Effects of NG‐nitro‐l‐arginine methyl ester on vasodilator responses to acetylcholine, 5′‐N‐ethylcarboxamidoadenosine or salbutamol in conscious rats

Abstract

1 Conscious, Long Evans rats (n = 16), chronically instrumented for the measurement of regional haemodynamics were given 3min, randomized infusions of two doses of sodium nitroprusside (1.5 and 15 μg min⁻¹), acetylcholine (0.4 and 4 μg min⁻¹), 5′-N-ethylcarboxamidoadenosine (NECA; 45 and 450 ng min⁻¹), and salbutamol (24 and 240 ngmin⁻¹) in the absence and in the presence of N^G-nitro-l-arginine methyl ester (l-NAME; 1 mg kg⁻¹ h⁻¹), a potent inhibitor of nitric oxide biosynthesis. 2 Sodium nitroprusside caused hyperaemic vasodilatation in the mesenteric, and common carotid vascular beds. These effects were enhanced in the presence of l-NAME, as was the hypotension. 3 Acetylcholine caused hyperaemic vasodilatation in the renal, internal carotid and common carotid vascular beds. These effects were attenuated in the presence of l-NAME, but the hypotension was unaffected. 4 NECA caused hyperaemic vasodilatation in the renal, mesenteric, hindquarters, internal carotid and common carotid vascular beds. However, only the hindquarters and internal carotid responses were diminished in the presence of l-NAME and the hypotension was unchanged. 5 Salbutamol caused hyperaemic vasodilatation in the hindquarters vascular bed only. This effect was reduced in the presence of l-NAME, but the hypotension was unchanged. 6 The results indicate marked regional variations in the sensitivity of vasodilator responses to l-NAME that can depend on the vasodilator agent chosen and the dose employed. It is clear from these findings also that measurement of mean arterial blood pressure alone cannot provide adequate information on which to judge the involvement of l-NAME-sensitive mechanisms in vasodilator responses in vivo.