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Effects of osmotic changes on the chemoreceptor cell of rat carotid body

Zoltán Molnár, Gábor L. Pethe o'', Csaba Fülöp and András Spät

The carotid body plays a crucial role in cardiorespiratory regulation. In the present study we investigated the effect of osmotic changes on cytoplasmic calcium concentration ([Ca²⁺]_c) and pH (pH_i) of isolated chemoreceptor cells of the rat carotid body. In CO₂/HCO₃^--buffered medium, reduction of osmolality from the control level of 300 mosmol kg^-1 to 250-285 mosmol kg^-1 resulted in a rise in [Ca²⁺]_c, as measured with Indo-1, whereas elevation of osmolality to 350 mosmol kg^-1 had no effect. The Ca²⁺ response required extracellular Ca²⁺ and was reduced by application of the L-type Ca²⁺ channel antagonist nifedipine (10 µM). The hyposmosis-induced Ca²⁺ response could be prevented by application of niflumic acid (300 µM), an inhibitor of the swelling-activated Cl^- channel. In whole-cell patch-clamp experiments niflumic acid abolished the swelling-activated Cl^- current but only slightly depressed the Ca²⁺ current. The inhibition of Ca²⁺ current by niflumic acid does not account for its action in preventing of hyposmosis-induced Ca²⁺ response, which seems to be initiated by Cl^--mediated depolarisation. Withdrawal of CO₂/HCO₃^- also prevented the Ca²⁺ response. Reduction of the osmotic concentration by 50 mosmol kg^-1 induced a small but sustained decrease in pH_i, while elevation by 50 mosmol kg^-1 had an inverse effect, as measured fluorimetrically with carboxy SNARF-1. Our conclusion is that in the rat chemoreceptor cell the activation of Cl^- channels, e.g. by hyposmotic challenge, induces depolarisation, which, in turn, activates voltage-gated Ca²⁺ channels.

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