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At least 379 records · Page 21Linked to original sources
PubMed1975

Inhibition by halothane of release of norepinephrine, but not of dopamine-beta-hydroxylase, from guinea-pig vas deferens.

Halothane strikingly decreases spontaneous and electrically stimulated release of norepinephrine from the isolated guinea pig hypogastric nerve--vas deferens preparation. This depression of adrenergic discharge appears to be a direct action on the sympathetic nerve endings and may in part account for the cardiovascular depression seen during halothane administration. Although halothane depressed stimulation-induced release of norepinephrine, it did not proportionately diminish release of dopamine-beta-hydroxylase. Possible mechanisms of the dissociation between catecholamine and enzyme release are discussed.

Animals↗
PubMed1980

Release of noradrenaline from the ligated cat hypogastric nerve.

After in vivo ligation for 24 of the cat hypogastric nerve, large amounts of noradrenaline (NA) and dopamine beta-hydroxylase (DBH) accumulated in the nerve segment immediately proximal to the ligature (P 1). In vitro incubation of 24-h-ligated nerves ((segments P1 and P2) in oxygenated Krebs solution at 37 degrees C in the presence of the ionophore X537A or high K+ concentrations caused a marked release of endogenously accumulated NA into the incubation medium. High-K+-evoked release was entirely dependent on extracellular Ca2+. Electrical nerve stimulation caused an 80% tissue NA loss, but the transmitter could not be found in the medium as intact NA. These results suggest that the in vivo ligated cat hypogastric nerve may serve as a useful model of adrenergic nerve terminals free of effector cells.

Animals↗
PubMed1980

Release of endogenous noradrenaline from ligated cat hypogastric nerve by veratridine.

The effect of veratridine on in vitro release of noradrenaline (NA) from ligated cat hypogastric nerve was investigated. After in vivo ligation for 24-48 h, large amounts of NA and dopamine-beta-hydroxylase (DBH) accumulated in the nerve segment immediately proximal to the ligature (P1). In vitro incubation of ligated nerves (segments P1 and P2) in oxygenated Krebs solution at 37 degrees C in the presence of veratridine caused a marked and dose-dependent release of endogenously accumulated NA into the incubation medium. The release continued to occur for a considerable time, even after washout of the drug. Veratridine-induced depletion of tissue NA was accounted for by its release, as NA, into the incubating medium. The secretory response to veratridine was readily blocked by tetrodotoxin (TTX). Veratridine-induced release was dependent on calcium and abolished by high magnesium. On the basis of the similarity between the NA secretory response to veratridine in this preparation and in adrenergically innervated organs, the results favour the view that the in vivo-ligated cat hypogastric nerve may serve as a useful model of adrenergic nerve terminals free of effector cells.

Animals↗
PubMed1985

Evidence that ATP is involved as a co-transmitter in the hypogastric nerve supplying the seminal vesicle of the guinea-pig.

Electrical field stimulation of the guinea-pig seminal vesicle (4 Hz and 16 Hz) produced a biphasic response. The initial rapid twitch response was blocked by desensitisation of the P2-purinoceptor with alpha, beta-methylene ATP. The slower tonic response was blocked by the alpha-adrenoceptor antagonist phentolamine (10 microM). The present results are similar to those found earlier for the guinea-pig vas deferens, indicating that ATP and NA may be released as co-transmitters from hypogastric nerve fibres.

Adenosine Triphosphate↗
PubMed1989

In vivo experiments for the evaluation of alpha 1-adrenoceptor antagonistic effects of SGB-1534 on canine urethra.

The alpha 1-adrenoceptor blocking effects of SGB-1534 on the urethral smooth muscle were compared in in vivo lower urinary tract preparations of anesthetized dogs, with the effects of other alpha 1-adrenoceptor antagonists, prazosin and bunazosin. Hypogastric nerve stimulation and selective administration of phenylephrine to the urethra and bladder through the cannulated right external iliac artery (i.a.) elicited reproducible frequency- and dose-dependent increases in intra-urethral pressure. Intra-bladder pressure was increased by the nerve stimulation but not by i.a. phenylephrine. SGB-1534, prazosin or bunazosin (0.1-10 micrograms/kg i.v.) dose dependently suppressed the urethral contraction evoked by the nerve stimulation and i.a. phenylephrine but did not influence the bladder contraction elicited by nerve stimulation. The alpha 1-adrenoceptor blocking potency of SGB-1534 was approximately 2.3 and 8.1 times greater than that of prazosin and bunazosin, respectively. The results indicate that alpha 1-adrenoceptors may mediate mainly the urethral contraction induced by hypogastric nerve stimulation and i.a. phenylephrine, and that SGB-1534 was more potent alpha 1-adrenoceptor blocking activity than prazosin and bunazosin in the canine urethra.

Adrenergic alpha-Antagonists↗
PubMed1996

The effect of NG-monomethyl-L-arginine on bladder function.

Recent studies have demonstrated the presence of nitric oxide synthase (NO synthase) in lower urinary tract tissues, however, its role in the detrusor is unclear. The current study was designed to determine if NO synthase inhibition alters detrusor activities, including micturition volume threshold, and inhibition of pelvic nerve-evoked contractions by various stimuli. In naive, anesthetized adult cats, inhibition of pelvic nerve-evoked bladder contractions, induced by hypogastric nerve stimulation or the intraarterial administration of NA, ATP, adenosine, beta,gamma-methylene ATP and 2-methylthio ATP, was measured before and after inhibition of NO synthase. The micturition volume threshold was also measured before and after NO synthase inhibition. L-NMMA decreased the micturition volume threshold by 38% (2 mg intravesical administration) or 80% (4 mg/kg i.a.). The magnitude of the micturition contractions was modestly increased. These results, and information in the literature, indicate that NO may play a role in the collection phase of the bladder cycle and any alteration of nitric oxide availability could induce or allow development of various bladder malfunctions, such as small bladder diseases, like interstitial cystitis.

Animals↗
PubMed1988

Factors affecting the relative viability of centrifascicular and subperineurial axons in acute peripheral nerve ischemia.

An acute reduction in nerve blood flow commonly results in centrifascicular fiber degeneration with subperineurial fiber sparing (CD-SS pattern) in experimental and human peripheral nerve. The mechanism of CD-SS pattern is uncertain. Three hypotheses for the better resistance to ischemic degeneration of subperineurial fibers have been suggested. The subperineurial region has been proposed to have (i) better anastomotic flow (ii) an increased capillary density, or (iii) an extra source of oxygen (from surrounding tissue). We developed methodology that permitted testing of these hypotheses. Nerve blood flow and oxygen tension were measured simultaneously in the central and subperineurial regions using microelectrodes and polarographic techniques. The longitudinal distribution of nerve blood flow was also determined. To test the first hypothesis, nerve blood flow was measured before and after arterial ligation. Well defined watershed areas of reduced flow were found in the longitudinal axis. However, even within these zones, there was a uniform rather than a differential radial reduction in nerve blood flow resulting from ligation. To test the second hypothesis, nerve blood flow was measured during induced arterial hypotension. Nerve blood flow was reduced in proportion to the severity of the ischemic insult but there was no physiologically significant difference between the central and subperineurial areas. To test the oxygen diffusion hypothesis, nerve oxygen tension was monitored simultaneously in the two sites at rest and during ischemia produced by arterial hypotension. Arterial hypotension resulted in severe centrifascicular hypoxia whereas subperineurial oxygen tension was much better maintained as a result of diffusion of oxygen into nerve from the surrounding pool of oil. These findings strongly suggest that the sparing of subperineurial axons in ischemic nerve trunks is due to the diffusion of oxygen from surrounding viable tissues rather than greater capillary density or anastomotic flow.

Animals↗
PubMed1993

Role of nitric oxide in sympathetic neurotransmission in opossum internal anal sphincter.

BACKGROUND: The role of nitric oxide in the gut in response to sympathetic nerve stimulation has not been examined. The present study examined the influence of the NO synthase inhibitor L-NG-nitro-arginine (L-NNA) on responses to hypogastric nerve stimulation (HGNS) in the opossum internal anal sphincter (IAS). METHODS: Resting pressures in the IAS (IASP) were monitored using low-compliance continuously perfused catheters. RESULTS: The predominant response to HGNS was an elevation of the resting tone in the IAS. The other responses of infrequent nature were a decrease in the IASP and a biphasic response (an initial increase followed by a decrease in the IASP). beta-Adrenoceptor antagonist propranolol had no significant effect on the increase in the IASP by HGNS but almost abolished the decrease in the IASP caused by HGNS and unmasked the excitatory responses. The IAS responses to HGNS were frequency dependent and abolished by guanethidine (adrenergic blocker). L-NNA caused significant and stereoselective suppression of all IAS responses to HGNS. The suppressed HGNS responses were completely reversed by the NO precursor L-arginine stereoselectively. The NO synthase inhibitor and guanethidine had no effect on the increase in IASP by phenylephrine. CONCLUSIONS: NO may play a significant role in the facilitatory modulation of sympathetic responses in the IAS.

Adrenergic alpha-Antagonists↗
PubMed1991

Prostaglandin E2 selectively affects purinergic transmission in guinea pig vas deferens.

The effect of prostaglandin E2 (PGE2) on the contractile response of the guinea pig vas deferens was examined. Postganglionic hypogastric nerve stimulation for 7 sec at 20 Hz induced a biphasic contractile response, consisting of fast phasic and delayed tonic components. Prostaglandin E2 delayed the onset and increased the maximum contractile responses. Stimulation in the presence of prazosin induced only a fast phasic contraction. Treatment with PGE2, in the presence of prazosin, delayed the onset of this response and increased its maximum. The delayed contraction, observed on stimulation in the presence of alpha,beta-methylene adenosine triphosphate (ATP), was enhanced moderately and concentration-dependently by PGE2. Short-term stimulation with 5 pulses induced a small fast phasic contraction. This contraction, which could be desensitized by alpha,beta-methylene ATP, was inhibited by PGE2 but not by prazosin. Prostaglandin E2 significantly enhanced the transient phasic contraction, induced by addition of exogenous ATP to the organ bath and had a similar but somewhat smaller effect on the tonic contraction induced by the addition of exogenous norepinephrine (NE). These findings suggest that PGE2 selectively delayed neurotransmission, mediated by ATP and enhanced contractions of the smooth muscle of guinea pig vas deferens, elicited by ATP or NE.

Adenosine Triphosphate↗