Release of nitric oxide by nerve stimulation in the human urogenital tract

Neurogenic ATP and nitric oxide (NO) may play important roles in the physiological control of gastrointestinal motility. However, the interplay between purinergic and nitrergic neurons in mediating the inhibitory neurotransmission remains uncertain. This study investigated whether neurogenic NO modulates the purinergic transmission to circular smooth muscles of the hamster proximal colon. Electrical activity was recorded from circular muscle cells of the hamster proximal colon by using the microelectrode technique. Intramural nerve stimulation with a single pulse evoked a fast purinergic inhibitory junction potential (IJP) followed by a slow nitrergic IJP. The purinergic component of the second IJP evoked by paired stimulus pulses at pulse intervals between 1 and 3 s became smaller than that of the first IJP. This purinergic IJP depression could be observed at pulse intervals <3 s, but not at longer ones, and failed to occur in the presence of NO synthase inhibitor. Exogenous NO (0.3–1 μM), at which no hyperpolarization is produced, inhibited purinergic IJPs, without altering the nitrergic IJP and exogenously applied ATP-induced hyperpolarization. In the presence of both purinoceptor antagonist and nitric oxide synthase (NOS) inhibitor, intramural nerve stimulation with 5 pulses at 20 Hz evoked vasoactive intestinal peptide (VIP)-associated IJPs, suggesting that VIP component may be masked in the IJPs of the hamster proximal colon. Our results suggest that neurogenic NO may modulate the purinergic transmission to circular smooth muscles of the hamster proximal colon via a prejunctional mechanism. In addition, VIP may be involved in the neurotransmitter in the hamster proximal colon.

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Mechanism underlying the response to vasodilator nerve stimulation in isolated dog and monkey cerebral arteries

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.259.5.h1511 ◽

1990 ◽

Vol 259 (5) ◽

pp. H1511-H1517 ◽

Cited By ~ 9

Author(s):

N. Toda ◽

T. Okamura

Keyword(s):

Nitric Oxide ◽

Electrical Stimulation ◽

Coronary Artery ◽

Substance P ◽

Nerve Stimulation ◽

Cerebral Arteries ◽

Inhibitory Effect ◽

Synthesis Inhibitor ◽

Transmural Stimulation ◽

Stimulation Of

Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips obtained from dogs and Japanese monkeys were abolished by tetrodotoxin and hexamethonium, respectively, and suppressed by treatment with NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor. The inhibitory effect was prevented and reversed by L-arginine but not by D-arginine. The relaxations suppressed by L-NMMA were not increased by exogenously applied NO. Endothelium denudation did not alter the response to transmural stimulation and nicotine or the inhibitory effect of L-NMMA. D-NMMA did not inhibit the response to vasodilator nerve stimulation. Dog coronary artery relaxations caused by transmural stimulation were not inhibited by L-NMMA but reversed to contractions by propranolol. Relaxations caused by substance P of dog cerebral arteries treated with indomethacin were dependent on endothelium and inhibited by L-NMMA, whereas those by NO and nitroglycerin, endothelium-independent relaxations, were unaffected. It is concluded that chemical and electrical stimulation of vasodilator nerves relaxes dog and monkey cerebral arteries, possibly by a mediation of NO rather than a stimulating action of NO on the release of vasodilator transmitter. Endothelium-dependent relaxations by substance P of dog cerebral arteries appear to be mediated by NO.

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Arteriolar wall Po 2 and nitric oxide release during sympathetic vasoconstriction in the rat intestine

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.2.h484 ◽

2000 ◽

Vol 279 (2) ◽

pp. H484-H491 ◽

Cited By ~ 11

Author(s):

Bryan A. Sauls ◽

Matthew A. Boegehold

Keyword(s):

Nitric Oxide ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Rat Intestine ◽

Nerve Activity ◽

Sympathetic Nerve Stimulation ◽

Nitric Oxide Release ◽

Sympathetic Vasoconstriction ◽

Arteriolar Wall

Endothelium-derived nitric oxide (NO) attenuates arteriolar constriction in the rat small intestine during periods of increased sympathetic nerve activity. This study was undertaken to test the hypothesis that a flow-dependent fall in arteriolar wall Po 2 serves as the stimulus for endothelial NO release under these conditions. Sympathetic nerve stimulation at 3–16 Hz induced frequency-dependent arteriolar constriction, with arteriolar wall O2 tension (Po 2) falling from 67 ± 3 mmHg to as low as 41 ± 6 mmHg. Arteriolar responses to nerve stimulation were enhanced after inhibition of NO synthase with N G-monomethyl-l-arginine (l-NMMA). Under a high-O2 (20%) superfusate, the fall in wall Po 2 was significantly attenuated, arteriolar constrictions were increased by 57 ± 9 to 66 ± 12%, and these responses were no longer sensitive tol-NMMA. The high-O2 superfusate had no effect on vascular smooth muscle responsiveness to NO (as judged by arteriolar responses to sodium nitroprusside) or on arteriolar wall oxidant activity (as determined by the reduction of tetranitroblue tetrazolium dye). These results indicate that a flow-dependent fall in arteriolar wall Po 2 may serve as a stimulus for the release of endothelium-derived NO during periods of increased sympathetic nerve activity.

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