Normotensive and spontaneously-hypertensive rats show differences in sensitivity to arginine-vasopressin as a modulator of noradrenaline release from brainstem slices.

The effect of arginine-vasopressin (AVP) on potassium ion-evoked release of [3H]noradrenaline (NA) from rat brainstem slices was investigated. In normotensive Sprague-Dawley (SD) and Wistar Kyoto (WKY) rats, AVP inhibited release of [3H]NA in a dose-dependent fashion, the magnitude and time course of inhibition at 10(-12)M AVP being similar to that observed using the alpha 2-adrenoceptor agonist, clonidine at 10(-7) M. However, it is unlikely that AVP functions through alpha-receptors since its effect is not blocked by phentolamine (10(-6) M). When brainstems from spontaneously-hypertensive (SH) rats (stroke-prone strain) were used, AVP was found to be without effect on [3H]NA-release at concentrations up to 10(-8) M. The potassium ion-evoked release appeared to have two components. The early phase of release was tetrodoxotin (TTX)-sensitive and was probably due to action potential conduction within the slices. The later phase, which was unaffected by tetrodotoxin, was probably a result of potassium-induced depolarization of nerve endings. AVP appeared to affect principally the early, TTX-sensitive release. In the presence of TTX (0.3 microM) the inhibitory effects of AVP were no longer seen. Thus, AVP may affect generation or conduction of action potentials within this tissue. There is published evidence that central vasopressinergic neurons may play a role in controlling the baroreceptor reflex arc. The present study provides a possible biochemical basis for this effect and is consistent with a neuromodulatory role of AVP in the CNS.