Carbon monoxide produced by isolated arterioles attenuates pressure-induced vasoconstriction

• Published in: American journal of physiology. Heart and circulatory physiology 2001-07, Vol.281 (1), p.H350-H358
• Main Authors: Zhang, Fan, Kaide, Jun-Ichi, Wei, Yuan, Jiang, Houli, Yu, Changhua, Balazy, Michael, Abraham, Nader G, Wang, Wenhui, Nasjletti, Alberto
• Format: Article
• Language: English
• Subjects: Animals; Arterioles - metabolism; Blood Pressure - physiology; Carbon Monoxide - metabolism; Electric Conductivity; Enzyme Inhibitors - pharmacology; Heme Oxygenase (Decyclizing) - antagonists & inhibitors; Heme Oxygenase (Decyclizing) - metabolism; In Vitro Techniques; Male; Mesoporphyrins - pharmacology; Muscle, Skeletal - blood supply; Muscle, Smooth, Vascular - cytology; Muscle, Smooth, Vascular - physiology; Potassium Channel Blockers; Potassium Channels - drug effects; Potassium Channels - physiology; Rats; Rats, Sprague-Dawley; Tetraethylammonium - pharmacology; Vasoconstriction - physiology
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.2001.281.1.h350

Department of Pharmacology, New York Medical College, Valhalla, New York 10595 Studies were conducted on isolated rat gracilis muscle arterioles to examine the role of vascular heme oxygenase (HO)-derived carbon monoxide (CO) on myogenic constrictor responses to stepwise increments in intraluminal pressure. The arterioles express HO-2 but not HO-1 and manufacture CO. Both HO-2 protein expression and CO production are reduced in arterioles maintained for 18   h before experimentation in media containing HO-2 antisense oligodeoxynucleotides (AS-ODN). Pressurization of arterioles mounted on a myograph over the pressure range of 40-100 mmHg elicits reduction of internal diameter. At pressures >40 mmHg, the internal diameter of vessels treated with either HO-2 AS-ODN, the HO inhibitor chromium mesoporphyrin (CrMP), or the K + channel blocker tetraethylammonium (TEA) are smaller than the corresponding control values. The inclusion of exogenous CO, but not of biliverdin, in the superfusion buffer attenuates pressure-induced vasoconstriction in CrMP-treated vessels. However, exogenous CO does not attenuate pressure-induced vasoconstriction in vessels treated with both CrMP and TEA. Collectively, these data suggest that CO of vascular origin attenuates pressure-induced arteriolar constriction via a mechanism involving a TEA-sensitive K + channel. heme oxygenase; potassium channels; vasodilatory mechanisms; vascular reactivity; myogenic tone