Baroreflex Control of Sympathetic Nerve Activity in Essential and Secondary Hypertension

TLDR

High blood pressure impairs baroreceptor control of heart rate, but it is unclear whether baroreceptor regulation of sympathetic activity is similarly affected. The study measured beat‑to‑beat arterial pressure, heart rate, and muscle sympathetic nerve activity in untreated essential and secondary hypertensive patients and normotensive controls while inducing baroreceptor stimulation and deactivation with phenylephrine and nitroprusside. Muscle sympathetic nerve activity rises with the severity of essential hypertension but remains unchanged in secondary hypertension, while baroreceptor control of heart rate is impaired in all hypertensives, yet baroreceptor modulation of sympathetic activity is preserved across both essential and secondary hypertension.

Abstract

Abstract —Studies performed in experimental animals and in humans have documented that high blood pressure markedly impairs baroreceptor control of heart rate. Whether a similar impairment also characterizes baroreceptor control of sympathetic activity modulating peripheral vasomotor tone is still unknown. In 28 untreated essential hypertensive subjects [14 of moderate and 14 of more severe degree, age 51.6±2.4 and 52.6±2.1 years (mean±SEM)] and in 13 untreated secondary hypertensives (renovascular or pheochromocytoma, age 50.1±4.6 years), we measured beat-to-beat arterial blood pressure (finger photoplethysmographic device), heart rate (electrocardiogram), and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Data were compared with those obtained in 15 age-matched normotensive control subjects. Muscle sympathetic nerve activity (bursts per 100 heart beats) showed a progressive and significant ( P <.01) increase from normotension (40.3±3.3) to moderate (55.6±4.1) and more severe essential hypertension (68.2±4.1), paralleling the progressive increase in blood pressure values. In contrast, muscle sympathetic nerve activity was not increased in secondary hypertensives (40.5±6.7) despite blood pressure values similar to or even greater than those of severe essential hypertensives. In both essential and secondary hypertensives, baroreceptor–heart rate control was displaced toward elevated blood pressure values and markedly impaired compared with normotensive subjects (average reduction, 38.5%). In contrast, the sympathoinhibitory and sympathoexcitatory responses to baroreceptor stimulation and deactivation were displaced toward elevated blood pressure values but similar in all groups. Thus, sympathetic activation characterizes essential but not secondary hypertension. Regardless of its nature, however, hypertension is not accompanied by an impairment of baroreceptor modulation of sympathetic activity.