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1 Department of Physiology, SL39, Tulane University School of Medicine, New Orleans,, Louisiana, United States
* To whom correspondence should be addressed. E-mail: fbotros{at}tulane.edu.
Heme oxygenases (HO-1, HO-2) catalyze the conversion of heme to carbon monoxide (CO), iron, and biliverdin. CO causes vasorelaxation via stimulation of soluble guanylate cyclase (sGC) and/or activation of KCa channels. Because nitric oxide (NO) exerts effects via the same pathways, we tested the interaction between CO and NO on rat afferent arterioles (AAs) using the blood-perfused juxtamedullary nephron preparation. AAs were superfused with either Tricarbonyldichlororuthenium (II) dimer, known as CO releasing molecule (CORM-2), 10 µmol/L CO solution, or 15 µmol/L Chromium mesoporphyrin (CrMP, HO inhibitor). AAs were also superfused with 1mmol/L nitro-L-arginine (NLA) to inhibit nitric oxide synthase (NOS) or 10 µmol/L ODQ to inhibit sGC and then CrMP was superfused during NOS inhibition or sGC inhibition. Treatment with 150 and 300 µmol/L CORM-2 or with CO (10 µmol/L) significantly dilated AAs (22.0±0.9 µm and 22.8±0.9 µm vs. 18.3± 0.9 µm, n=5, p<0.05), and (26.0±1.4 µm vs. 18.8±0.7 µm, n=5, p<0.05). In untreated vessels, HO inhibition did not alter AAs diameter (17.5±0.7 µm vs. 17.2±0.6 µm, n=7, p>0.05); however during inhibition of NO production, which constricted arterioles to 14.6±1.2 µm, n=6, p<0.05, concurrent HO inhibition led to further vasoconstriction (11.7±1.6 µm, n=6, p<0.05). CORM-2 attenuated the NLA-induced vasoconstriction. Inhibition of sGC caused significant constriction (15.7±0.4 µm vs. 18.8±0.4 µm, n=6, p<0.05). HO inhibition during sGC inhibition did not cause further change in AAs (15.5±0.7 µm, n=6). We conclude that endogenously-produced CO does not exert a perceptible influence on AAs diameter in the presence of intact NO system; however, when NO production is inhibited, CO serves as an important renoprotective reserve mechanism to prevent excess afferent arteriole constriction.
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