ABSTRACT
1. Electrical and mechanical responses of epididymal and prostatic regions of rat, rabbit and guinea-pig vas deferens have been examined to investigate regional variation in purinergic and adrenergic mechanisms. 2. Noradrenaline was significantly more potent in producing contraction in epididymal segments of the muscle than in prostatic segments. 3. ATP and alpha,beta,methylene ATP were significantly more potent in producing contraction of prostatic segments than epididymal segments. 4. In guinea-pig vas deferens the resting membrane potential was greater in smooth muscle cells in the prostatic region than in the epididymal. Excitatory junction potentials (EJPs) in both the epididymal and prostatic regions were of similar magnitude and were almost abolished by the P2x-purinoceptor antagonist suramin. 5. The alpha-adrenoceptor antagonist phentolamine had no inhibitory action on EJPs in either region of the guinea-pig vas deferens.
Subject(s)
Muscle, Smooth/drug effects , Receptors, Adrenergic/physiology , Receptors, Purinergic/physiology , Vas Deferens/physiology , Adenosine Triphosphate/analogs & derivatives , Adenosine Triphosphate/pharmacology , Animals , Dose-Response Relationship, Drug , Electric Stimulation , Epididymis , Guinea Pigs , Male , Membrane Potentials/drug effects , Muscle Contraction/drug effects , Norepinephrine/pharmacology , Prostate , Rabbits , Rats , Receptors, Adrenergic/drug effects , Receptors, Purinergic/drug effects , Suramin/pharmacology , Vas Deferens/drug effectsABSTRACT
Isolated tail arteries from spontaneously hypertensive rats (SHR) were more responsive than those from Wistar-Kyoto (WKY) control rats to exogenously applied noradrenaline (NA), ATP, alpha,beta-methylene ATP (mATP), KCl and sympathetic nerve stimulation. The sympathetic contractile responses of the SHR and WKY were both reduced to 10-20% of control by alpha 1-adrenoceptor antagonism. The pressor responses to sympathetic nerve stimulation were significantly greater in the SHR than the WKY rats at all stimulation frequencies examined (1-10 Hz). There was no significant difference between SHR and WKY rats in the magnitude of pressor responses produced by i.v. administration of NA or mATP. The pressor responses to sympathetic nerve stimulation in the pithed SHR were no more resistant to alpha-adrenoceptor antagonism than those of the WKY. The results suggest that the contribution by ATP to sympathetic vasoconstriction is no greater in SHR than WKY.
Subject(s)
Muscle, Smooth, Vascular/innervation , Receptors, Purinergic/physiology , Sympathetic Nervous System/physiology , Adenosine Triphosphate/pharmacology , Adrenergic alpha-Antagonists/pharmacology , Animals , Arteries/drug effects , Blood Pressure/drug effects , Electric Stimulation , In Vitro Techniques , Male , Muscle Contraction/drug effects , Norepinephrine/pharmacology , Rats , Rats, Inbred SHR , Rats, Inbred WKY , Species Specificity , Vasoconstriction/drug effectsABSTRACT
Contractile responses of the dog mesenteric artery were obtained (after removal of endothelium) to transmural stimulation of the perivascular nerves and to exogenous application of ATP, noradrenaline, dopamine, 5-hydroxy-tryptamine and high potassium solution. The alpha-adrenoceptor antagonists prazosin and phentolamine preferentially reduced the response to noradrenaline and the secondary phase of the biphasic contractile response to nerve stimulation, whilst the addition of alpha, beta-methylene-ATP, which selectively desensitizes P2-purinoceptors, reduced only the contractions to ATP and the portion of the nerve-mediated response which was resistant to the alpha-adrenoceptor antagonists. The responses to nerve stimulation were reduced by the selective P1-purinoceptor agonist 2-chloroadenosine, and its effect was reversed by the P1-purinoceptor antagonist 8-phenyltheophylline. These results suggest that in dog mesenteric artery part of the response to sympathetic nerve stimulation is mediated by ATP acting on P1-purinoceptors on the arterial smooth muscle, and that P1-purinoceptors on the sympathetic nerve terminal can inhibit release of the neurotransmitters.
