Subject(s)
Prostaglandins/history , Animals , Blood Circulation , Chemistry , Digestive System Physiological Phenomena , Fatty Acids/analysis , Female , Fever/physiopathology , History, 20th Century , Humans , Inflammation/physiopathology , Male , Nervous System Physiological Phenomena , Pain/physiopathology , Prostaglandins/metabolism , Prostaglandins/physiology , Prostaglandins, Synthetic/pharmacology , Reproduction , Respiratory Physiological PhenomenaSubject(s)
Neurochemistry/history , Neurotransmitter Agents/physiology , Synaptic Transmission , Acetylcholine/physiology , Animals , Atropine/pharmacology , Biological Evolution , Epinephrine/physiology , History, 19th Century , History, 20th Century , Humans , Male , Muscle Contraction , Neuromuscular Junction/physiology , Norepinephrine/physiology , Receptors, Adrenergic/physiology , Receptors, Cholinergic/physiology , Substance P/physiology , Sympathetic Nervous System/physiology , Synapses/physiology , Vas Deferens/physiologySubject(s)
Prostaglandins/physiology , Animals , Biochemistry/history , Dogs , Female , History, 20th Century , Horses , Humans , Male , Prostaglandins/isolation & purification , Rabbits , Semen/analysis , Sheep , SwineABSTRACT
Noradrenaline as well as the indirectly acting amines tyramine and phenethylamine either enhance or inhibit the twitch response of the transmurally stimulated, isolated guine-pig vas deferens, thus partly confirming previous reports. In both cases enhancement is annulled by alpha-adrenoceptor blockers. The twitch inhibition caused by noradrenaline is abolished by alpha- + beta2-adrenoceptor blockers, but not by either blocker alone. The inhibition caused by the indirectly acting amines is largely abolished by alpha-adrenoceptor blockers. Clonidine strongly inhibits the twitch. This effect if promptly removed by phentolamine. After blockade of the neurally induced twitch by tetrodotoxin, noradrenaline and the indirectly acting amines have no effect or slightly enhance the twitch elicited by transmural stimulation of the smooth muscle. It is concluded that exogenous noradrenaline acts on postjunctional stimulatory alpha-adrenoceptors and on inhibitory alpha- and beta2-adrenoceptors, which are presumably prejunctional. In the unstimulated preparation contracted by acetylcholine, noradrenaline causes further contraction which is changed into relaxation after phentolamine. This relaxation is abolished by butoxamine, suggesting that noradrenaline may also act on inhibitory postjunctional beta2-adrenoceptors. The twitch-inhibiting effect of endogenous noradrenaline, released by nerve stimulation or by indirectly acting amines, appears to be primarily mediated by prejunctional alpha-adrenoceptors.
Subject(s)
Neuromuscular Junction/physiology , Receptors, Adrenergic , Synaptic Transmission , Vas Deferens/physiology , Animals , Clonidine/pharmacology , Guinea Pigs , Isoproterenol/pharmacology , Male , Methoxamine/pharmacology , Muscle Contraction/drug effects , Norepinephrine/pharmacology , Receptors, Adrenergic, alpha/drug effects , Receptors, Adrenergic, beta/drug effects , Synaptic Transmission/drug effects , Terbutaline/pharmacology , Tyramine/pharmacologyABSTRACT
The twitch response to nerve activity in the vas deferens does not behave as if it were adrenergic since it is enhanced by adrenoceptor blockers and often inhibited by noradrenaline and other sympathomimieic amines. Potassium (K+) ions have a strong reinforcing action on the twitch and easily restore it after blockade by lanthanum. The hypothesis is advanced that K+ ions have a transmitter function in the vas deferens and that K+ ions released in conjunction with the nerve stimulus may reach a concentration at the postsynaptic membrane sufficient to excite the muscle cell and produce a twitch.
