Cardiac Baroreflex in Hypertension: Role of the Heart and Angiotensin II

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Abstract
Sigmoid logistic function curves provide a powerful means of characterizing the baroreceptor-heart rate reflex. In hypertension the operating range of the reflex is reset in the direction of the elevated resting BP; this can be accounted by rapid resetting of the threshold of the arterial baroreceptors. In addition, there is a deficit in the vagal component of the heart rate (HR) range. Reduction in gain occurs in moderate/severe hypertension, but may be absent in young primary hypertensives. All the changes are reversible, and reversibility of HR range and gain is related to reducing left ventricular hypertrophy or central blood volume rather than to reduction in BP. High plasma angiotensin II can further accentuate the vagal deficit. An input-output model has been developed from comparison of perivascular cuff and drug methods for eliciting the reflex, which place different loads on the heart; the greater load changes simulate many of the alterations in reflex properties observed in hypertension. We conclude that during changes in vasomotor tone in normal animals, about 70% of the drive for the cardiac baroreflex comes from arterial baroreceptors and about 30% from low threshold cardio-pulmonary baroreceptors. In hypertension, the vagal deficit in HR range is due to afferent interactions involving arterial and low and high threshold cardio-pulmonary baroreceptors.