Corticotrophin releasing factor attenuates N^G-Nitro-L-arginine Methyl Ester induced increases in blood pressure in the anaesthetised rat

Abstract

In vitro corticotrophin releasing factor (CRF) causes a prolonged endothelium-dependent vasodilatation which is blocked by inhibitors of nitric oxide (NO) synthase (NOS). Here the role of NO in CRF-induced reductions in blood pressure (BP) has been investigated using anaesthetised rats. Infusion of N^G-Nitro-L-arginine Methyl Ester (L-NAME) increased mean arterial pressure (MAP) but did not reduce the fall in BP caused by CRF injection. Bolus injection of L-NAME produced a marked vasopressor effect when given alone. However, when administered 20 min after CRF, L-NAME restored MAP to basal levels, but the marked vasopressor response observed in control animals was completely blocked. This indicates that the increase in BP occurring on bolus injection of L-NAME is not simply due to an inhibition of NO-dependent vasodilatation.