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New mechanism of heart protection by angiotensin receptor blockers.

Cardiac hypertrophy is often seen in hypertensive patients and is associated with arrhythmia, stroke, sudden death and heart failure. Mechanical stretching has been cited as the cause of cardiac hypertrophy, and investigation into this process with angiotensin receptor blockers (ARBs) has indicated that AT(1) receptors are involved in stretch-induced hypertrophic responses. The effects of stretching have also been found to be independent of angiotensin II. These experiments showed that there are two types of ARBs. One is a competitive antagonist, and the other is the inverse agonist which is able to inhibit the activity of the receptors even in the absence of their ligands. Inverse agonism on AT(1) receptors has been demonstrated with candesartan, which may have clinical significance depending on the presence or absence of angiotensin II and the expression of AT(1) receptors.