Conducted Arteriolar Dilations Persist in the Presence of Nitroarginine

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Abstract
At least two mechanisms of arterial dilations are induced by the application of muscarinic agonists. One is caused by nitric oxide, and the second is the result of the release of an endothelium-dependent hyperpolarizing factor (EDHF) that has yet to be clearly defined. This study was performed to determine whether two modes of dilation also are present in the microcirculation. Arterioles (38 μm maximal diameter) in the cheek pouch of anesthetized hamsters were stimulated with the micropipette application of a muscarinic-receptor agonist (methacholine 10−4M; MCh). A single microapplication of MCh (5 s) caused dilation at the tip of the pipette, as well as a dilation remote from the site of application. Two modes of muscarinic receptor-induced dilation were suggested within arterioles because nitroarginine (10−6−10−3M) significantly decreased the local dilation from control of 14 ± 1.8 μm to 5 ± 0.9 μm in the presence of 10−4M nitroarginine, without significantly affecting the conducted response (control, 4.7 ± 0.8 μm; with 10−4M nitroarginine, 3.1 ± 0.5 μm). Therefore, in hamster cheek-pouch arterioles there are two modes of dilation caused by muscarinic agonists, and they are mediated by different mechanisms: one is nitric oxide and the other is consistent with a hyperpolarizing factor.