Nakazato Y, Sekine H, Isogaya M, Ito S, Ohga A
Department of Pharmacology, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan.
J Auton Nerv Syst. 1987 Jul;20(1):35-42. doi: 10.1016/0165-1838(87)90079-8.
Stimulation of the greater splanchnic nerve with relatively weak intensity caused a relaxation which was reversed to a contraction as the intensity of stimulation increased. This contraction was abolished or reversed to a relaxation after intravenous injection of atropine and phenoxybenzamine. When hexamethonium was further administered, a long lasting contraction appeared in response to the greater splanchnic nerve stimulation. Perivascular (postganglionic) nerve stimulation did not cause the long lasting contraction until an adrenergic neuron blocking agent, such as guanethidine, and atropine were administered. The long lasting contraction was not affected by the histamine H1 receptor blocking agent, mepyramine. Close arterial injection of substance P (SP) caused a dose-dependent contraction of the stomach which was partly inhibited by atropine. When SP was repeatedly injected at intervals of a few minutes, the response to SP progressively declined. Under this condition, the long lasting contraction induced by greater splanchnic nerve stimulation was reversibly inhibited. This experiment shows that stimulation of the greater splanchnic nerve causes a long lasting contraction of the stomach which is revealed by either hexamethonium or guanethidine in the atropinized dog. A possible involvement of SP in the long lasting contraction was discussed.
