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HYPERTENSION

Hypertensionelevated blood pressure (>130/ >90 mmhg). Hypertension is a majorrisk

factor forstroke,myocardial infarction,heart failure,aneurysms of the arteriesperipheral arterial

disease and is a cause ofchronic kidney disease.Even moderate elevation of arterial blood pressure is

associated with a shortenedlife expectancy.

BASIS:

130/85mmhg

Medication History (verapamil and propanolol)

TREATMENT OBJECTIVES

Prevent complications

Normalize blood pressure 120/80 mmhg

NON-PHARMACOLOGICAL TREATMENT

Lifestyle modifications:

Weight reduction

Dash diet

Sodium restriction

Moderation in alcohol consumption

PHARMACOLOGICAL TREATMENT

ANGIOTENSIN RECEPTOR BLOCKER

LOSARTAN VALSARTAN

EFFICACY +++ +++

SUITABILITY+++ +++

SAFETY +++ +++

COST ++ +

DIURETICS VASODILATORS CCB ACEI ARBS BB

EFFICACY +++ +++ +++ +++ +++ +++

SUITABILITY + + ++ ++ +++ ++

SAFETY + + + ++ +++ ++

COST +++ ++ ++ ++ ++ ++

http://en.wikipedia.org/wiki/Risk_factorhttp://en.wikipedia.org/wiki/Risk_factorhttp://en.wikipedia.org/wiki/Strokehttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Aneurysmhttp://en.wikipedia.org/wiki/Peripheral_arterial_diseasehttp://en.wikipedia.org/wiki/Peripheral_arterial_diseasehttp://en.wikipedia.org/wiki/Chronic_kidney_diseasehttp://en.wikipedia.org/wiki/Life_expectancyhttp://en.wikipedia.org/wiki/Life_expectancyhttp://en.wikipedia.org/wiki/Life_expectancyhttp://en.wikipedia.org/wiki/Chronic_kidney_diseasehttp://en.wikipedia.org/wiki/Peripheral_arterial_diseasehttp://en.wikipedia.org/wiki/Peripheral_arterial_diseasehttp://en.wikipedia.org/wiki/Aneurysmhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Strokehttp://en.wikipedia.org/wiki/Risk_factorhttp://en.wikipedia.org/wiki/Risk_factor

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LOSARTAN

Mechanism Of Action:

is a selective, competitiveangiotensin II receptor type 1 (AT1) receptor

antagonist, reducing the end organ responses to angiotensin II. Losartan administration

results in a decrease in total peripheral resistance (afterload) and cardiac venous return

(preload) All of the physiological effects of angiotensin II, including stimulation of

release ofaldosterone,are antagonized in the presence of losartan. Reduction in blood

pressure occurs independently of the status of therenin-angiotensin system.As a result

of losartan dosing, plasma renin activity increases due to removal of the angiotensin II

feedback.

Pharmacokinetics:

Losartan is well absorbed following oral administration and undergoes significant first-

pass metabolism to produce 5-carboxylic acid metabolite, designated as EXP3174. This

metabolite is a long-acting (6 to 8 hr), noncompetitive antagonist at the AT1receptor, and

contributes to the pharmacological effects of losartan. EXP3174 is 10-40 times more potent in

blocking AT1receptors than losartan. Losartan's bioavalability is about 32%.

Metabolism is primarily by cytochrome P450 isoenzymes CYP2C9 and CYP3A4.

Peak plasma concentrations of losartan and E-3174 occur about one hour and three to

four hours, respectively, after an oral dose. Both losartan and E-3174 are more than 98%

bound to plasma proteins. Losartan is excreted in the urine, and in the feces via bile, as

unchanged drug and metabolites. About 4% of an oral dose is excreted unchanged in

urine, and about 6% is excreted in urine as the active metabolite. The terminal

elimination half lives of losartan and E-3174 are about 1.5 to 2.5 hours and 3 to 9 hours,

respectively.

http://en.wikipedia.org/wiki/Angiotensin_II_receptor_type_1http://en.wikipedia.org/wiki/Aldosteronehttp://en.wikipedia.org/wiki/Renin-angiotensin_systemhttp://en.wikipedia.org/wiki/Renin-angiotensin_systemhttp://en.wikipedia.org/wiki/Aldosteronehttp://en.wikipedia.org/wiki/Angiotensin_II_receptor_type_1