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Wenzel RR et al.  
Interaction of the Sympathetic Nervous System with other Pressor Systems in Antihypertensive Therapy

Journal of Clinical and Basic Cardiology 2001; 4 (3): 185-192

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Fig. 4: Moxonidin - SNS-‹beraktivitšt Fig. 5: Moxonidin - Herzfrequenz

Keywords: EndothelEndothelinantagonistenEndothelinsystemKardiologieMikrozirkulationRenin-Angiotensin-SystemStickoxidsympathisches Nervensystemcardiologyendothelin antagonistsendothelin systemendotheliummicrocirculationmuscle sympathetic nerve activitynitric oxiderenin-angiotensin system

Regulation of blood pressure homeostasis and cardiac function is importantly regulated by the sympathetic nervous system (SNS) and other pressor systems including the renin-angiotensin system (RAS) and the vascular endothelium. Increases in SNS activity increase mortality in patients with hypertension, coronary artery disease and congestive heart failure. This review summarizes some of the interactions between the main pressor systems, ie, the SNS, the RAS and the vascular endothelium including the endothelin-system. Different classes of cardiovascular drugs interfere differently with the SNS and the other pressor systems. Beta-blockers, ACE-inhibitors and diuretics have no major effect on central SNS activity. Pure vasodilators including nitrates, alpha-blockers and DHP-calcium channel blockers increase SNS activity. In contrast, central sympatholytic drugs including moxonidine reduce SNS activity. The effects of angiotensin-II receptor antagonist on SNS activity in humans are not clear, experimental data are discussed in this review. There are important interactions between the pressor systems under experimental conditions. Endothelin-A-receptor-antagonists inhibit angiotensin II and noradrenaline induced vasoconstriction. On the other hand, with L-NMMA and yohimbine, alpha-2-adrenoceptor-mediated endothelial vasodilation can be unmasked. Ongoing and future studies have to assess the impact of combination therapy with different antihypertensive classes on SNS activity and on the other pressor systems and establish the ideal combination regarding hard end points, efficacy and side effects. It can be assumed, that in cardiovascular diseases with already enhanced SNS activity drugs, which do not increase SNS activity or even lower it, are preferable. Whether this reflects in lower mortality has to be investigated in intervention trials.
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