muscle, effects on cardiac metabolism, and vasoconstriction of blood vessels.' In addition, clinical studies demonstrating the efficiency of angiotensin converting enzyme (ACE) inhibitors in the treatment of heart failure,2 myocardial ischemia,3 4and hypertension5.6 suggest that Ang II directly promotes pathological cell growth that participates in remodeling of the failing heart. Several animal studies have implicated Ang II in cardiac hypertrophy associated with hypertension; for instance, in a rat model of "pressure-overload" cardiac hypertrophy, treatment with an ACE inhibitor prevented the increase in left ventricular mass with no effect on afterload,7 suggesting that the growth effects of Ang II are direct. Moreover, chronic infusion of Ang II into rats increased left ventricular mass, even when the pressor activity of Ang II was blocked or a subpressor dose of Ang II was used.8 Recent experiments using cultured embryonic chick cardiomyocytes lend further support to the hypothesis that Ang II can directly produce cellular hypertrophy.9"10 It has not been established whether Ang II also has a direct growth effect on nonmyocyte cells of the heart, although recent studies suggest that cardiac fibroblasts are a target for Ang II; for instance, treatment with the ACE inhibitor captopril prevented myocardial fibrosis in a rat model with renovascular hypertension" and with induced myocardial infarction.12 In the latter study,

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In many nonexcitable cells, activation of phospholipase C (PLC)-linked receptors results in a release of Ca²⁺ from intracellular stores followed by a transmembrane Ca²⁺ entry. This Ca²⁺ entry underlies the sustained phase of [Ca²⁺]_i increase, is important for various cellular functions including gene expression, secretion and cell proliferation, and is supported by agonist-activated Ca²⁺-permeable ion channels. Ca²⁺-permeable channels which are activated by store depletion and which are therefore referred to as store- operated channels or SOCs form a major pathway for agonist-induced Ca²⁺ influx. So far, the molecular structures of these channels have not been identified. Potential candidates are encoded by members of the TRP family, a class of ion channels initially discovered in Drosophila and involved in the PLC-dependent transduction of visual stimuli. Here, we review recent evidence that agonist-induced Ca²⁺ influx and especially SOCs are present in different cell types of the heart and of the cardiovascular system and compare these findings with the possible functions and tissue-specific expression of mammalian TRP proteins.

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