Extreme vasoreactivity of rat epineurial arterioles to
vasopressin.
Sasaki, Hideyuki, and Phillip A. Low.
Neurophysiology Laboratory, Department of Neurology, Mayo
Foundation, Rochester, MN 55905 USA, Phone: (507) 284-3375, Fax:
(507) 284-1814
APStracts 3:0134H, 1996.
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 rat sciatic NBF, evaluated its interactions with
[alpha]-adrenoreceptors, and its effect on ischemic conduction
failure. NBF was measured using microelectrode hydrogen polarography.
Vasopressin was administered both intraarterially and topically (to
epineurium). Intra-arterial lysine-vasopressin (LVP) or arginine
-vasopressin (AVP) reduced NBF, with a dose causing 50% of maximal
effect (ED50) of 10-23.8 M and 10-22.5 M; the asymptote was 54.6% and
55.7% of NBF reduction for LVP and AVP respectively. Topical
epineurial application of LVP also caused a concentration-dependent
reduction of NBF (EC50 = 10-20.2 M; asymptote = 69.2% NBF reduction).
The topical application of the subthreshold concentrations of LVP
(10-24 M) and norepinephrine (NE; 10-8 M) alone resulted in no change
in NBF, but combined application resulted in a dramatic reduction in
NBF (72.3%). Subthreshold phentolamine reduced the effects of LVP.
The ratio of amplitudes of muscle compound action potential evoked on
proximal to distal stimulation was used as an index of the presence
of a ischemic conduction block. This ratio was significantly reduced
following the combined topical application of supramaximal
concentrations of LVP (10-5 M) and NE (10-4 M). These findings
suggest that vasopressin is an extremely potent neural
vasoconstrictor, that there are interactions between vasopressin and
[alpha]-adrenergic receptors, and that vasoconstriction caused by
combined LVP and NE can produce partial conduction block of sciatic
-tibial nerve.
Received 6 April 1995; accepted in final form 20 March 1996.
APS Manuscript Number H337-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 April 96