Baroreceptors and Hypertension

Abstract

Baroreceptors are deformation receptors whose output is limited by wall strain. Experimental hypertension in animals is associated with a resetting of the baroreceptors such that the threshold pressure and set point are raised and gain decreased. These changes begin within a few days, are reversible, and are probably due to a splinting of the receptors by a stiffer arterial wall. The pulsatile pattern of impulse activity in the sinus nerve is maintained. Studies of the baroreflex arc in hypertensive man using the phenylephrine method have shown both resetting and a diminished sensitivity; the same changes occur with ageing. Neurogenic hypertension produced by baroreceptor denervation remains controversial, possibly due to species differences. Deafferentation may augment renal hypertension. Interaction between the baroreflex and the brain works both ways; situations where there is a heightened level of arousal may be associated with an inhibition of the cardiac limb of the reflex, while baroreceptor stimulation tends to lower the level of arousal. Malfunction of the baroreceptors might exacerbate hypertension by impairing the buffering of pressor stimuli and altering renal arterial resistance, resetting the relation between pressure and urine flow. Essential hypertension in human does not show the same degree of lability seen in experimental neurogenic hypertension in animals, but impairment of the reflex could be related to changes in distensibility of the sinus wall.