Effects of angiotensin-converting enzyme inhibition on leptin and adiponectin levels in essential hypertension.

Activation of the renin-angiotensin-aldosterone system (RAAS) and abnormal adipokine levels are biological alterations that affect blood pressure regulation and interact to link hypertension, obesity and metabolic diseases. While imbalanced levels of hormones produced by adipocytes including hypo-adiponectinaemia and hyperleptinaemia were reported in hypertension, little is known about how antihypertensive therapy affects these alterations. This study aimed to evaluate the effects of enalapril on plasma adiponectin and leptin levels in hypertensive individuals. Thirty-seven untreated hypertensive patients were prospectively treated with enalapril for 8 weeks. Blood samples were collected at baseline and after the treatment with enalapril. Plasma adiponectin and leptin levels were measured by enzyme-linked immunoassay. We found significant increases in adiponectin levels after enalapril treatment (5.4 ± 3.7 versus 6.0 ± 4.5 µg/mL, mean ± S.D., p = 0.04). Conversely, leptin levels were unchanged (18.0 ± 14.7 versus 18.4 ± 14.8 ng/mL, mean ± S.D., p = 0.31). Multiple linear regression revealed that baseline leptin is a significant predictor of systolic blood pressure reduction (ß=0.269, p = 0.01) in hypertensive individuals treated with enalapril. While enalapril increases adiponectin levels in hypertensive individuals, baseline leptin levels predict blood pressure reduction in response to this therapy. These findings support the idea of an important relationship between RAAS and adipose tissue in hypertension and suggest that enalapril improves the adipokine profile, possibly allowing beneficial effects to overweight or obese hypertensive individuals.