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Am J Physiol Heart Circ Physiol 281: H350-H358, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 1, H350-H358, July 2001

Carbon monoxide produced by isolated arterioles attenuates pressure-induced vasoconstriction

Fan Zhang, Jun-Ichi Kaide, Yuan Wei, Houli Jiang, Changhua Yu, Michael Balazy, Nader G. Abraham, Wenhui Wang, and Alberto Nasjletti

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


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