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1 Internal Medicine, The University of Iowa, Iowa City, IA
2 Veterian Affair Medical Center, Iowa City, IA
ABSTRACT
We demonstrated that Acid-Sensing Ion Channel 2 (ASIC2) contributes to mechanoelectrical transduction in baroreceptor neurons. Its expression in nodose sensory ganglia (NG) is decreased in association with development of hypertension in spontaneously hypertensive rats (SHR) (FASEB J, 21:A1407, 2007). Since NG neurons relay sensory signals from various visceral organs we sought to define more specifically the expression of ASIC2a in aortic baroreceptor nodose neurons (ABRNs) of SHR. We hypothesized that ASIC2a expression is reduced in ABRNs of SHR to account for the suppressed depolarizing potential responses to mechanical stimulation we observed earlier in SHR (FASEB J, 19:A607, 2005). ABRNs in NG were labeled with DiI injected into the aortic arch adventitia of SHR and WKY rats at 10 weeks of age. Two weeks later, both NG were removed and neurons were dissociated and cultured. Individual DiI labeled ABRNs and non-labeled neurons were selected by fluorescence microscopy for quantitative single cell RT-PCR. The results indicate first that DiI labeled ABRNs (n = 24) had a significant higher level of ASIC2 mRNA (2.99 ± 0.93) than non-DiI neurons (1.00 ± 0.97) (p < 0.05). Second, the ASIC2a mRNA level in DiI neurons relative to non-DiI labeled neurons from the same ganglia was significantly lower in SHR (1.97 ± 0.59, n = 12) than in WKY (5.91 ± 0.61, n = 12) (p < 0.05). The single cell RT-PCR results were confirmed by RT-PCR of pooled neurons (n = 10/grougp). We propose that the development of hypertension and impaired baroreceptor sensitivity in SHR are associated with significant reduction of ASIC2 expression (HL14388).
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