Anti-hypertensive drugs in metabolic syndrome
Abstract
There are two basic aspects to metabolic syndrome which constitute the pathophysiological basis for its multiple manifestations: insulin resistance and visceral fat adipocytes. Insulin-resistant adipocytes possess all the elements of the reninangiotensin system. These metabolic interactions between the adipocyte's renin-angiotensin system, insulin action and insulin resistance, explain in part the findings relating to a reduced risk of progression to diabetes and the improvement of the insulin-resistance parameters in trials using ACE inhibitors and ARA II (UKPDS, HOPE and MICROHOPE, meta-analyses of ABCD, CAPPP, FACET and UKPDS, LIFE and VALUE). The ARA II may act along two different pathways: via the PPAR-gamma by reducing insulin resistance, dislipidemia and inflammation, and via the angiotensin II pathway by diminishing cell proliferation, hypertension and oxidation.
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