In the last few years, the large family of transient receptor potential (TRP) channels has been associated with the development of several cardiovascular diseases. 28 mammalian TRP-related proteins have been cloned, which are divided in 6 subfamilies: the classical TRPs (TRPC1-7); the vanilloid receptor TRPs (TRPV1-6); the melastatin TRPs (TRPM1-8); the mucolipins (TRPML1-3); the polycystins (TRPP1-3); and ankyrin transmembrane protein 1 (TRPA1). The proteins of the TRP family exhibit a 6-transmembrane domain architecture and form cation channels activated by, among others, temperature, receptor stimulation, chemical agonists, or possibly mechanical forces. In this way, they may contribute directly to transplasmalemmal Ca2+ influx and/or influence intracellular Ca2+ concentration ([Ca2+]i) indirectly by setting the membrane potential or regulating Ca2+ release from intracellular organelles. Depending on the cell type, TRP channel-mediated changes in cellular Ca2+ homeostasis can lead to alterations in vascular and cardiac contractility, neurotransmitter release, secretion of vasoactive hormones, mineral absorption, and body fluid balance to regulate blood pressure. In the heart, neuroendrocrine stimuli like noradrenaline, adrenaline and Angiotensin II lead to activation of G-protein-dependent signaling pathways that evoke Ca2+ entry and Ca2+-dependent processes, e.g. activation of Calcineurin/NFAT, CaM-Kinase and protein kinase C leading to the development of myocyte growth and cardiac hypertrophy. Although this represents an adaptive response preserving cardiac function initially, the persistent activation of this pathway during long-term cardiac stress may lead to cardiac failure in many cardiovascular disease entities including hypertension, ischemic or valvular heart disease. A specific pharmacology is still lacking for most TRPs. Therefore, studies to unravel the roles of TRP channels currently rely on experiments using transgenic animals and our findings about the role of individual TRP proteins for blood pressure regulation and development of cardiac hypertrophy using TRP-deficient mice will be presented.