A pharmacological study of the rabbit saphenous artery <i>in vitro</i>: a vessel with a large purinergic contractile response to sympathetic nerve stimulation

Burnstock, Geoffrey; Warland, Jennifer J.I.

doi:10.1111/j.1476-5381.1987.tb16830.x

Cited by 126 publications

(93 citation statements)

References 28 publications

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“…It seems clear, however, that the proposed ATP-mediated com-ponent of the smooth muscle response of isolated blood vessels is a rapid short-lasting contraction where the ATP contribution relative to NA is inversely related to stimulation frequency (i.e. relatively largest at low stimulation frequencies) Burnstock & Warland, 1987). In contrast, the remaining nerve stimulation-evoked responses in the pig spleen after reserpine were slowly developing, long-lasting and were most pronounced at high frequencies.…”

Section: Discussionmentioning

confidence: 61%

“…Increasing evidence based on observations from in vitro experiments on isolated blood vessels (Kugelgen & Starke, 1985;Kennedy et al, 1986;Burnstock & Warland, 1987;Muramatsu, 1987) and vas deferens (Fedan et al, 1981;Sneddon et al, 1982;Stjarne & Astrand, 1985), suggests that ATP is a co-transmitter with NA in the electrical and/or contractile responses of smooth muscle cells evoked by sympathetic nerve stimulation. It seems clear, however, that the proposed ATP-mediated com-ponent of the smooth muscle response of isolated blood vessels is a rapid short-lasting contraction where the ATP contribution relative to NA is inversely related to stimulation frequency (i.e.…”

Section: Discussionmentioning

confidence: 99%

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Evidence for co‐transmitter role of neuropeptide Y in the pig spleen

Lundberg

Rudehill

Sollevi

et al. 1989

British J Pharmacology

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1 The possible involvement of neuropeptide Y (NPY) in relation to noradrenaline (NA) and adenosine triphosphate (ATP) mechanisms in the sympathetic nervous control of the vascular tone and capsule contraction in the blood perfused pig spleen was investigated in vivo. 2 Local injections or infusions of NA, NPY and a-, f-methylene ATP (mATP) caused vasonconstriction (perfusion pressure increase) and capsule contraction (increased venous blood flow). ATP only evoked vasodilatation. NPY was about 50 fold more potent than NA as a vasoconstrictor, and the NPY response was more long-lasting. Reserpine treatment did not change the effects of NPY. 3 Electrical stimulation of the splenic nerves in control animals caused a frequency-dependent, guanethidine-sensitive output of both NPY-like immunoreactivity (-LI) and NA, suggesting corelease. The output of NPY-LI relative to NA was enhanced at high frequency stimulation. Furthermore, a-adrenoceptor blockade by phentolamine enhanced both the output of NPY-LI and NA while inhibition of the neuronal uptake of NA with desipramine reduced the low frequency stimulation-evoked overflow of NPY-LI. Preganglionic denervation did not change the output of NPY-LI or NA. 4 Reserpine treatment reduced both the splenic content of NA and NPY-LI. Preganglionic denervation inhibited the reserpine-induced depletion of the NPY content but not of NA in terminal areas. The stimulation-evoked NPY overflow was markedly enhanced, especially at low-frequency stimulation after resperpine, and the plasma levels of NPY-LI in the venous effluent were then in the nmolar range (i.e. where exogenous NPY induced vasoconstriction). The perfusion-pressure increase upon stimulation in reserpine-treated, preganglionically-denervated animals was highly correlated (r = 0.91) to the NPY overflow. The functional 0.5 Hz responses were reduced after reserpine, while at higher frequencies the functional effects were of similar magnitude to controls but longer-lasting.5 Tyramine induced a release of NA but not of NPY-LI. Furthermore, the increase in perfusion pressure induced by tyramine was absent after reserpine.6 After tachyphylaxis to the vasoconstrictor effects of mATP, the nerve stimulation-evoked, functional response as well as the NA and NPY-LI overflow were unchanged. After reserpine treatment, both the perfusion-pressure increase and NPY-LI overflow to nerve stimulation were reduced after mATP tachyphylaxis. 7 In conclusion, release of NPY rather than ATP may explain the long-lasting, non-adrenergic, splenic functional responses in reserpinized animals upon sympathetic stimulation. However, NA is most likely the main splenic transmitter when low-frequency stimulation is used under control conditions. Neuropeptide Y (NPY), a peptide with 36 amino porcine brain (Tatemoto, 1982), co-exists with noracid residues which was originally isolated from adrenaline (NA) in postganglionic, sympathetic nerves in a variety of peripheral organs (Lundberg et

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Evidence for co‐transmitter role of neuropeptide Y in the pig spleen

Lundberg

Rudehill

Sollevi

et al. 1989

British J Pharmacology

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“…Both purinergic (prazosin-resistant) component and adrenergic (prazosinsensitive) component were shown to involve the neurogenic vasoconstriction induced by electrical field stimulation in different types of blood vessels including the rabbit ear [1], saphenous [2], hepatic [3], and splenic artery [4]. However, the ratio of NA:ATP released by the sympathetic nerves supplying different blood vessels is variable.…”

Section: Introductionmentioning

confidence: 99%

Physiological significance of P2X receptor-mediated vasoconstriction in five different types of arteries in rats

Jia²,

Chen

et al. 2011

Purinergic Signalling

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P2X 1 receptors, the major subtype of P2X receptors in the vascular smooth muscle, are essential for α,β-methylene adenosine 5′-triphosphate (α,β-MeATP)-induced vasoconstriction. However, relative physiological significance of P2X 1 receptor-regulated vasoconstriction in the different types of arteries in the rat is not clear as compared with α 1 -adrenoceptor-regulated vasoconstriction. In the present study, we found that vasoconstrictive responses to noncumulative administration of α,β-MeATP in the rat isolated mesenteric arteries were significantly smaller than those to single concentration administration of α,β-MeATP. Therefore, we firstly reported the characteristic of α,β-MeATP-regulated vasoconstrictions in rat tail, internal carotid, pulmonary, mesenteric arteries, and aorta using single concentration administration of α,β-MeATP. The rank order of maximal vasoconstrictions for α,β-MeATP (E max·α,β-MeATP ) was the same as that of maximal vasoconstrictions for noradrenaline (E max·NA ) in the internal carotid, pulmonary, mesenteric arteries, and aorta. Moreover, the value of (E max·α,β-MeATP /E max·KCl )/(E max·NA /E max·KCl ) was 0.4 in each of the four arteries, but it was 0.8 in the tail artery. In conclusion, P2X 1 receptor-mediated vasoconstrictions are equally important in rat internal carotid, pulmonary, mesenteric arteries, and aorta, but much greater in the tail artery, suggesting its special role in physiological function.

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“…Furthermore, the identity of the neurotransmitter(s) released from lumbar sympathetic fibres which mediate contractions of colon circular muscle is as yet not known. It could involve the corelease of adenosine 5'-triphosphate (ATP) or a related nucleotide and noradrenaline, as has been shown in vas deferens (Sneddon et al, 1982;Meldrum & Burnstock, 1983;Sneddon & Westfall, 1984;Burnstock & Sneddon, 1985;von Kugelgen et al, 1989) and in arteries and submucosal arterioles (von Kugelgen & Starke, 1985;1991;Burnstock & Warland, 1987;Evans & Surprenant, 1992).…”

Section: Introductionmentioning

confidence: 99%

Stimulation of lumbar sympathetic nerves evokes contractions of cat colon circular muscle mediated by ATP and noradrenaline

Venkova

Krier

1993

British J Pharmacology

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1 The action of the lumbar sympathetic nerves to cat colon was studied in vitro using isolated muscle strips with attached lumbar colonic nerves (LCN) orientated in the axis of circular muscle layer. Electrical stimulation of LCN caused frequency-dependent increases in resting tension and in amplitude of spontaneous contractions. Contractile responses were abolished by tetrodotoxin (31M) and by guanethidine (30 JAM), indicating that they were neurogenic, involving the release of neurotransmitter from sympathetic fibres.2 Propranolol (I-9 J1M), a B-adrenoceptor antagonist, caused a concentration-dependent potentiation of LCN-evoked contractile responses. Propranolol (3 JAM) potentiated contractile responses to exogenously applied noradrenaline but not to phenylephrine.3 Phentolamine (1-9 JAM), an a-adrenoceptor antagonist, and prazosin (1-9 pM), an xl-adrenoceptor antagonist, caused a concentration-dependent reduction of amplitude but did not abolish LCN-evoked contractile responses. Prazosin (3 AM) or phentolamine (3 jaM) antagonized contractile responses to noradrenaline and phenylephrine.4 Desensitization of purinoceptors with the P2x-receptor agonist, a,j3-methylene ATP, caused a decrease in amplitude of LCN-evoked contractile responses and abolished contractile responses to ATP. In muscle strips where xl-adrenoceptors were blocked with prazosin (3 JAM) and P2-purinoceptors were desensitized with a,-methylene ATP, the amplitude of contractile responses was reduced by 82-100%.5 The P2X-purinoceptor antagonists, arylazido amino propyl adenosine triphosphate (ANAPP3) and suramin, affected LCN-evoked contractile responses. ANAPP3 (50-100 AIM) caused a concentrationdependent reduction in the amplitude of contractile response. Suramin (100 JiM) caused a small reduction in amplitude of contractile responses but potentiated their amplitude at a concentration of 500 JAM.6 ANAPP3 (100 AM) irreversibly inhibited contractions to X,P-methylene ATP or ATP. Suramin (100-500 JiM) inhibited contractions to ax,P-methylene ATP (0.5-1IJM) or low concentrations of ATP (10-50 AM) but potentiated contractions at higher concentrations. ANAPP3 (100 JiM) and suramin (100, 500 JAM) had no affect on contractile responses to noradrenaline. 7 Clonidine (0.05-1 JAM), a selective 'X2-adrenoceptor agonist, caused a concentration-dependent reduction in amplitude of LCN-evoked contractile responses, at 10 Hz, while yohimbine (0.1-1 JAM), a selective a2-adrenoceptor antagonist, increased them. At 1 JAM, both compounds affected LCN-evoked contractions at all frequencies. This suggests that prejunctional M2-receptors are involved in autoinhibition at sympathetic terminals. 8 In summary, LCN-evoked contractile responses involve the corelease of noradrenaline and ATP or a related purine nucleotide from sympathetic fibres. It is likely that the neurogenic responses are mediated through excitatory postjunctional ax-adrenoceptors, excitatory suramin-sensitive and suramin-insensitive P2X-purinoceptors and inhibitory ,-adrenoceptors. Also, autoinhibitor...

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A pharmacological study of the rabbit saphenous artery in vitro: a vessel with a large purinergic contractile response to sympathetic nerve stimulation

Cited by 126 publications

References 28 publications

Evidence for co‐transmitter role of neuropeptide Y in the pig spleen

Evidence for co‐transmitter role of neuropeptide Y in the pig spleen

Physiological significance of P2X receptor-mediated vasoconstriction in five different types of arteries in rats

Stimulation of lumbar sympathetic nerves evokes contractions of cat colon circular muscle mediated by ATP and noradrenaline

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