Abstract
Acid sensing ion channel 2 (ASIC2) has been implicated as a mechanosensor in sensory nerves (Nature 407:2000). Previously, we demonstrated a blunting of increases in baroreceptor (BR) activity during increases in blood pressure (BP) in ASIC2 deficient (ASIC2−/−) mice, suggesting that ASIC2 contributes to BR mechanoelectrical transduction (FASEB J. 15(5):2001). We hypothesized that a defect in BR sensory function in ASIC2−/−mice will translate into impaired BR control of heart rate (HR), decreased parasympathetic tone, and increased sympathetic tone. BP and HR were measured by telemetry in conscious control (n=6) and ASIC2−/− (n=5) male mice. BR sensitivity (BRS) was calculated from spontaneous reciprocal fluctuations in BP and HR using the sequence method. Resting mean BP was similar in control (98±4 mmHg) and ASIC2−/− (101±5 mmHg) mice, whereas HR was significantly higher in ASIC2−/− mice (552±19 vs. 495±18 bpm, *P<0.05). This pattern was also observed during periods of spontaneous locomotor activity (see table). ASIC2−/− mice exhibited decreased BRS, reduced HR response to methylatropine (parasympathetic tone), and increased HR response to propranolol (sympathetic tone). Taken together with our previous findings, these results support the hypothesis that ASIC2 is a component of the BR mechanosensitive channel complex. (NIH HL14388 and AHA#0525745Z)
Published Version
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