At Low Dose, Arginine Vasotocin Has Vasopressor Rather Than Vasodepressor Effect in Chickens

Abstract

It is widely accepted that both arginine vasopressin (AVP), and its avian analogue, arginine vasotocin (AVT) are vasopressor (VP) in mammals, but vasodepressor (VDP) in birds. The rat VP and chicken VDP assays were used to characterize neurohypophysial peptides and their analogues. However, these assays use pharmacological doses. Like AVP in mammals, AVT is secreted in birds during dehydration, when peripheral vasoconstriction rather than vasodilatation is needed. Mature White Leghorn cockerels with permanent cannulas in brachial artery and vein were put restrained in a sling. Mean arterial pressure (MAP); heart rate; and rectal, shank, skin, and comb temperatures were continuously recorded. The i.v. infusion regimen was: 1 hr of 0.05 ml/kg * min of saline followed by an hour of tested drug and another hour of saline. The drugs were: AVT, V1-agonist ([Phe2 Orn8]VT), and V2-agonist (DDAVP), in dosage of 50 pmol/kg * min each. AVT and to a lesser extent the V1-agonist increased MAP, caused bradycardia, and reduced thermal conductivity between core and skin or comb. The V2-agonist had no significant effect. Thus, at a low dosage AVT has a VP rather than a VDP effect. Bolus i.v. injection of 2 nmol AVT/kg caused an immediate and large drop in MAP accompanied by tachycardia which subsided within 20-30 sec. This was followed by a small rise in MAP and significant bradycardia. Bolus injection of 2 nmol/kg of either agonist had no hypotensive effect and only the V1-agonist caused the second-phase bradycardia. Thus, bolus injection of AVT at a high dose causes an immediate VDP response that subsides and is followed by a VP one. The V1-agonist elicits only the VP effect. The VDP effect of AVT is mediated by a receptor different than either V1 or V2.