Extreme vasoreactivity of rat epineurial arterioles to vasopressin
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Published:1996-10-01
Issue:4
Volume:271
Page:H1307-H1313
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ISSN:0363-6135
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Container-title:American Journal of Physiology-Heart and Circulatory Physiology
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language:en
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Short-container-title:American Journal of Physiology-Heart and Circulatory Physiology
Affiliation:
1. Department of Neurology, Mayo Foundation, Rochester, Minnesota 55905, USA.
Abstract
Vasopressin is a potent vasoconstrictor to most blood vessels but is a vasodilator to some. The role of vasopressin in the regulation of nerve blood flow (NBF) is not known. We undertook a dose-effect study of vasopressin on NBF and evaluated its interactions with alpha-adrenoreceptors and its effect on ischemic conduction failure. NBF was measured using microelectrode hydrogen polarography. Vasopressin was administered topically (to epineurium). Topical epineurial application of vasopressin caused a concentration -dependent reductin of NBF (EC 50 = 6.6 x 10(-9) M; asymptote = 73.9% NBF reduction). The topical application of subthreshold concentrations of vasopressin and norepinephrine alone resulted in no change in NBF, but combined application resulted in a dramatic reduction in NBF (72.3%). The ratio of amplitudes of muscle compound action potential evoked on proximal to distal stimulation was used as an index of the presence of an ischemic conduction block. This ratio was significantly reduced following the combined topical application of supramaximal concentrations of vasopressin and norepinephrine. These findings suggest that vasopressin is a potent neural vasoconstrictor and that vasoconstriction caused by combined vasopressin and norepinephrine can produce partial conduction block of sciatic-tibial nerve [corrected].
Publisher
American Physiological Society
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Cited by
3 articles.
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