Abstract
Arterial strips from rat tail, rabbit ear, and dog mesentery, which are partially contracted by norepinephrine (NE), relax below the initial level of contraction in a frequency-dependent manner after cessation of transmural electrical stimulation. Antagonism of poststimulant relaxation by several pharmacologically unrelated agents suggests that the phenomenon is probably not due to release of a specific dilator neurotransmitter. Indeed, electrical stimulation of modified Krebs bicarbonate solution (contains EDTA) and NE in the absence of tissue abolishes the ability of the mixture to elicit a contraction when transferred to a second bath containing unstimulated tissue. Electrical stimulation does not measurably alter bath pH and temperature nor the ability of NE and 5-hydroxytryptamine to elicit contractions when they are added to the bath after stimulation has ended. Electrical stimulation (30-s train, 16 Hz, 0.5 A, rectilinear pulse width 0.5 ms) of modified Krebs bicarbonate solution and radiolabelled NE in the presence or absence of tissue results in alteration of a major portion of the labelled NE with appearance of several unidentified products. High concentrations of a known NE metabolite (3,4-dihydroxyphenylglycol) interfere with the ability of NE to maintain a contraction, and the possibility that NE breakdown products may interfere with NE's pharmacological action as an additional mechanism for a portion of poststimulant relaxation is not excluded. It is concluded that 'field' stimulation under the present conditions causes oxidation of NE in spite of the usual precaution of adding EDTA to the bath solution.
Publisher
Canadian Science Publishing
Subject
Physiology (medical),Pharmacology,General Medicine,Physiology
Cited by
16 articles.
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