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Neuroeffector transmission to different layers of smooth muscle in the rat penile bulb
Author(s) -
Hashitani Hikaru
Publication year - 2000
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2000.t01-2-00549.x
Subject(s) - niflumic acid , cyclopiazonic acid , medicine , ouabain , excitatory postsynaptic potential , extracellular , endocrinology , inhibitory postsynaptic potential , membrane potential , stimulation , biology , biophysics , channel blocker , chemistry , intracellular , biochemistry , sodium , calcium , organic chemistry
1 Using intracellular recording techniques, two distinct layers of smooth muscle were identified in the rat penile bulb. The inner muscle layer (parenchyma) exhibited spontaneous action potentials, while the outer sheet (sac) was electrically quiescent. 2 In the parenchyma, transmural stimulation initiated non‐adrenergic, non‐cholinergic (NANC) inhibitory junction potentials (IJPs) which were abolished by N ωnitro‐L‐arginine (LNA) or 1 H ‐[1,2,4]oxadiazolo[4,3‐ a ]quinoxalin‐1‐one (ODQ). The amplitude of IJPs was reduced by ouabain, dinitrophenol or decreasing the extracellular potassium concentration ([K + ] o ) but not by several K + channel blockers. 3 The parenchyma also received an excitatory innervation mediated by α‐adrenoceptors which caused a contraction that was not associated with a membrane potential change. 4 In the sac, transmural stimulation initiated two component excitatory junction potentials (EJPs) mediated by α‐adrenoceptors and associated action potentials. The initial component was more dramatically suppressed than the secondary component by caffeine, ryanodine or cyclopiazonic acid (CPA). Lowering of the extracellular chloride concentration ([Cl − ] o ) selectively inhibited the rapid component of EJPs, while niflumic acid was less potent. 5 These results suggest that IJPs in the parenchyma result from the release of NO which stimulates sodium pump activity following the activation of guanylate cyclase. In the sac, the activation of α‐adrenoceptors initiates EJPs by releasing Ca 2+ from intracellular stores which activates Ca 2+ ‐activated channels.