Angiotensin II receptor blockers (ARBs) have beneficial effects similar to those of ACE inhibitors, but angioedema occurs less, and cough rarely occurs compared to ACE inhibitors.
A. Mechanism of Action
Angiotensin I can be formed by nonrenin enzymes such as cathepsin or tonin. Angiotensin I may be converted to angiotensin II by trypsin, cathepsin, or the heart chymase, but the exact contribution of these alternative pathways to the formation of angiotensin II remains unclear. Angiotensin II activates two subtypes of angiotensin II receptors, AT1 and AT2, but only the AT1 receptor mediates all the known clinical effects of angiotensin II described above in Section I. AT1 receptors are present in the heart, kidney, vascular smooth muscle cells, brain, adrenal glands, platelets, the placenta, and in adipocytes. The AT2 receptor affects the inhibition of cell growth, promotion of cell differentiation, tissue repair, apop-tosis, and perhaps to a small degree, the production of bradykinin, NO, and prostaglandins in the kidney. Other effects may emerge with further research. The AT2 receptors have been cloned and are present at a low level in the adrenal gland, heart, brain, kidney, and uterus.

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