For the management of hypertension alone or in combination with other classes of antihypertensive agents. Also used as a first-line agent in the treatment of diabetic nephropathy, as well as a second-line agent in the treatment of congestive heart failure (only in those intolerant of ACE inhibitors).
Angiotensin II, the principal pressor agent of the renin-angiotensin system, is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme [kininase II]. It is responsible for effects such as vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Eprosartan selectively blocks the binding of angiotensin II to the AT1 receptor, which in turn leads to multiple effects including vasodilation, a reduction in the secretion of vasopressin, and reduction in the production and secretion of aldosterone. The resulting effect is a decrease in blood pressure.
Mode of Action:
Eprosartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT_ receptor found in many tissues (e.g., vascular smooth muscle, adrenal gland). There is also an AT_ receptor found in many tissues but it is not known to be associated with cardiovascular homeostasis. Eprosartan does not exhibit any partial agonist activity at the AT_ receptor. Its affinity for the AT_ receptor is _,000 times greater than for the AT_ receptor. In vitro binding studies indicate that eprosartan is a reversible, competitive inhibitor of the AT_ receptor. Eprosartan has also been shown to bind to AT_ receptors both presynaptically and synaptically. Its action on presynaptic AT_ receptors results in the inhibition of sympathetically stimulated noradrenaline release. Unlike ACE inhibitors, eprosartan and other ARBs do not interfere with response to bradykinins and substance P, which allows for the absence of adverse effects that are present in ACE inhibitors (eg. dry cough).
Eprosartan is not metabolized by the cytochrome P450 system. It is mainly eliminated as unchanged drug. Less than 2% of an oral dose is excreted in the urine as a glucuronide.
There was no mortality in rats and mice receiving oral doses of up to 3000 mg eprosartan/kg and in dogs receiving oral doses of up to 1000 mg eprosartan/kg.
Ruilope L, Jager B, Prichard B: Eprosartan versus enalapril in elderly patients with hypertension: a double-blind, randomized trial. Blood Press. 2001;10(4):223-9. Pubmed Hedner T: The clinical profile of the angiotensin II receptor blocker eprosartan. J Hypertens Suppl. 2002 Jun;20(5):S33-8. Pubmed Puig JG, Lopez MA, Bueso TS, Bernardino JI, Jimenez RT: Clinical profile of eprosartan. Cardiovasc Drugs Ther. 2002 Dec;16(6):543-9. Pubmed Ruilope L, Jager B: Eprosartan for the treatment of hypertension. Expert Opin Pharmacother. 2003 Jan;4(1):107-14. Pubmed de la Sierra A, Ram CV: Introduction: The pharmacological profile of eprosartanãimplications for cerebrovascular and cardiovascular risk reduction. Curr Med Res Opin. 2007 Nov;23 Suppl 5:S1-3. Pubmed Blankestijn PJ, Rupp H: Clinical profile of eprosartan: a different angiotensin II receptor blocker. Cardiovasc Hematol Agents Med Chem. 2008 Oct;6(4):253-7. Pubmed
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