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Transient receptor potential, TRP channels are a new superfamily of functionally versatile non-selective cation channels present from yeast to mammals. On the basis of their structural homology, TRP channels are subdivided in 7 groups : TRPC 1-7 Canonical, TRPV 1-6 Vanilloid, TRPM 1-8 Melastatin, TRPP 1-3 Polycystin, TRPML Mucolipin, TRPA Ankyrin and TRPN (NO mechanotransducer potential C), the latter not expressed in mammals. Their cloning and heterologous expression allowed to demonstrating that these channels are generally weakly voltage-dependent. They are activated by various ligands involving a signal transduction cascade as well as directly by multiple compounds, heat and pH. TRP channels are found in a broad range of cell types. TRP channels are essential in allowing animals to sense the outside world and cells to sense their local environment. Following mutations or anomalous behaviour, these channels have a major role in several human diseases.

General properties of the calcium channel are analyzed in the myocardium under voltage clamp conditions both in multicellular properties and in single isolated cells. More recently the patch-clamp has allowed us to study single channels. In normal conditions, the selectivity of the calcium channel to Ca2+ ions is very high; however, in the absence of calcium many divalent cations and even Na ions can go through this channel. Kinetic analysis shows: calcium channel inactivation depends on Ca2+ entry rather than on membrane potential, opening of this channel requires at least two transitions of closed states before the open state. Many works refer to pharmacology of the calcium channel in heart tissue. beta-adrenergic stimulation induces a large increase in current amplitude related to the increase in maximal conductance without variation in the unitary conductance. Two interpretations are available: an increase in the opening probability and/or an increase in the number of available channels, both are consecutives to phosphorylations of the channel. Cholinergic stimulation seems to have little effect. Studies of calcium antagonists have revealed that all these substances have, at various levels, use-dependent and voltage-dependent inhibitory effect. Moreover, some dihydropyridine derivatives can even, activate the channel. Antiarrhythmic as well as general anaesthetic agents have an inhibitory action on the calcium channel besides their effects on the sodium channel or the Na-Ca exchange. Very recently, the existence of another calcium conductance was demonstrated. It is characterized by a low threshold, a pure voltage-dependent inactivation, a relatively weak sensitivity to anticalcic agents and neurotransmettors.

The importance of respecting the ionic equilibrium of cardioplegic solutions was studied experimentally in rat papillary muscle by observing the mechanical and metabolic changes after altering the ionic composition of the washing fluid. The first part of the study demonstrated the nature of the "rigor" of sustained tension induced by the inhibition of the respiratory activity of the mitochondria: this observation showed that this tension was essentially related to the energy deficit induced by poisoning. In the second part, it was shown that calcium overload induced by changing the ionic composition of the nutrient fluid (replacing some of the Na+ ions by K+ or Li+), that is to say related to dysfunction of the Na+-Ca++ exchange induced a contraction which also rapidly evolved to a tension of rigor. This effect was accompanied by a significant reduction in the adenosine triphosphate (ATP) and creatine phosphate (CP) content. The mechanical consequences of prolonged hypoxia or calcium overload are directly related to the reduction in energy reserves producing a marked deficit of ATP in the myofibrils, and resulting in a stable but reversible increase in cardiac muscle rigidity (or rigor). The prevention of calcium overload during the use of cardioplegic solutions is discussed in the context of metabolic myocardial protection. The inhibitory substances of calcium influx such as the calcium antagonist drugs or Mg++ may have an important role to play, in addition to the maintenance of ionic concentrations, especially that of sodium, close to those of the external fluid.