THE ROLE OF CYTOSOLIC CA2-VITRO PERFUSED RECTAL GLAND TUBULES OF SQUALUS-ACANTHIAS( IN THE SECRETION OF NACL IN ISOLATED IN)

In many exocrine glands cytosolic Ca2+ ([Ca2+](i)) plays a pivotal rol e in stimulation-secretion coupling. In the rectal gland of the dogfis h Squalus acanthias this appears not to be the case and it is believed that secretion is mainly controlled by the Cl- conductance of the lum inal membrane. We have examined this question in a study of isolated i n vitro perfused rectal gland tubules (RGT). Three types of measuremen ts were performed: (1) measurements of [Ca2+](i) by the fura-2 techniq ue; (2) measurements of transepithelial electrical parameters, i.e. tr ansepithelial voltage (V-te), transepithelial resistance (R-te), the e quivalent short-circuit current (I-sc) and the voltage across the baso lateral membrane (V-bl), and (3) whole-cell patch-clamp measurements o f cellular voltage (V-m), conductance (G(m)) and membrane capacitance (C-m). The data indicates that carbachol (CCH) increases [Ca2+](i) by increasing store release and Ca2+ influx. Other agonists, producing cy tosolic cAMP, also increased [Ca2+] by enhancing Ca2+ influx. CCH hype rpolarized these cells and enhanced G(m) significantly. The effect of CCH on V-te and i(sc) was most marked under control conditions and dis appeared in RGT otherwise stimulated by agonists that lead to cAMP pro duction. It is concluded that [Ca2+](i) plays a major role in the stim ulation of NaCl secretion in RGT by enhancing the basolateral K+ condu ctance. cAMP-producing agonists enhance [Ca2+](i) by increased Ca2+ in flux. CCH releases Ca2+ from respective stores. CCH, unlike the cAMP-p roducing agonists, only increases basolateral K+ conductance. It modul ates secretion especially under conditions in which the cAMP pathway i s not fully activated.