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Carbon monoxide of vascular origin attenuates the sensitivity of renal arterial vessels to vasoconstrictors

2001; American Society for Clinical Investigation; Volume: 107; Issue: 9 Linguagem: Inglês

10.1172/jci11218

1558-8238

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

Neuroscience of respiration and sleep

Rat renal interlobar arteries express heme oxygenase 2 (HO-2) and manufacture carbon monoxide (CO), which is released into the headspace gas. CO release falls to 30% and 54% of control, respectively, after inhibition of HO activity with chromium mesoporphyrin (CrMP) or of HO-2 expression with antisense oligodeoxynucleotides (HO-2 AS-ODN). Patch-clamp studies revealed that CrMP decreases the open probability of a tetraethylammonium-sensitive (TEA-sensitive) 105 pS K channel in interlobar artery smooth muscle cells, and that this effect of CrMP is reversed by CO. Assessment of phenylephrine-induced tension development revealed reduction of the EC50 in vessels treated with HO-2 AS-ODN, CrMP, or TEA. Exogenous CO greatly minimized the sensitizing effect on agonist-induced contractions of agents that decrease vascular CO production, but not the sensitizing effect of K channel blockade with TEA. Collectively, these data suggest that vascular CO serves as an inhibitory modulator of vascular reactivity to vasoconstrictors via a mechanism that involves a TEA-sensitive K channel.