Abstract
Systemic hypoxia (inspired oxygen of 10%) constricts large arterioles (A1) and dilates small arterioles (A3) in striated muscle. The possible role of endothelium-derived relaxing factor (EDRF) or prostaglandins in mediating these responses was examined, as were the arteriolar response to systemic hypoxia in 1K1C (1-kidney, 1-clip) hypertensive rats and EDRF involvement in this response. In the cremaster muscles of anesthetized rats, hypoxia-induced A1 constriction was similar in normotensive and hypertensive animals and was not affected by the blockade of prostaglandin synthesis with mefenamic acid or by EDRF inhibition with hydroquinone (an EDRF inactivator) or L-Nω-nitro-arginine (L-NNA) (an EDRF synthesis inhibitor). A3 dilation in normotensive animals was unaffected by mefenamic acid, but was significantly (p < 0.05) attenuated by hydroquinone and L-NNA. Arteriolar dilation during systemic hypoxia was significantly less (p < 0.05) in the hypertensive compared with the normotensive groups and not alter...
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