Article Details

Background and Objective: Across species, from insects to mammals, the heart adjusts its beating rate when exposed to various physiological or pathological stresses. This regulation occurs through direct mechanical stretch of cardiac cells and through hormonal and neural inputs. Stretch-induced increases in contractility are seen in both larval heart tubes and the complex ventricles of mammals. A major contributor to this response is the family of stretch-activated ion channels, including transient receptor potential ankyrin (TrpA) channels. Although TrpA channels are known to increase in several mammalian cardiac disorders, it remains unclear whether this upregulation is adaptive or harmful. The present study aimed to determine whether enhanced expression of the mechanosensitive TrpA1 channel in the larval Drosophila heart plays a functional role in maintaining heart rate during prolonged pulsatile perfusion.

Materials and Methods: Transgenic Drosophila lines were generated so that the F1 progeny selectively overexpressed TrpA1 in cardiac tissue. Third-instar larvae were dissected to expose the heart, which was then subjected to pulsatile perfusion for four hours. Heart rates were recorded throughout the experiment, and statistical significance was assessed using ANOVA or the Wilcoxon rank-sum test.

Results: Pulsatile supra-perfusion supported stable cardiac contractions for more than four hours in situ, allowing extended physiological and pharmacological assessment. Both the parental line (UAS-TrpA1) and the overexpression line (Tinc>TrpA1) maintained relatively consistent heart rates at 20°C across the four-hour period. At 30°C, however, the parental line preserved heart rate more effectively than the TrpA1-overexpressing larvae. The TrpA1 inhibitor HC-030031, at concentrations of 30 μM, 100 μM, and 1 mM, failed to block temperature-induced depolarization of body wall muscles in larvae expressing TrpA1, and the control groups also showed no observable drug effect.

Conclusion: Overexpression of TrpA1 did not enhance temperature-dependent maintenance of heart rate during prolonged pulsatile perfusion, and pharmacological inhibition with HC-030031 did not attenuate the depolarization response. These findings suggest that TrpA1 may not play a central regulatory role under these experimental conditions.