressure-diameter curves were obtained with and without the contact of DV and the myocardium. The direct contact shifted the pressure-diameter curve upward (P < 0.05 vs. without contact), and myogenic tone was reduced by approximately 40%. When endothelium of DV was denuded, the shift persisted, but the degree of shift was reduced to 10% (P < 0.05 vs. with endothelium). The shift was abolished by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker. A similar upward shift was induced by rapid pacing, but the shift was not blocked by glibenclamide. We conclude that the beating myocardium counteracts myogenic tone by releasing transferable vasoactive signals that affect the endothelium and the vascular smooth muscle, and that the signals are solely mediated by the activation of K(ATP) channels, unlike the rapid pacing-induced vasoactive factors.
authors.affiliation: Dept. of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Aoba-ku, Sendai 980-8574, Japan.
authors.forename: Satoru
authors.initials: S
authors.lastname: Takeda
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Komaru
authors.forename: Katsuaki
authors.initials: K
authors.lastname: Takahashi
authors.forename: Kouichi
authors.initials: K
authors.lastname: Sato
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kanatsuka
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Kokusho
authors.forename: Kunio
authors.initials: K
authors.lastname: Shirato
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Shimokawa
mesh_terms: D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D003331:Coronary Vessels / Q000502:physiology*; D004285:Dogs; D005260:Female; D005905:Glyburide / Q000494:pharmacology; D006321:Heart / Q000187:drug effects; D008297:Male; D008833:Microcirculation / Q000502:physiology*; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism; D024661:Potassium Channels, Inwardly Rectifying / Q000187:drug effects / Q000502:physiology*; D011817:Rabbits; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D000889:Anti-Arrhythmia Agents; D024661:Potassium Channels, Inwardly Rectifying; D000255:Adenosine Triphosphate; D005905:Glyburide