Inhibition of adrenergic neurotransmission in canine vascular smooth muscle by histamine: mediation by H2-receptors.

McGrath, Michael A.; Shepherd, John T.

doi:10.1161/01.res.39.4.566

Cited by 100 publications

(59 citation statements)

References 31 publications

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“…Further, the positive inotropic and chronotropic responses to stimulation were progressively reduced by successively higher concentrations of histamine, whereas the S-I efflux of radioactivity was reduced by low concentrations of histamine and enhanced by a high concentration. The concentrations of histamine that inhibited transmitter noradrenaline release in guinea-pig atria were similar to those found by McGrath & Shepherd (1976) to produce this effect in isolated strips of canine blood vessels. Lokhandwala (1978) showed that in the dog heart in situ, histamine in concentrations too low to elicit postjunctional responses, nevertheless inhibited responses of the heart to sympathetic nerve stimulation.…”

Section: Discussionsupporting

confidence: 80%

“…The development of the concept of modulation of transmitter noradrenaline release mediated by the action of endogenous substances acting on specific prejunctional receptors (see reviews by Starke, 1977;Westfall, 1977) led to the exploration of a similar role for histamine. Thus the ability of histamine to depress responses to sympathetic nerve stimulation by a prejunctional mechanism has been demonstrated in canine blood vessels (McGrath & Shepherd, 1976) and heart (Lokhandwala, 1978). The histamine receptors involved were characterized by these workers as the H2-type since the inhibitory effects of histamine were attenuated by the H2-receptor antagonist, metiamide.…”

Section: Introductionmentioning

confidence: 99%

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EFFECTS OF HISTAMINE ON THE RESTING AND STIMULATION‐INDUCED RELEASE OF [³H]‐NORADRENALINE IN GUINEA‐PIG ISOLATED ATRIA

Rand

Story

Wong-Dusting

1982

British J Pharmacology

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The sympathetic transmitter stores of guinea‐pig isolated atria were labelled with [3H]‐noradrenaline. The effects of histamine (0.3 to 100 μmol/l) on resting and stimulation‐induced (S‐I, 2 Hz for 10 s) release of radioactivity were investigated. Histamine, in low concentrations (0.3 and 1 μmol/l) had no effect on resting release but inhibited S‐I release of radioactivity. The inhibition was abolished by the H2‐receptor antagonist, cimetidine (10 μmol/l) and also by the H1‐receptor antagonist, mepyramine (1μmol/l). The inhibitory actions of histamine on S‐I release were not due to indirect effects involving α‐adrenoceptors, β‐adrenoceptors, muscarinic cholinoceptors or prostaglandin synthesis. Histamine in a high concentration (100 μmol/l) increased the resting and S‐I release of radioactivity. The increase in resting release was abolished by the neuronal uptake blocking drug cocaine (30 μmol/l) but the increase in S‐I release was only partially blocked by cocaine.

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

EFFECTS OF HISTAMINE ON THE RESTING AND STIMULATION‐INDUCED RELEASE OF [³H]‐NORADRENALINE IN GUINEA‐PIG ISOLATED ATRIA

Rand

Story

Wong-Dusting

1982

British J Pharmacology

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“…Inhibition was apparent at frequencies of sympathetic stimulation (up to 10 Hz) that are close to rates of firing found in vivo in efferent sympathetic fibres in the airways of the dog or cat (Widdicombe, 1966). It has been shown that histamine can inhibit sympathetic contractions of dog saphenous vein and tibial artery (McGrath & Shepherd, 1976), seemingly by reducing the output of noradrenaline from sympathetic nerve terminals during electrical stimulation. There may be a similar effect at sympathetic nerve terminals in the guinea-pig trachea.…”

Section: Discussionmentioning

confidence: 65%

Autonomic responses of the isolated, innervated trachea of the guinea‐pig: interaction with autonomic drugs, histamine and 5‐hydroxytryptamine

McCaig

1986

British J Pharmacology

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1 Intraluminal pressure was measured in the isolated, fluid-filled trachea of the guinea pig, with autonomic innervation on the right side intact. Increases or decreases in intraluminal pressure reflected excitatory or inhibitory responses respectively, in the tracheal smooth muscle. 2 Stimulation of the cervical vagus nerve evoked a cholinergic excitatory response. After cholinergic blockade with atropine, a non-adrenergic, non-cholinergic inhibitory response was obtained.3 Stimulation of the cervical sympathetic trunk, or stellate ganglion, evoked P-adrenergic inhibitory responses. In the presence of propranolol, sympathetic stimulation evoked x-adrenergic excitatory responses which were of low amplitude (< 5% of cholinergic excitatory responses). In the presence of phentolamine but not prazosin, P-adrenergic inhibitory responses were potentiated.4 Neostigmine potentiated responses to vagal stimulation, increasing the amplitude and duration of response. At higher concentrations neostigmine (i) raised intraluminal pressure, a response blocked by atropine, and (ii) attenuated sympathetic inhibitory responses, an effect largely blocked by atropine. 5 Histamine increased intraluminal pressure and this response was attenuated by atropine. In the presence of histamine, vagal excitatory responses were attenuated. Sympathetic inhibitory responses at low frequencies of stimulation (up to 10 Hz) were inhibited by histamine. 6 5-Hydroxytryptamine (5-HT) increased intraluminal pressure also, an effect partially blocked by atropine. 5-HT had no effect on vagal excitatory responses. Like histamine, 5-HT attenuated sympathetic inhibitory responses at lower frequencies of stimulation.

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“…Acetylcholine, 8 ' "• 17 histamine, 18 and also moderate increases in potassium concentrations 19 have been demonstrated to inhibit release of norepinephrine in canine blood vessels during nerve stimulation. The present studies extend this list of prejunctional vasodilators to adenosine and the adenine nucleotides.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of sympathetic neurotransmission in canine blood vessels by adenosine and adenine nucleotides.

Verhaeghe¹,

Vanhoutte²,

Shepherd³

1977

Circulation Research

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174

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SUMMARY Adenosine and the adenine nucleotides caused a greater relaxation of strips of canine saphenous vein and tibial artery when they had been contracted by nerve stimulation than by exogenous norepinephrine. An infusion of adenosine into the dogs' lateral saphenous vein, perfused at constant flow, caused a greater relaxation of this vein when constricted by electrical stimulation of the lumbar sympathetic chain than by exogenous norepinephrine. That this difference was due to inhibition by these compounds of the output of neurotransmirter from the sympathetic nerve endings was demonstrated by column chromatographic analysis of the radioactivity in the supervision fluid of vein strips, previously incubated with tritiated norepinephrine. Both adenosine and adenosine triphosphate (10"' M) reduced the efflux of 3 H-norepinephrine during nerve stimulation with electrical impulses. Adenosine also reduced the efflux caused by potassium (30 mM), but not that caused by tyramine (6 x 10~6 M). Theophylline antagonized the inhibitory effect of adenosine on the sympathetic neurotransmission. We found that at 4 x 10 4 M adenosine triphosphate still caused a decreased efflux of neurotransmitter during electrical stimulation, but with adenosine the 3 H-norepinephrine efflux no longer decreased and the overflow of deaminated compounds increased. Furthermore, the same concentration of adenosine increased the efflux of 3 H-norepinephrine and deaminated compounds in unstimulated strips, and the increase of 3 H-norepinephrine was enhanced after monoamine oxidase inhibition. Thus, we conclude that at higher concentrations adenosine increases the intraneuronal leakage of norepinephrine out of the storage vesicles.ADENOSINE and the adenine nucleotides by a local action on blood vessels cause their dilation. This has been demonstrated both in vivo and in vitro. '" 3 There is evidence that these substances can inhibit neuromuscular transmission in the rat phrenic nerve-diaphragm and frog sartorius preparations 4 ' 5 and cholinergic neurotransmission in the intestinal wall. 6 The present experiments were performed to determine whether adenosine and related nucleotides inhibit adrenergic neurotransmission in canine blood vessels. Methods STUDIES IN VITROHelical strips of lateral saphenous veins and anterior tibial arteries, isolated from dogs (15-25 kg) anesthetized with sodium pentobarbital (30 mg/kg, iv), were placed in an organ bath filled with Krebs-Ringer solution (NaCl, 118.2 mM; KC1, 4.7 mM; MgSO 4 , 1.2 mM; KH 2 PO 4 , 1.2 mM; CaCl 2 , 2.5 mM; NaHCO 3 , 25 mM; calcium disodium ethylenediaminetetraacetate (EDTA) 0.026 mM; and glucose, 5.5 mM) maintained at 37°C and aerated with a 95% O 2 -5% CO 2 mixture. The strips were attached to a force transducer (Grass FT 03C) for isometric tension recording. The transducer was mounted on a movable support allowing fine adjustments of the strip length and connected to a pen writing recorder (Gould Brush 220). For electrical stimulation of the preparations, two rectangular platinum electr...

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Inhibition of adrenergic neurotransmission in canine vascular smooth muscle by histamine: mediation by H2-receptors.

Cited by 100 publications

References 31 publications

EFFECTS OF HISTAMINE ON THE RESTING AND STIMULATION‐INDUCED RELEASE OF [³H]‐NORADRENALINE IN GUINEA‐PIG ISOLATED ATRIA

EFFECTS OF HISTAMINE ON THE RESTING AND STIMULATION‐INDUCED RELEASE OF [³H]‐NORADRENALINE IN GUINEA‐PIG ISOLATED ATRIA

Autonomic responses of the isolated, innervated trachea of the guinea‐pig: interaction with autonomic drugs, histamine and 5‐hydroxytryptamine

Inhibition of sympathetic neurotransmission in canine blood vessels by adenosine and adenine nucleotides.

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Inhibition of adrenergic neurotransmission in canine vascular smooth muscle by histamine: mediation by H2-receptors.

Cited by 100 publications

References 31 publications

EFFECTS OF HISTAMINE ON THE RESTING AND STIMULATION‐INDUCED RELEASE OF [3H]‐NORADRENALINE IN GUINEA‐PIG ISOLATED ATRIA

EFFECTS OF HISTAMINE ON THE RESTING AND STIMULATION‐INDUCED RELEASE OF [3H]‐NORADRENALINE IN GUINEA‐PIG ISOLATED ATRIA

Autonomic responses of the isolated, innervated trachea of the guinea‐pig: interaction with autonomic drugs, histamine and 5‐hydroxytryptamine

Inhibition of sympathetic neurotransmission in canine blood vessels by adenosine and adenine nucleotides.

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EFFECTS OF HISTAMINE ON THE RESTING AND STIMULATION‐INDUCED RELEASE OF [³H]‐NORADRENALINE IN GUINEA‐PIG ISOLATED ATRIA

EFFECTS OF HISTAMINE ON THE RESTING AND STIMULATION‐INDUCED RELEASE OF [³H]‐NORADRENALINE IN GUINEA‐PIG ISOLATED ATRIA