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• W2076269811 abstract "CORM-A1 is a newly described water-soluble carbon monoxide (CO) releasing molecule (CORM) that can deliver CO to various vascular beds in the absence of dramatic changes in blood carboxy-hemoglobin (COHb) levels. We tested the in vivo and in vitro renal vascular effects of CORM-A1 administration using anesthetized mice instrumented with a renal flow probe as well as in isolated, pressurized renal interlobar arteries. Administration of CORM-A1 (0.96 micromol) resulted in a significant increase in renal blood flow (RBF) of 33 +/- 6% as compared to control. Administration of acetylcholine (50 pmol) caused a similar increase in RBF (25 +/- 4%). In order to determine if the vasodilatory effect of CORM-A1 in vivo was mediated through activation of soluble guanylate cyclase (sGC), mice were pretreated with the sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 1 nmolkg(-1)min(-1)) for 30min. Pretreatment with ODQ significantly reduced the CORM-A1 mediated increase in RBF to 9 +/- 5% of control. In isolated pressurized renal interlobar arteries, CORM-A1 caused dose dependent vasodilatation of phenylephrine constricted arteries. The CORM-A1 mediated vasodilatation was significantly attenuated by ODQ to similar levels as observed in vivo. Inhibition of calcium activated potassium channels (Kca) with iberiotoxin resulted in a complete blockade of the CORM-A1 mediated vasodilatation in pressurized renal interlobar arteries. We conclude that CO released from CORM-A1 causes an increase in RBF and a decrease in vascular resistance through activation of sGC and opening of Kca channels in the kidney of the mouse." @default.
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• W2076269811 date "2006-07-01" @default.
• W2076269811 modified "2023-09-27" @default.
• W2076269811 title "Renal vascular responses to CORM-A1 in the mouse" @default.
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• W2076269811 doi "https://doi.org/10.1016/j.phrs.2006.01.012" @default.
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