Enhanced sympathetic nervous system activity may be an early expression of the genetic predisposition to develop hypertension in spontaneously hypertensive rats.
Does not inform human hypertension care; leaves open whether early sympathetic drive initiates genetic hypertension in rats.
The present study describes developmental changes in autonomic controls of heart rate in a strain of rats genetically predisposed to hypertension (spontaneously hypertensive rats or SHR) and in a normotensive strain of rats (Wistar-Kyoto rats or WKY). Rat pups were tested at 4, 8, 12, and 16 days to determine heart rate changes after selective pharmacological treatments. Specifically, freely moving pups were treated with selective beta-adrenergic and muscarinic receptor blockers (i.e., atenolol and atropine methylnitrate), using procedures designed to produce minimal pain or discomfort. The results indicated that by 4 days of age there is a substantial sympathetic acceleratory influence on heart rate. Comparison of inferred autonomic control of the heart in prehypertensive SHR and normotensive WKY pups suggested exaggeration of this early sympathetic influence among SHR pups. After 2 wk of age, however, equivalent autonomic control of heart rate was seen in SHR and WKY rats, with the higher basal heart rate of SHR rats being mediated by an increased intrinsic heart rate (i.e., heart rate after combined blockade). These findings suggest that enhanced sympathetic nervous system activity may be an early expression of the genetic predisposition to develop hypertension.
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Tucker et al. (1984) studied this question.
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