Why the study?
Endoglin is involved in regulating endothelial function and homeostasis, but the effect of candesartan compared with other BP-lowering regimens on plasma soluble endoglin was not established.
Does long-term treatment with candesartan reduce plasma levels of soluble endoglin compared to other antihypertensive agents in hypertensive patients?
Does long-term treatment with candesartan reduce plasma levels of soluble endoglin compared to other antihypertensive agents in hypertensive patients?
Long-term treatment with candesartan is associated with lower levels of soluble endoglin, a biomarker of endothelial dysfunction, compared to other antihypertensive classes.
Candesartan-associated lower sEng warrants caution in interpreting endothelial effects; leaves open whether this biomarker change improves hypertension outcomes.
Endoglin is a transmembrane glycoprotein involved in regulating endothelial function and homeostasis. We investigated the effect of candesartan compared with that of different regimens of blood pressure (BP)-lowering agents on the plasma level of soluble endoglin (sEng), a biomarker involved directly in endothelial homeostasis. A total of 395 patients were enrolled, of which 129 had normal BP (group A, control group), 133 were hypertensive patients treated with candesartan (8, 16, or 32 mg/day) in monotherapy (group C) and 133 were hypertensive patients treated with different types of antihypertensive agents (beta-blockers, calcium-channel blockers, diuretics) as monotherapy (group B). Classical methods of assessing endothelial damage (flow-mediated dilatation, intima-media thickness) as well as other biochemical parameters and investigations were undertaken. Correlations with the plasma level of sEng were performed. A lower plasma level of sEng was found in patients undergoing long-term BP-lowering treatment with candesartan compared with that in hypertensive patients undergoing longterm treatment with beta-blockers, calcium-channel blockers, or diuretics (p < 0.001). Diastolic BP and the blood urea nitrogen (BUN) levels were protective factors for sEng. The end-diastolic diameter of the left ventricle and neutrophil count were risk factors for soluble endoglin and thus for endothelial dysfunction. By quantifying a glycoprotein involved in endothelial function/homeostasis regulation, sEng, could be a specific biomarker of vascular and cardiac lesions and predict the efficacy of antihypertensive treatment.
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Valentina Buda (2022) studied this question.
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