Genetic ablation of Ttn3 in mice induced ambient hypertension (MAP 124.4 vs 103.2 mmHg), tachycardia, and impaired baroreflex sensitivity, demonstrating its essential role in sensing blood pressure.
TTN3 is an essential mechanosensitive ion channel in aortic arch baroreceptors that detects dynamic blood pressure changes to regulate arterial pressure and heart rate.
Absolute Event Rate: 124.4% vs 103.2%
p-value: p=<0.05
The baroreceptor reflex is a powerful neural feedback that regulates arterial pressure (AP). Mechanosensitive channels transduce pulsatile AP to electrical signals in baroreceptors. Here we show that tentonin 3 (TTN3/TMEM150C), a cation channel activated by mechanical strokes, is essential for detecting AP changes in the aortic arch. TTN3 was expressed in nerve terminals in the aortic arch and nodose ganglion (NG) neurons. Genetic ablation of Ttn3 induced ambient hypertension, tachycardia, AP fluctuations, and impaired baroreflex sensitivity. Chemogenetic silencing or activation of Ttn3+ neurons in the NG resulted in an increase in AP and heart rate, or vice versa. More important, overexpression of Ttn3 in the NG of Ttn3-/- mice reversed the cardiovascular changes observed in Ttn3-/- mice. We conclude that TTN3 is a molecular component contributing to the sensing of dynamic AP changes in baroreceptors.
Lu et al. (Mon,) conducted a other in Blood pressure regulation (Baroreceptor function). Genetic ablation of Ttn3 vs. Wild-type (WT) mice was evaluated on Mean arterial pressure (MAP) over 24 hours (p=<0.05). Genetic ablation of Ttn3 in mice induced ambient hypertension (MAP 124.4 vs 103.2 mmHg), tachycardia, and impaired baroreflex sensitivity, demonstrating its essential role in sensing blood pressure.