The role of aldosterone and aldosterone blockade in hypertension

Hypertension is the most prevalent and significant modifiable risk factor for cardiovascular disease.1 It has been estimated that 7.6 million premature deaths and 54% of stroke and 47% of ischemic heart disease worldwide are attributable to elevated blood pressure levels.2 Blood pressure regulation is a complex process involving several organs, including the heart, brain, kidneys and vasculature. The renin-angiotensin-aldosterone system (RAAS) has a central role in blood pressure regulation. A decrease in renal perfusion leads to the synthesis and release of renin by the juxtaglomerular cells in the afferent arterioles of the kidney. Renin converts angiotensinogen, which is produced in the liver, to angiotensin I (Ang I). This is subsequently converted to angiotensin II (Ang II) by angiotensin-converting enzyme (ACE) in vascular tissues. Ang II increases blood pressure via Ang II type 1 receptor (AT1R)-mediated vasoconstriction, by increasing sympathetic tone and by stimulation of arginine vasopressin release.3 Ang II also stimulates sodium and water reabsorption by a direct action in the kidney, and indirectly by stimulating aldosterone synthesis and release in the adrenal gland.3 When blood pressure goes up, the increase in renal perfusion will slow down renin release, thereby providing a negative feedback mechanism regulating RAAS activity to its required level. Figure 1 shows a schematic overview of the RAAS.

• View at Worldcat

Free Full Text ( Final Version , 9mb )