Dissociation of autonomic controls of heart rate in weaning-aged borderline hypertensive rats by perinatal NaCl.

The ontogeny of functional sympathetic neural, adrenal medullary, and extra-adrenal components of adrenergic control of heart rate was investigated in borderline hypertensive rats exposed to either high or low sodium chloride (NaCl) from conception through weaning. Borderline hypertensive rats were produced by mating spontaneously hypertensive females with normotensive Wistar-Kyoto males. Females were maintained on diets containing either low (0.12% NaCl) or high (3% NaCl) dietary NaCl throughout pregnancy and lactation. At 28 days of age, baseline heart rates recorded from awake and unrestrained pups did not differ between low and high NaCl-exposed pups. Overall sympathetic tone, inferred from heart rate change after beta 1-adrenergic blockade with atenolol, did not differ between high and low NaCl-exposed pups. Early NaCl exposure did not alter the neural component of sympathetic control of heart rate as inferred from heart rate decrease after bretylium tosylate. Parasympathetic nervous system control, as reflected by tachycardic response to muscarinic receptor blockade with atropine methyl nitrate was also unchanged by early NaCl exposure. The adrenal catecholamine component of sympathetic control of heart rate was inferred from bradycardia following administration of the ganglion blocking agent, chlorisondamine, to pups pretreated with bretylium and atropine methyl nitrate. Pups exposed to low NaCl showed increased adrenal control of heart rate compared to high NaCl-exposed pups. The influence of residual catecholamines on heart rate was inferred from bradycardia following administration of the beta 1-adrenergic receptor blocking agent, atenolol, in pups pretreated with bretylium, atropine methyl nitrate, and chlorisondamine. Residual catecholamine influence was greater in rats exposed to high NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)