Prejunctional Regulation by Endogenous and Exogenous Acetylcholine of Adrenergic Nerve Function in Isolated Canine Mesenteric Arteries.

Abstract

Transmural electrical stimulation (5-30 Hz) produced a frequency-dependent increase in the perfusion pressure of isolated, perfused dog mesenteric artery segments without the endothelium, which was abolished by prazosin or tetrodotoxin. Physostigmine inhibited the pressor response to transmural electrical stimulation, whereas atropine potentiated the response. Treatment with acetylcholine (10-6 and 10-5 M) dose-dependently inhibited the response to electrical nerve stimulation. The effect was reversed by the addition of atropine and AF-DX 116 at a concentration (10-~ M) that selectively blocked the M2 receptor subtype, but not by pirenzepine or 4-DAMP. Acetylcholine did not alter the pressure raised by norepinephrine in perfused arterial segments nor the contraction caused by exogenous norepinephrine in the artery strips. 3H-overflow evoked by transmural electrical stimulation from tissues prelabeled with [3H] norepinephrine was decreased by acetylcholine (10-6 M) in the superfused dog mesenteric arterial strips. It is concluded that acetylcholine inhibits adrenergic neurogenic contractions by interfering with the release of norepinephrine, which possibly results from activation of the prejunctional M2 receptor subtype. (Hypertens Res 1997; 20: 119-125)

Cilostazol's Effect on the Response to Perivascular Nerve Stimulation in Isolated Dog Cerebral and Mesenteric Arteries

“…In the present study, CZ did not potentiate contractions induced by TES or nicotine in dog mesenteric arteries, which contraction is caused by noradrenergic nerve stimulation (27,28). However, the same concentration of the agent enhanced the relaxation induced by nitrergic nerve stimulation with TES or nicotine in the cerebral arteries, suggesting that CZ selectively potentiated nitrergic nerve function without affecting noradrenergic nerve function.…”

Hemodynamic consequences of chronic parasympathetic blockade with a peripheral muscarinic antagonist

“…Finally, ACh is known to inhibit the release of norepinephrine from sympathetic nerve terminals via stimulation of prejunctional muscarinic receptors (36). Thus an additional possibility is that blockade of these receptors by SMB could effectively increased sympathetic tone at the level of the heart and vasculature.…”