Genetically hypertensive rats: relationship between the development of hypertension and the changes in norepinephrine turnover of peripheral and central adrenergic neurons.

Abstract

In genetically hypertensive rats, the norepinephrine turnover of peripheral and central adrenergic neurons was determined either by the decline in endogenous norepinephrine after inhibition of tyrosine hydroxylase or by the decay in the specific activity of norepinephrine after labelling the stores by intravenous or intraventricular injection of3H-norepinephrine. In the periphery (heart and submaxillary gland), the norepinephrine turnover of genetically hypertensive rats was reduced in proportion to the rise in systolic blood pressure. In the hypothalamus, medulla-pons and the residual parts of the brain, the turnover was unchanged both in the prehypertensive and the hypertensive state. The results indicate that the central adrenergic neurons, involved in the control of blood pressure, may act independently from the activity of peripheral baroreceptors. The elevated blood pressure resulting from an enhanced peripheral vascular reactivity to the physiological neurotransmitter norepinephrine may induce a compensatory inhibition of the activity of the peripheral adrenergic neurons. In the genetically hypertensive rats, neither the peripheral nor the central adrenergic nervous system seems to play a primary role in the development of hypertension.