Abstract

We have demonstrated that palmitic acid methyl ester (PAME) is the major perivascular adipose tissue (PVAT)‐derived relaxing factor. PAME also was shown to inhibit nicotinic acetylcholine receptor (nAChR)‐mediated inward currents on the superior cervical ganglionic neurons. The present study, therefore, was designed to determine if PAME released from the PVAT inhibited nicotine‐induced neurogenic relaxation of isolated endothelium‐denuded small mesenteric arterial (sMA) rings of 8‐week old male Sprague‐Dawley rats. In tissue bath myography study, nicotine (100 μM) induced small, basal relaxation in sMA rings with PVAT. The relaxation was significantly enhanced in arteries without PVAT. Transmural nerve stimulation (TNS) also elicited tetrodotoxin‐sensitive relaxation of sMA rings with or without PVAT. The relaxations in both ring preparations, however, were not significantly different. In sMA preparations with PVAT, TNS‐elicited relaxation or nicotine‐induced small, basal relaxation was not significantly affected by 4‐propargylglycine (10 mM, an inhibitor for H2S synthesis). These results suggest that PVAT, most likely via release of PAME but not H2S, modulates the neurogenic control of the sMA tone. (supported by Tzu Chi Univ & Foundation, NSC and NHRI of Taiwan).

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