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Aldosterone and ENaC: From Genetics to Physiology

Extracellular Ca²⁺ regulates the stimulation of Na⁺ transport in A6 renal epithelia

¹Laboratory of Physiology, Biomedical Research Institute, Limburgs Universitair Centrum, Universitaire Campus, B-3590 Diepenbeek; and ²Laboratory of Physiology, Katholieke Universiteit Leuven, Campus Gasthuisberg O/N, B-3000 Leuven, Belgium

Submitted 3 November 2003 ; accepted in final form 8 June 2004

We investigated the involvement of intracellular and extracellular Ca²⁺ in the stimulation of Na⁺ transport during hyposmotic treatment of A6 renal epithelia. A sudden osmotic decrease elicits a biphasic stimulation of Na⁺ transport, recorded as increase in amiloride-sensitive short-circuit current (I_sc) from 3.4 ± 0.4 to 24.0 ± 1.3 µA/cm² (n = 6). Changes in intracellular Ca²⁺ concentration ([Ca²⁺]_i) were prevented by blocking basolateral Ca²⁺ entry with Mg²⁺ and emptying the intracellular Ca²⁺ stores before the hyposmotic challenge. This treatment did not noticeably affect the hypotonicity-induced stimulation of I_sc. However, the absence of extracellular Ca²⁺ severely attenuated Na⁺ transport stimulation by the hyposmotic shock, and I_sc merely increased from 2.2 ± 0.3 to 4.8 ± 0.7 µA/cm². Interestingly, several agonists of the Ca²⁺-sensing receptor, Mg²⁺ (2 mM), Gd³⁺ (0.1 mM), neomycin (0.1 mM), and spermine (1 mM) were able to substitute for extracellular Ca²⁺. When added to the basolateral solution, these agents restored the stimulatory effect of the hyposmotic solutions on I_sc in the absence of extracellular Ca²⁺ to levels that were comparable to control conditions. None of the above-mentioned agonists induced a change in [Ca²⁺]_i. Quinacrine, an inhibitor of PLA₂, overruled the effect of the agonists on Na⁺ transport. In conclusion, we suggest that a Ca²⁺-sensing receptor in A6 epithelia mediates the stimulation of Na⁺ transport without the interference of changes in [Ca²⁺]_i.

intracellular calcium concentration; magnesium; phospholipase A₂; osmolality

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