Key result
Adrenergic neuro-effector interactions in hypertensive animals adapt long-term by increasing sympathetic control efficiency in the heart while reducing it in blood vessels.
The ability of the blood vessel wall to synthesize noradrenaline is augmented at the early stages of genetic hypertension in animals. It usually is normal, or reduced in chronic hypertension. 2. The exocytotic release of noradrenaline is greater than normal, in the early stages of a number of experimental models of hypertension. 3. Postjunctional receptors for noradrenaline are not uniform throughout the vascular tree. Their sensitivity changes during the development of high blood pressure. 4. In chronic hypertension neuronal uptake and the extraneuronal disposition of released noradrenaline is depressed in the heart, but accelerated in the blood vessel wall. 5. The adrenergic neuro-effector interaction undergoes a diverging long-term adaptation in the heart and the blood vessels of hypertensive animals. In the former this tends to increase, but in the latter to reduce, the efficiency of sympathetic nervous control.
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Vanhoutte et al. (1980) conducted a review in Hypertension. Adrenergic neuro-effector interaction was evaluated on Sympathetic nervous control efficiency and noradrenaline kinetics. Adrenergic neuro-effector interactions in hypertensive animals adapt long-term by increasing sympathetic control efficiency in the heart while reducing it in blood vessels.
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