Differential Expression of Acid‐Sensing Ion Channel (ASIC) Subunits in Rat Carotid Body

Abstract

Attempts to elucidate the molecular basis and location of mechano- and chemosensors are ongoing in several laboratories. Our work suggests that the DEG/ENaC channels and particularly the ASIC subunits may play an important role in cardiovascular sensory signaling. Specifically, we recently observed that disruption of ASIC2 in mice suppresses the carotid occlusion baroreflex (mechanosensory), whereas disruption of ASIC1 and 3 may suppress a carotid chemoreceptor reflex (chemosensory). In this study, we carried out quantitative PCR on the carotid body where glomus cells are the major site of peripheral chemoreceptor sensory transduction. Total RNA was obtained from the carotid bodies of five Sprague-Dawley rats (9 weeks of age). The results shown in the figure indicate a relatively high expression of ASIC3 and 1b and low or absent expression of ASIC2a, 2b, 1a. Of interest also is the higher expression of the large conductance Ca2+ activated K+ channel (BK), a channel known to mediate hypoxic responses and the low expression of TRPC1, a putative mechanosensitive ion channel. It appears that the selective expression of the mRNA of these channels in the carotid body parallels the functional responses, i.e. differentially higher expression of primarily chemosensitive channels (ASIC1 and 3, BK) as chemoreceptors in the carotid body in contrast to the lower expression of the putative mechanosensitive subunits or channels (ASIC2 and TRPC1). This conclusion assumes protein expression that reflects the quantitative mRNA levels. (HL14388) Figure 1Open in figure viewerPowerPoint