Comparative Pharmacological and Histochemical Evidence for Purinergic Inhibitory Innervation of the Portal Vein of the Rabbit, but Not Guinea‐pig

Cocks

Crowe

1978

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1 Fluorescence histochemical localization of quinacrine (which binds to adenosine 5'-triphosphate (ATP)) revealed nerve fibres running singly and in bundles in both rat and rabbit anococcygeus muscle. Single neurone cell bodies and ganglia containing between 2 and 50 cells were also observed. 2 Catecholamine fluorescence studies revealed a dense adrenergic ground plexus, but no adrenergic ganglion cells were detected. No acetylcholinesterase-positive nerve fibres or ganglion cells were seen in the rat. 3 When the tone was raised with guanethidine, a relaxation in response to field stimulation was revealed, which was unaffected by atropine but blocked by tetrodotoxin. 4 Release of ATP increased 3 to 6 times above background during stimulation of these non-adrenergic, non-cholinergic, inhibitory nerves. 5 Neither quinacrine staining nor the release of ATP during inhibitory nerve stimulation was affected by 6-hydroxydopamine treatment, which abolished catecholamine fluorescence. 6 Exogenous ATP produced relaxation in high tone preparations of the rabbit anococcygeus muscle. ATP produced either contraction or a small relaxation followed by a contraction of the rat anococcygeus muscle, but treatment with low concentrations of the prostaglandin synthesis inhibitor indomethacin, converted the contraction to a relaxation. 7 These data are consistent with the view that the anococcygeus muscle is innervated by purinergic inhibitory nerves.

Section: Discussionmentioning

confidence: 66%

Evidence for Purinergic Innervation of the Anococcygeus Muscle

Cocks

Crowe

1978

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“…Effects of 2-chloroadenosine on contractions due to exogenous noradrenaline (NA) Since postjunctional purinoceptors are present in each of the three preparations (Sjoberg & Wahlstr6m, 1975;Burnstock et al, 1979;Ishii & Shimo, 1983) the postjunctional actions of 2-chloroadenosine were also considered. NA, 2 x 10-7 M, elicits a contraction similar in magnitude to that caused by nervous stimulation at the parameters used above.…”

Section: -mentioning

confidence: 99%

“…Quinacrine fluorescence Portal veins dissected from rabbits (n = 6), guinea-pigs (n = 6) and rats (n= 6) were washed in modified Krebs solution (see Burnstock et al, 1979) at room temperature and were then incubated for 1 h in Krebs solution containing 5 x 10-7M quinacrine dihydrochloride and continually gassed with 95% 02, 5% C02. At the end of the incubation period they were washed for a further 20-30 min with quinacrine-free Krebs solution.…”

Section: Histochemistrymentioning

confidence: 99%

Indirect evidence that purinergic modulation of perivascular adrenergic neurotransmission in the portal vein is a physiological process

Crowe

Kennedy

et al. 1984

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1The effects of adenine nucleotides and nucleosides on the contractile response to perivascular nerve stimulation were compared in the isolated portal vein of rabbit, rat and guinea-pig. 2 2-Chloroadenosine was more potent than adenosine and ATP, which were equipotent in producing inhibition of neurogenic contractions in the rabbit and rat via prejunctional P1-purinoceptors. 3 In contrast, neurogenic contractions of the guinea-pig portal vein were not inhibited by adenosine and were potentiated by 2-chloroadenosine and, to a lesser extent, by ATP. 4 Fluorescence histochemical localization of quinacrine, which binds to high levels of ATP, revealed a dense perivascular nerve plexus in the portal vein of rabbit and rat but not of guinea-pig. 5After chemical sympathectomy, quinacrine-positive nerves persisted in the rabbit (supporting other evidence for the presence of purinergic nerves) but not in the rat (supporting other evidence for ATP as a cotransmitter in adrenergic nerves). 6 It is concluded that a prejunctional purinergic modulatory mechanism operates in adrenergic neurotransmission in the portal vein of rabbit and rat but not guinea-pig, and it is suggested that this indicates a physiological mechanism.

“…Thus, exogenous ATP in the rabbit mesenteric artery may be acting upon receptors which would be stimulated physiologically by sensory rather than sympathetic nerves. The rabbit portal vein is innervated by sympathetic nerves but is also supplied with non-sympathetic (purinergic) nerves which release ATP and mediate vasodilatation (Burnstock et al, 1979;Reilly et al, 1987;Su, 1987). These non-adrenergic nerves are the source of approximately 50% of the purines released by electrical field stimulation (Levitt & Westfall, 1982) and may account for the presence of the P2y-purinoceptor on the smooth muscle in this vessel.…”

Section: Basal Tone Preparationsmentioning

confidence: 99%

Vasodilator response of coronary smooth muscle to the sympathetic co‐transmitters noradrenaline and adenosine 5′‐triphosphate

Corr

1991

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1 Vasodilator and vasoconstrictor responses to noradrenaline (NA), adenosine and adenosine 5'-triphosphate (ATP) were examined in isolated ring segments of the left anterior descending coronary artery of the rabbit in the absence of endothelium.2 NA caused dose-dependent relaxation of potassium-constricted vessels in the absence of aladrenoceptor blockade, with a pD2 of 5.96 + 0.21. This was inhibited by 1 gM propranolol. Constrictor responses of vessels at baseline tension were only seen at concentrations greater than 1 mm, and reached a maximum of 6% of the contraction to 30 mm KCI. 3 ATP caused relaxation of the potassium-constricted ring segments in a dose-dependent manner, although a transient constriction often preceded the relaxation. Adenosine was equipotent with ATP in producing relaxation; this was significantly inhibited by the Pl-purinoceptor antagonist, 8-phenyltheophylline (8-PT). The responses to ATP were little affected by 8-PT, indicating that ATP was not acting through breakdown to adenosine. At basal tone, ATP produced transient vasoconstriction only at concentrations greater than 0.1 mm, reaching a maximum of 38% of the contraction to 30mM KCl. 4 We conclude that in the rabbit coronary artery both NA and ATP produce vasodilatation by a direct action on the smooth muscle.