Nitric oxide as a regulator of adrenal blood flow

To determine whether nitric oxide (NO) is involved in adrenal medullary vasodilation during splanchnic nerve stimulation (NS)-induced catecholamine secretion, blood flow (Q) and secretory responses were measured in pentobarbital-anesthetized dogs before and after administration of the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME). L-NAME (40 mg/kg iv over 5 min, followed by 40 mg · kg^-1 · h^-1) reduced NO synthase activity of medullary and cortical homogenates from 5.2 ± 0.3 to 0.7 ± 0.1 pmol · min^-1 · mg protein^-1 and from 1.2 ± 0.2 pmol · min^-1 · mg protein^-1 to undetectable levels, respectively. L-NAME reduced resting medullary and cortical Q̇ by 42 and 60%, respectively. NS before L-NAME increased medullary Q̇ from 181 ± 16 to 937 ± 159 ml · min^-1 · 100 g^-1 and epinephrine secretion from 1.9 ± 0.8 to 781 ± 331 ng/min. NS after L-NAME had no effect medullary Q̇ (103 ± 14 vs. 188 ± 34 ml · min^-1 · 100 g^-1), while epinephrine secretion increased to the same extent as in control animals (1.9 ± 0.7 vs. 576 ± 250 ng/min). L-NAME also unmasked NS-induced cortical vasoconstriction; cortical Q̇ decreased from 96 ± 8 to 50 ± 5 ml · min^-1 · 100 g^-1. Administration of hexamethonium (30 mg/kg iv), a nicotinic receptor antagonist, reduced NS- induced epinephrine secretion by 90%. These data suggest independent neural control of medullary Q̇ and catecholamine secretion, the former by NO and the latter by acetylcholine.