The mechanism underlying the essential hypertension is
complex and has not yet been completely defined, but it is evident that the
activation of the SNS plays an important role in its pathogenesis.
Blockade of beta-AR interferes with the sympathetic regulation
of the heart. The HR and contractility are only marginally affected by the BAA
administration at rest, but it suppresses prominently the increases in HR and
cardiac contractility induced by stress and/or physical exercises. The
mechanism of antihypertensive effects of BAAs is like-wise unknown, even though
a number of explanations have been proposed to play an essential role. They
include the following effects:
-
Reduction of cardiac output
-
Central nervous system
effects
-
Renin-angiotensin-
aldosterone system inhibition
-
Reduction of plasma volume
-
Peripheral vascular
resistance reduction
-
Improvement of vascular
compliance
-
Baroreceptor resetting
-
Reduction of pressor
response to exercise and stress-related catecholamines.
All these effects are possible proposition of a solution in the pursuit of finding the best treatment for the state of hypertension and its sequelae .
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