Extreme vasoreactivity of rat epineurial arterioles to vasopressin

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 and evaluated its interactions with α-adrenoreceptors and its effect on ischemic conduction failure. NBF was measured using microelectrode hydrogen polarography. Vasopressin was administered both intra-arterially 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 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 an 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 1) vasopressin is an extremely potent neural vasoconstrictor, 2) there are interactions between vasopressin and α-adrenergic receptors, and 3) vasoconstriction caused by combined LVP and NE can produce partial conduction block of sciatic-tibial nerve.