Does vasopressin-induced vasoconstriction persist during prolonged infusion in dogs?

I have examined the systemic and regional hemodynamic effects of an intravenous arginine vasopressin (AVP) infusion at a rate of 220 pg X kg-1 X min-1 maintained for 48 h in 12 conscious dogs. Plasma AVP concentration increased from 2.8 +/- 1.1 to 8.2 +/- 1.4 pg/ml, and plasma osmolality fell from 294.8 +/- 1.4 to 287.1 +/- 1.5 mosmol/kg. Mean arterial pressure increased slightly but significantly despite a reduction in blood volume. Contrary to what we previously observed with 1-h AVP infusion at the same rate, cardiac output and heart rate did not decrease, and total peripheral resistance did not increase. Most vascular beds sensitive to the acute vasoconstrictor effects of AVP, such as those of the skeletal muscle, fat, colon, and skin, did not show any significant reduction in blood flow after 48 h. Only in the pancreas and in the thyroid gland was there a significant flow decrease, which was similar in magnitude to that measured after 1 h of infusion. It therefore appears that vasoconstriction induced by modest increases in plasma concentrations of AVP is not maintained during prolonged administration in most vascular beds. However, injection of a specific antagonist of the pressor action of AVP [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin, 10 micrograms/kg, induced a significant increase in cardiac output and heart rate, as well as a fall in total peripheral resistance and significant increases in myocardial, fat, and skin blood flows after 48 h of AVP infusion.(ABSTRACT TRUNCATED AT 250 WORDS)