Thermal receptors detect temperature changes and can alter the activity of the cells. A subtype referred to as TrpA1 responds to increased temperature and increases expression in the heart of mammals when the heart is injured or is reduced in oxygen. It is not known if this is beneficial or detrimental to the heart. Thus, we examined the effect on heart activity of altering heart expression of TrpA1 in larval fruit flies at varied temperatures. Hearts of normal larvae stopped beating at 37 °C but hearts expressing high levels of TrpA1 stopped beating at 30 °C. In contrast, unmodified larvae of a blowfly species that grows at higher temperatures showed increased heart rate with increased temperature to 37 °C. It is not known if blowflies alter their expression of the thermal receptors. Thermal receptors can also be activated by physical stretch. Thus, it is possible an increase in expression in mammalian hearts within a narrow temperature range could be helpful in maintaining heart rate, as activation of TrpA1 receptors may be modulated by the stretching and relaxing of the heart itself. More research is needed in examining the function of TrpA1 receptors in mammalian hearts.
The transient receptor potential (TrpA—ankyrin) receptor has been linked to pathological conditions in cardiac function in mammals. To better understand the function of the TrpA1 in regulation of the heart, a Drosophila melanogaster model was used to express TrpA1 in heart and body wall muscles. Heartbeat of in intact larvae as well as hearts in situ, devoid of hormonal and neural input, indicate that strong over-expression of TrpA1 in larvae at 30 or 37 °C stopped the heart from beating, but in a diastolic state. Cardiac function recovered upon cooling after short exposure to high temperature. Parental control larvae (UAS-TrpA1) increased heart rate transiently at 30 and 37 °C but slowed at 37 °C within 3 min for in-situ preparations, while in-vivo larvae maintained a constant heart rate. The in-situ preparations maintained an elevated rate at 30 °C. The heartbeat in the TrpA1-expressing strains could not be revived at 37 °C with serotonin. Thus, TrpA1 activation may have allowed enough Ca 2+ influx to activate K( Ca) channels into a form of diastolic stasis. TrpA1 activation in body wall muscle confirmed a depolarization of membrane. In contrast, blowfly Phaenicia sericata larvae increased heartbeat at 30 and 37 °C, demonstrating greater cardiac thermotolerance.