Olsart Plus

Hypertension: The usual starting dose is 20/12.5 mg one tablet once daily. Dosing should be individualized. Depending on the blood pressure response, the dose may be titrated at intervals of 2-4 weeks to two tablets 40/25 once daily.

The common side-effects are nausea, headache, dizziness, hyperuricemia, upper respiratory tract infection and urinary tract infection. Other adverse effects are chest pain, back pain, peripheral edema, abdominal pain, dyspepsia, gastroenteritis, diarrhea.

Olmesartan: Limited data are available in regard to overdosage in humans. The most likely manifestation of overdosage would be hypotension and tachycardia. Supportive treatment should be instituted.

Hydrochlorothiazide: The most common signs and symptoms observed are those caused by electrolyte depletion (hypokalemia, hypochloremia, and dehydration) resulting from excessive diuresis. If digitalis has also been administered, hypokalemia may accentuate cardiac arrhythmias.

Olmesartan Medoxomil & Hydrochlorothiazide combination is indicated for the treatment of hypertension.

Angiotensin-II formed from angiotensin-I in a reaction catalyzed by angiotensin-converting enzyme (ACE), is a potent vasoconstrictor, the primary vasoactive hormone of the renin-angiotensin system and an important component in the pathophysiology of hypertension. It also stimulates aldosterone secretion by the adrenal cortex. Olmesartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin-II by selectively blocking the binding of angiotensin-II to the AT 1 receptor found in many tissues (e.g. vascular smooth muscle, adrenal gland). In-vitro-binding studies indicate that Olmesartan is a reversible & competitive inhibitor of AT 1 receptor. Olmesartan does not inhibit ACE (kinase-I, the enzyme that converts angiotensin-I to angiotensin-II and degrades bradykinin).

Hydrochlorothiazide is a thiazide diuretic. Thiazides affect the renal tubular mechanisms of electrolyte reabsorption, directly increasing the excretion of Sodium and Chloride in approximately equivalent amounts. Indirectly, the diuretic action of Hydrochlorothiazide reduces plasma volume with consequent increases in plasma renin activity, increases Aldosterone secretion & urinary Potassium loss and decreases serum Potassium. The renin-aldosterone link is mediated by angiotensin-II. So, co-administration of an angiotensin-II receptor antagonist tends to reverse the potassium loss associated with these diuretics.

Combined antihypertensive preparations