ENDOTHELIUM, VASOPRESSIN RECEPTORS, AND RESISTANCE TO DOCA-SALT HYPERTENSION

Mesenteric artery rings from Wistar and Wistar-Furth rats subcutaneous ly treated with deoxycorticosterone acetate (DOCA) and 1% NaCl drinkin g water were used to measure endothelial modulation of contractile sen sitivity and vasopressin receptor function and affinity. DOCA-salt hyp ertension reduced contractile sensitivity to arginine vasopressin (AVP ) and did not affect contractile sensitivity to norepinephrine in arte ries from Wistar rats. Endothelial removal caused a threefold increase in contractile sensitivity to AVP and norepinephrine in DOCA-salt hyp ertensive Wistar rats. In Wistar-Furth rats, DOCA-salt treatment did n ot affect contractile sensitivity to AVP, lysine vasopressin, oxytocin , and norepinephrine or the affinity of the vasopressin receptor for a gonists or antagonists. Removal of endothelium did not affect vasopres sin contractile sensitivity but caused a 15-fold increase in contracti le sensitivity to norepinephrine in untreated or DOCA-salt-treated Wis tar-Furth rats. These data show that reduced vasopressin receptor func tion and increased endothelial function that compensate for increased contractile sensitivity in arteries from DOCA-salt hypertensive Wistar rats are not the cause of resistance of DOCA-salt-treated Wistar-Furt h rats to the development of enhanced contractile sensitivity and hype rtension.