Role of sympathetic nervous system in hypertension and effects of cardiovascular drugs.
The sympathetic nervous system (SNS) plays an important role in the regulation of cardiac performance and peripheral circulation. Changes in SNS activity measured as catecholamines in plasma or organ spillover have been implicated in the pathogenesis of hypertension. Recent studies using microneurography to directly assess peripheral sympathetic nerve activity have demonstrated an increase in sympathetic activity in patients with borderline hypertension at rest and during hypoxia. We have recently shown that resting muscle sympathetic nerve activity is comparable in offspring of hypertensive and normotensive parents. However, during mental arithmetic the increase in muscle sympathetic nerve activity and blood pressure was significantly more pronounced in offspring of hypertensive than in offspring of normotensive parents, but resting blood pressure was in the normotensive range and comparable in both groups. These data indicate that the response to mental stress results in a more pronounced activation of SNS in normotensive subjects with a genetic background of hypertension. In other cardiovascular disease states such as acute myocardial infarction and heart failure activity of the SNS may determine prognosis significantly. Some calcium antagonists which are successfully used to treat patients with hypertension and stable angina pectoris may have unfavourable effects in patients with impaired left ventricular function. This could be due in part to baroreceptor-mediated activation of the SNS, an effect which seems to be related to pharmacokinetics and pharmacodynamics of the drugs. In contrast, angiotensin converting enzyme inhibitors seem to directly decrease sympathetic nerve activity. This may explain at least in part their beneficial effects in patients with impaired left ventricular function. Thus, the SNS as a regulator of the cardiovascular system also plays an important role in the pathophysiology of cardiovascular diseases such as hypertension, myocardial infarction and heart failure. Furthermore, drug therapy could have a significant impact on the activity of the SNS.
Noll
G
G
Cardiology, University Hospital Zürich, Switzerland.
Wenzel
R R
RR
Binggeli
C
C
Corti
C
C
Lüscher
T F
TF
D001143:Arousal / Q000187:drug effects* / Q000502:physiology; D002317:Cardiovascular Agents / Q000009:adverse effects / Q000627:therapeutic use*; D002395:Catecholamines / Q000097:blood; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D011379:Prognosis; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000503:physiopathology
D002317:Cardiovascular Agents; D002395:Catecholamines