Role of transmitters in mediating hypothalamic control of electrolyte excretion

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Abstract
Changes in urinary volume and electrolyte excretion were monitored after the injection of cholinergic and monoaminergic drugs into the 3rd cerebral ventricle of conscious male rats made diuretic by an i.v. infusion of 5% dextrose. A natriuretic and kaliuretic response was induced by the intraventricular injection of norepinephrine (NE) or carbachol, whereas dopamine (DA) had no effect. The .beta.-receptor stimulator isoproterenol (ISO) induced an antinatriuretic and antikaliuretic effect. Intraventricular injection of the .alpha.-adrenergic blocker phentolamine abolished the natriuretic response to NE and carbachol and to intraventricular hypertonic saline (HS). The .beta.-adrenergic blocker propranolol induced a natriuresis and kaliuresis when injected alone and an additive effect when its injection was followed by NE or HS. Propranolol potentiated the natriuretic response to carbachol. Cholinergic blockade with atropine diminished the response to NE and blocked the natriuretic response to HS. Na receptors in the ventricular wall may modify renal Na excretion via a stimulatory pathway involving cholinergic and .alpha.-adrenergic receptors and may inhibit Na excretion via a tonically active .beta.-receptor pathway.