Xipamide, a sulfonamide diuretic drug, can block sodium reabsorption in distal tubules of the kidney and the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel. It is used for the treatment of oedema and hypertension.
Xipamide is a sulfonamide-based diuretic. Xipamide is an antihypertensive agent able to selectively inhibit the anion exchanger (AE). The efficacy of xipamide 20 to 40 mg once daily in patients with mild to moderate hypertension is comparable to that of bendrofluazide 5 mg, bumetanide 1 mg or hydrochlorothiazide 50 mg when used alone in newly treated or previously treated patients[3]. 10 mg or 20 mg of xipamide daily is effective in lowering blood pressure in hypertensive patients but is associated with hypokalaemia[4]. The plasma concentration of alpha-atrial natriuretic peptide fell after 1 week of xipamide administration and increased during prolonged xipamide administration but remained reduced. The changes in plasma alpha-ANP observed after 1 week of xipamide were negatively correlated with the changes in hematocrit and hemoglobin. The xipamide-induced changes in PRA (Plasma renin activity) and PAC (aldosterone concentration) were positively correlated with the changes in the hematocrit and hemoglobin[5]. In newborn rat cardiomyocytes, xipamide reduced amiloride-induced cell acidification at similar concentrations as in H9c2 cardiocytes, but with a slightly higher extent of maximal inhibition (70-80%). Xipamide reduced amiloride-dependent cell acidification in the rat heart myogenic H9c2 cell line and in newborn rat cultured cardiomyocytes[6].
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