Electrophysiology of neuromuscular transmission in guinea-pig mesenteric veins.
1. Neuromuscular transmission in the smooth muscle of mesenteric veins has been investigated by recording intracellular potential changes resulting from stimulation of the sympathetic nerves and comparing these potential changes with responses obtained by ionophoresis of noradrenaline. 2. Neural stimulation or exogenous noradrenaline acted similarly to cause two excitatory depolarizations, a slow response reported previously (Suzuki, 1981) and a separate fast depolarization. 3. The fast depolarization was distinct from the slow depolarizing response in that it had a different dependence on the level of stimulation, was readily desensitized and was more suppressed in low-chloride solution. 4. The fast but not the slow depolarization shared certain characteristics with constriction. The fast depolarization and constriction both increased with the intensity of stimulation; inactivation in both was dependent on the recovery interval between trains of stimuli and both were suppressed to a similar degree by antagonists to alpha-adrenoceptors. The fast depolarization was, however, not a prerequisite for constriction to occur. 5. The fast and slow depolarizations were activated after a long latency which had a high temperature coefficient consistent with the postulate that these responses are rate limited by intracellular biochemical reactions. 6. The fast depolarization was preferentially suppressed by prazosin, an antagonist to the alpha 1-adrenoceptor subtype. Suppression of the slow depolarization required relatively higher concentrations of antagonist, indicating that these responses were mediated by receptor interactions involving a different alpha-adrenoceptor subtype. 7. It is concluded that neuromuscular transmission in mesenteric veins occurs through activation of alpha-adrenoceptors. A number of responses result, including voltage-independent constriction and two distinct excitatory depolarizations which can lead to voltage-dependent constriction.
Van Helden
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DF
Department of Pharmacology, John Curtin School of Medical Research, Australian National University, Canberra, A.C.T.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002712:Chlorides / Q000494:pharmacology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008642:Mesenteric Veins / Q000294:innervation / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000294:innervation / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects*; D013696:Temperature; D013997:Time Factors
D002712:Chlorides; D009638:Norepinephrine; D010646:Phentolamine