Pharmacological evidence that the sympathetic nervous system mediates the increase in secretion of renin produced by p-chloroamphetamine

The increase in plasma renin activity produced by p-chloroamphetamine in unanesthetized rats is blocked by p-chlorophenylalanine and by lesions of the dorsal raphe nucleus and the mediobasal hypothalamus. To determine whether the pathway from these areas of the brain to the kidneys that mediates the renin response is sympathetic, the effect of β-adrenergic blockade and ganglionic blockade on the renin response to p-chloroamphetamine was studied. The increase in plasma renin activity 60 min after the administration of p-chloroamphetamine (10 mg/kg, i.p.) was prevented by the β-adrenergic antagonist (−)-propranolol (1 mg/kg, i.p.), but not by (+)-propranolol (1 mg/kg, i.p.), given 30 min before p-chloroamphetamine. Sotalol (30 mg/kg, i.p.) injected 30 min before p-chloroamphetamine also blocked the renin response. The ganglionic-blocking drug chlorisondamine lowered blood pressure and increased plasma renin activity by itself. However, p-chloroamphetamine administered 30 min after chlorisondamine produced no further increase in plasma renin activity. Chlorisondamine, by itself, did not produce maximal secretion of renin, since isoproterenol, 30 min after chlorisondamine, produced a large increase in plasma renin activity. The data indicate that the increase in plasma renin activity produced by p-chloroamphetamine is mediated via the sympathetic nervous system.