Angiotensin+receptor+blockers+(ARB's)

__General Pharmacology__ These drugs have very similar effects to [|angiotensin converting enzyme (ACE) inhibitors] and are used for the same indications ([|hypertension], [|heart failure], post-[|myocardial infarction]). Their mechanism of action, however, is very different from ACE inhibitors, which inhibit the formation of angiotensin II. ARBs are receptor antagonists that block type 1 angiotensin II (AT1) receptors on bloods vessels and other tissues such as the heart. These receptors are coupled to the [|Gq-protein and IP3 signal transduction pathway] that stimulates vascular smooth muscle contraction. Because ARBs do not inhibit ACE, they do not cause an increase in bradykinin, which contributes to the vasodilation produced by ACE inhibitors and also some of the side effects of ACE inhibitors (cough and angioedema). ARBs have the following actions, which are very similar to ACE inhibitors: __Therapeutic Uses__ ARBs are used in the treatment of hypertension and heart failure in a similar manner as ACE inhibitors (see [|ACE inhibitors] for details). They are not yet approved for post-myocardial infarction, although this is under investigation. __Specific Drugs__ ARBs include the following drugs: Note that each of the ARBs named above ends with "sartan." __Side Effects and Contraindications__ As a drug class, ARBs have a relatively low incidence of side effects and are well-tolerated. Because they do not increase bradykinin levels like ACE inhibitors, the dry cough and angioedema that are associated with ACE inhibitors are not a problem. ARBs are contraindicated in pregnancy. Patients with bilateral renal artery stenosis may experience renal failure if ARBs are administered. The reason is that the elevated circulating and intrarenal angiotensin II in this condition constricts the efferent arteriole more than the afferent arteriole within the kidney, which helps to maintain glomerular capillary pressure and filtration. Removing this constriction by blocking angiotensin II receptors on the efferent arteriole can cause an abrupt fall in glomerular filtration rate. This is not generally a problem with unilateral renal artery stenosis because the unaffected kidney can usually maintain sufficient filtration after AT1 receptors are blocked; however, with bilateral renal artery stenosis it is especially important to ensure that renal function is not compromised.
 * Angiotensin Receptor Blockers (ARBs)**
 * Dilate arteries and veins and thereby reduce arterial pressure and [|preload] and [|afterload] on the heart.
 * Down regulate sympathetic adrenergic activity by blocking the effects of angiotensin II on sympathetic nerve release and reuptake of norepinephrine.
 * Promote renal excretion of sodium and water ([|natriuretic] and [|diuretic] effects) by blocking the effects of angiotensin II in the kidney and by blocking angiotensin II stimulation of [|aldosterone] secretion.
 * Inhibit cardiac and vascular remodeling associated with chronic [|hypertension], [|heart failure], and [|myocardial infarction].
 * **candesartan**
 * **eprosartan**
 * **irbesartan**
 * **losartan**
 * **telmisartan**
 * **valsartan**