摘要
Angiotensin II directly stimulates muscle sympathetic nerve activity and facilitates adrenergic sympathetic transmission. The hypotheses that the chronic blockade of angiotensin II receptors(AT1 type)reduces muscle sympathetic activity and that there is an interaction with baroreceptor function in patients with mild to moderate hypertension were investigated. Muscle sympathetic nerve activity decreased from 51.7±3.5 to 45.9±4.2 bursts/-min(p=0.022), and cardiac baroreceptor sensitivity increased from 3.2±1.3 to 4.9±1.8 ms/mm Hg(p=0.007). This study for the first time demonstrates that in hypertensive patients, chronic AT1 receptor antagonism inhibits muscle sympathetic nerve activity and that baroreceptor function is improved under these conditions.
Angiotensin II directly stimulates muscle sympathetic nerve activity and facilitates adrenergic sympathetic transmission. The hypotheses that the chronic blockade of angiotensin II receptors(AT1 type)reduces muscle sympathetic activity and that there is an interaction with baroreceptor function in patients with mild to moderate hypertension were investigated. Muscle sympathetic nerve activity decreased from 51.7±3.5 to 45.9±4.2 bursts/-min(p=0.022), and cardiac baroreceptor sensitivity increased from 3.2±1.3 to 4.9±1.8 ms/mm Hg(p=0.007). This study for the first time demonstrates that in hypertensive patients, chronic AT1 receptor antagonism inhibits muscle sympathetic nerve activity and that baroreceptor function is improved under these conditions.
