Mechanosensitivity describes the ability to respond to a mechanicalstimulus. The heart can respond to a mechanical stimulus through the action ofmechanosensitive ion channels (MSCs). MSCs provide a direct link betweenstretch and electrical activity. However, the heart does not react to stretch solelythrough the action of MSCs. The mammalian myocardium possesses a biphasicresponse to stretch: first, there is an immediately increase in the force of cardiaccontraction, known as the Frank-Starling response; secondly, there is a slowpositive inotropic response, known as the slow force response (SFR) that occursover the minutes following the initial stretch. Fish are unique amongst vertebrates as, with a few exceptions, they relymore heavily on changes in stroke volume than heart rate when regulatingcardiac output. Rainbow trout (Oncorhynchus mykiss) are particularly sensitiveto the Frank-Starling response and small increases in filling pressure lead to largeincreases in stroke volume (300 %) during strenuous exercise. The ability of fishhearts to undertake these large dilations makes them an ideal model whenlooking at the effect of stretch on cardiac muscle as they may exhibit morepronounced responses to mechanical stimuli. Despite this, the role of mechanicalregulation in the fish heart has undergone sparse investigation. The aim of this thesis was to investigate the mechanosensitivity of thefish heart at a number of resolutions. Chapter three looks at the effect of stretchon the isolated whole rainbow trout heart. I found that MSCs are activated atphysiological extremes of input and output pressures. The trout ortholog of acandidate MSC, TRPC1, was cloned and its presence in the heart was verified. Both MSCs and exaggerated cardiac transmural electrical heterogeneity cancause re-entrant arrhythmias in the mammalian heart. As the piscine heart hasshown resistance to these arrhythmias I examined the transmural electricalheterogeneity of the tuna heart in Chapter four. I found no evidence oftransmural electrical heterogeneity in the tuna heart which may explain thereduced susceptibility of the fish heart to re-enterant arrhythmias. In Chapter fiveI investigated the effect of stretch on ventricular trabecular bundle preparationsand isolated ventricular myocytes of the rainbow trout. This study was the first tofind a lack of a SFR in a vertebrate heart and provides evidence for theimportance of the Na+ /H+ -exchanger in the SFR. Finally the study in Chaptersix examined the length-dependent Ca2+ sensitivity of skinned ventricular rat andtrout myocytes. I show that the increased length-dependent Ca2+ sensitivity of thetrout myocytes may account for the extended functional limb of the piscinelength-tension relationship. Skinned trout myocytes were shown to develop ahigh passive tension that could not be explained by the trout titin isoform ratio,but may be explained by increased phosphorylation of titin in vivo. My PhD research has produced clear and novel evidence for theimportance of mechanosensitivity in the fish heart. From the level of the wholeheart to the level of the individual sarcomere, stretch induces physiologicalchanges in this vital organ. A greater understanding of piscine cardiacmechanosensitivity will greatly improve general knowledge ofmechanosensitivity in general and will provide an evolutionary point ofcomparison for the studies of mechanosensitivity in other organisms.