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1 Laboratory of Neurophysiology and Neuropharmacology, Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts
Isometric tension changes of the iris sphincter of the cat were investigated in vitro. Electrical stimulation resulted in contraction followed by relaxation. Elimination of the cholinergic component by chronic parasympathetic denervation or by atropine, or both, markedly reduced electrically induced contraction, but had little influence on relaxation. Norepinephrine produced contraction, relaxation, or slight relaxation followed by contraction. Isoproterenol elicited virtually pure relaxation. The actions of dichloroisoproterenol and phentolamine indicated that relaxation induced electrically or by drug was due mainly to activation of beta receptors and contraction was due to activation of alpha receptors. Proper choice of electrical stimulus parameters (high versus low stimulus rate) allowed activation predominantly of relaxing beta adrenergic, or of contractile alpha adrenergic mechanisms, respectively. These studies also confirm earlier observations that electrical stimuli act indirectly, i.e., via excitation of nerve terminals and release of transmitter, and that the sphincter muscle is not directly excitable by electrical shocks.
Note:
With the Technical Assistance of Myrna Dodd and P. T. Scardino
Key Words: dual adrenergic innervation of iris sphincter alpha adrenergic receptors in iris sphincter beta adrenergic receptors in iris sphincter electrical activation of iris sphincter electrical inexcitability of iris muscle iris sphincter isolated cat norepinephrine on cat isolated iris sphincter isoproterenol on cat isolated iris sphincter tyramine on cat isolated iris sphincter atropine on cat isolated iris sphincter dichloroisoproteronol on cat isolated iris sphincter phentolamine on cat isolated iris sphincter
Submitted on December 4, 1963
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