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The European Society of Cardiology

Emerging insights into hypertension and dyslipidaemia synergies

A.C. Sposito*

Heart Institute (InCor), Zerbini Foundation, Brasilia, Brazil

* Correspondence: Andrei C. Sposito, Department of Cardiology, Heart Institute (InCor-DF), Zerbini Foundation, Brasilia, Brazil. Tel.: +55 61 403 5404; fax: +51 61 403 5486 (E-mail: sposito{at}zerbini.org.br).

Abstract

Hypertension frequently occurs in conjunction with metabolic disturbances, most notably hypercholesterolaemia. If there is an association between hypertension and hypercholesterolaemia, it is important to understand the mechanisms responsible and investigate whether elevated blood pressure (BP) increases the atherogenicity of cholesterol-rich lipoproteins. Evidence from studies suggests that hypercholesterolaemia contributes to the progression of hypertension via a number of possible mechanisms: low nitric oxide bioavailability, enhanced activity of the renin–angiotensin–aldosterone system, enhanced endothelin levels and receptor expression, and endothelial dysfunction. Other possible mechanisms include salt sensitivity (which is worsened by endothelial dysfunction), the secretion of vasoconstrictive molecules and an enrichment of cholesterol in cellular membranes, all of which reduce membrane fluidity and ion channel transporter activity. In response to cholesterol-enriched cellular membranes, the fractional clearance rate of sodium is reduced, which, in turn, favours sodium retention. Enriched cellular membrane cholesterol can also affect the transport of calcium in vascular smooth muscle cells, allowing an influx of calcium into these cells, which in turn increases conductivity and leads to microvessel constriction. Conversely, it is also evident that arterial distension and increased intra-luminal pressure induced by hypertension can increase the accumulation of atherogenic lipoproteins in the arterial wall. To optimize the management of cardiovascular disease, future treatment strategies should be directed at controlling both BP and cholesterol, particularly in high-risk patients.

Keywords Hypertension; Hypercholesterolaemia; Nitric oxide; Endothelial dysfunction; Renin–angiotensin system


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