Amlodipine, Hydrochlorothiazide, Olmesartan medoxomil
Indications
Amlodipine, Hydrochlorothiazide, Olmesartan medoxomil is used for:
Olmesartan
Olmesartan is indicated for the treatment of hypertension either alone or associated with other antihypertensive agents.[FDA label] Hypertension is a sustained elevation of resting blood pressure. The hypertensive effect can affect the systolic blood pressure, diastolic blood pressure or both. This condition tends to be asymptomatic until it reaches a severe or long-standing state.[L5569]
Amlodipine
Amlodipine may be used alone or in combination with other antihypertensive and antianginal agents for the treatment of the following conditions [FDA label]: 䮢 Hypertension 䮢 Coronary artery disease 䮢 Chronic stable angina 䮢 Vasospastic angina (Prinzmetal?s or Variant angina) 䮢 Angiographically documented coronary artery disease in patients without heart failure or an ejection fraction < 40%
Hydrochlorothiazide
For the treatment of high blood pressure and management of edema.
Olmesartan is indicated for the treatment of hypertension either alone or associated with other antihypertensive agents.[FDA label] Hypertension is a sustained elevation of resting blood pressure. The hypertensive effect can affect the systolic blood pressure, diastolic blood pressure or both. This condition tends to be asymptomatic until it reaches a severe or long-standing state.[L5569]
Amlodipine
Amlodipine may be used alone or in combination with other antihypertensive and antianginal agents for the treatment of the following conditions [FDA label]: 䮢 Hypertension 䮢 Coronary artery disease 䮢 Chronic stable angina 䮢 Vasospastic angina (Prinzmetal?s or Variant angina) 䮢 Angiographically documented coronary artery disease in patients without heart failure or an ejection fraction < 40%
Hydrochlorothiazide
For the treatment of high blood pressure and management of edema.
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Amlodipine, Hydrochlorothiazide, Olmesartan medoxomil :
Mechanism of Action
Olmesartan
Olmesartan is a selective angiotensin II-type I receptor blocker with a large affinity. It has been shown to present an IC50 of 8 nmol/L while showing a very minimal affinity towards angiotensin-II type II receptor. The blockage of olmesartan is done by the displacement of angiotensin II converting it hence, in a competitive antagonist.[A175330] The activity of olmesartan is mainly performed in vascular smooth muscle cells and hence its activity prevents the vasoconstrictor effects of angiotensin II.[A175342]
Amlodipine
**Mechanism of action on blood pressure** Amlodipine is considered a peripheral arterial vasodilator that exerts its action directly on vascular smooth muscle to lead to a reduction in peripheral vascular resistance, causing a decrease in blood pressure. Amlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the influx of calcium ions into both vascular smooth muscle and cardiac muscle. Experimental studies imply that amlodipine binds to both _dihydropyridine_ and _nondihydropyridine_ binding sites, located on cell membranes. The contraction of cardiac muscle and vascular smooth muscle are dependent on the movement of extracellular calcium ions into these cells by specific ion channels. Amlodipine blocks calcium ion influx across cell membranes with selectivity. A stronger effect of amlodipine is exerted on vascular smooth muscle cells than on cardiac muscle cells [FDA label]. Direct actions of amlodipine on vascular smooth muscle result in reduced blood pressure [F3757]. **Mechanism of action in angina** The exact mechanism by which amlodipine relieves the symptoms of angina have not been fully elucidated to this date, however, the mechanism of action is likely twofold: Amlodipine has a dilating effect on peripheral arterioles, reducing the total peripheral resistance (afterload) against which the cardiac muscle functions. Since the heart rate remains stable during amlodipine administration, the reduced work of the heart reduces both myocardial energy use and oxygen requirements [F3757]. Dilatation of the main coronary arteries and coronary arterioles, both in healthy and ischemic areas, is another possible mechanism of amlodipine reduction of blood pressure. The dilatation causes an increase in myocardial oxygen delivery in patients experiencing coronary artery spasm (Prinzmetal's or variant angina) and reduces coronary vasoconstriction caused by smoking [F3757].
Hydrochlorothiazide
Hydrochlorothiazide, a thiazide diuretic, inhibits water reabsorption in the nephron by inhibiting the sodium-chloride symporter (SLC12A3) in the distal convoluted tubule, which is responsible for 5% of total sodium reabsorption. Normally, the sodium-chloride symporter transports sodium and chloride from the lumen into the epithelial cell lining the distal convoluted tubule. The energy for this is provided by a sodium gradient established by sodium-potassium ATPases on the basolateral membrane. Once sodium has entered the cell, it is transported out into the basolateral interstitium via the sodium-potassium ATPase, causing an increase in the osmolarity of the interstitium, thereby establishing an osmotic gradient for water reabsorption. By blocking the sodium-chloride symporter, hydrochlorothiazide effectively reduces the osmotic gradient and water reabsorption throughout the nephron.
Olmesartan is a selective angiotensin II-type I receptor blocker with a large affinity. It has been shown to present an IC50 of 8 nmol/L while showing a very minimal affinity towards angiotensin-II type II receptor. The blockage of olmesartan is done by the displacement of angiotensin II converting it hence, in a competitive antagonist.[A175330] The activity of olmesartan is mainly performed in vascular smooth muscle cells and hence its activity prevents the vasoconstrictor effects of angiotensin II.[A175342]
Amlodipine
**Mechanism of action on blood pressure** Amlodipine is considered a peripheral arterial vasodilator that exerts its action directly on vascular smooth muscle to lead to a reduction in peripheral vascular resistance, causing a decrease in blood pressure. Amlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the influx of calcium ions into both vascular smooth muscle and cardiac muscle. Experimental studies imply that amlodipine binds to both _dihydropyridine_ and _nondihydropyridine_ binding sites, located on cell membranes. The contraction of cardiac muscle and vascular smooth muscle are dependent on the movement of extracellular calcium ions into these cells by specific ion channels. Amlodipine blocks calcium ion influx across cell membranes with selectivity. A stronger effect of amlodipine is exerted on vascular smooth muscle cells than on cardiac muscle cells [FDA label]. Direct actions of amlodipine on vascular smooth muscle result in reduced blood pressure [F3757]. **Mechanism of action in angina** The exact mechanism by which amlodipine relieves the symptoms of angina have not been fully elucidated to this date, however, the mechanism of action is likely twofold: Amlodipine has a dilating effect on peripheral arterioles, reducing the total peripheral resistance (afterload) against which the cardiac muscle functions. Since the heart rate remains stable during amlodipine administration, the reduced work of the heart reduces both myocardial energy use and oxygen requirements [F3757]. Dilatation of the main coronary arteries and coronary arterioles, both in healthy and ischemic areas, is another possible mechanism of amlodipine reduction of blood pressure. The dilatation causes an increase in myocardial oxygen delivery in patients experiencing coronary artery spasm (Prinzmetal's or variant angina) and reduces coronary vasoconstriction caused by smoking [F3757].
Hydrochlorothiazide
Hydrochlorothiazide, a thiazide diuretic, inhibits water reabsorption in the nephron by inhibiting the sodium-chloride symporter (SLC12A3) in the distal convoluted tubule, which is responsible for 5% of total sodium reabsorption. Normally, the sodium-chloride symporter transports sodium and chloride from the lumen into the epithelial cell lining the distal convoluted tubule. The energy for this is provided by a sodium gradient established by sodium-potassium ATPases on the basolateral membrane. Once sodium has entered the cell, it is transported out into the basolateral interstitium via the sodium-potassium ATPase, causing an increase in the osmolarity of the interstitium, thereby establishing an osmotic gradient for water reabsorption. By blocking the sodium-chloride symporter, hydrochlorothiazide effectively reduces the osmotic gradient and water reabsorption throughout the nephron.