Changes of Vascular Reactivity Induced by Low Vasopressin Concentrations: Interactions with Cortisol and Lithium and Possible Involvement of Prostaglandins*

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Abstract
Arginine vasopressin in physiological concentrations potentiated the vascular effects of various vasoconstrictor agents. By using the isolated rat mesenteric artery preparation, the pressor effects of norepinephrine [NE], angiotensin II and KCl were all significantly increased when vasopressin was added to the perfusion buffer. Cortisol and Li both inhibited the potentiating effect of vasopressin but had no effect on the control pressor response to NE. When the vascular effects of NE were first blocked with indomethacin and then restored by the addition of prostaglandin E2, the potentiation by vasopression was almost completely prevented. This suggests that vasopressin may be acting by stimulating prostaglandin biosynthesis. Cortisol and Li may exert their inhibitory effects by preventing the activation of prostaglandin synthesis by vasopressin. These findings may be of clinical significance because the phenomena occur well within the range of vasopressin levels found in human plasma.