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Electrophysiological studies on the interaction of 5-hydroxytryptamine with sympathetic transmission in the guinea pig inferior mesenteric artery and ganglion

AG Meehan and DL Kreulen

Department of Pharmacology, College of Medicine, University of Arizona, Tucson.

The interaction of 5-hydroxytryptamine (5-HT) with sympathetic transmission was investigated in the guinea pig inferior mesenteric artery (IMA) and ganglion (IMG). Intracellular recordings of membrane potential were made using glass microelectrodes. Superfusion of 5-HT (0.3 microM) reduced the amplitudes of stimulation-evoked excitatory junction potentials in the IMA. 5-HT had no effect on depolarizing responses to pressure-ejection of adenosine triphosphate or norepinephrine in the IMA. The inhibitory effect of 5-HT on excitatory junction potentials in the IMA was abolished by methysergide (3 microM), but was unaffected by the following antagonists: methiothepin (1 microM), MDL 72222 (3 microM), MDL 11939 (0.3 microM) or by phentolamine (10 microM). In the IMG, pressure-ejection of 5-HT (10 mM) evoked fast and slow depolarizing responses in 77% of neurons tested; the fast depolarizing responses to 5-HT were reduced in the presence of MDL 72222 (5 microM). Superfusion of 5-HT (0.3-3 microM) had no effect on stimulation-evoked fast excitatory postsynaptic potentials in the IMG. Thus, the results of the present study suggest that, depending on its site of interaction with postganglionic sympathetic neurons, 5-HT may have excitatory or inhibitory effects on sympathetic transmission. 5-HT may inhibit transmitter release through the activation of as yet unidentified 5-HT receptors on the sympathetic nerve endings in mesenteric blood vessels. Whereas, in the prevertebral ganglion, 5-HT may act to facilitate sympathetic transmission, in part, through activation of 5-HT3, receptors on the somata of principal neurons.

Volume 256, Issue 1, pp. 82-87, 01/01/1991
Copyright © 1991 by American Society for Pharmacology and Experimental Therapeutics




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Copyright © 1991 by the American Society for Pharmacology and Experimental Therapeutics.