Abstract
The aim of the present study was to examine the role of protein kinase G (G-kinase) in the mechanism of endogenous nitric oxide (NO) deficiency-induced supersensitivity to the nitrovasodilator sodium nitroprusside (SNP) in isolated rat pulmonary artery. Tension experiments and cGMP measurements were carried out on isolated rat pulmonary artery to assess the influence of NO deficiency, caused by either N-nitro-L-arginine methyl ester (L-NAME) treatment or endothelium removal on the vasodilator potency of SNP. Sodium nitroprusside was more potent (pD2; 8.21 +/- 0.04) in relaxing arterial rings treated with 100microM L-NAME or denuded of the endothelium (pD2; 8.44 +/- 0.11) compared with the endothelium-intact controls (pD2; 7.61 +/- 0.05). Similarly, the tissue sensitivity to 8-Br-cGMP, a G-kinase activator, was significantly (P < 0.05) greater after L-NAME treatment (pD2; 5.04 +/- 0.09) or endothelium removal (pD2; 5.28 +/- 0.11) in comparison with the controls (pD2; 4.22 +/- 0.17). On the other hand, dibutyryl cAMP, an activator of protein kinase A, was equipotent in dilating control (pD2; 4.14 +/- 0.04) and L-NAME-treated (pD2 4.21 +/- 0.05) vessels. Further, L-NAME treatment significantly (P < 0.05) decreased the basal cGMP b...Continue Reading
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