Abstract
Blood pressures of Otago genetically hypertensive (GH) rats are higher than those of genetically related normotensive (N) rats as early as 35 days after birth. At this age, the elevation of blood pressure is entirely neurogenic, as both GH and N animals have similar blood pressures following ganglion blockade; however, by age 45 days an additional non-neural component of the hypertension has appeared, and this persists into adulthood. Chronic treatment with propranolol or atenolol (1 mg/kg/day) over days 28–90 does not attenuate the development of hypertension. Neonatal sympathectomy with guanethidine almost abolishes resting sympathetic tone even in adult (GH) animals, but does not prevent the appearance of the non-neural component of the hypertension. It is concluded that although sympathetic nervous tone contributes to the absolute level of blood pressure in GH rats, it is not a causative factor in the development of hypertension.
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