Isoproterenol and nucleotide induced stimulation of Ca2+ uptake by microsomal fractions from kidney and isolated glomeruli.

Renal cortical microsomal vesicles possess an ATP-dependent Ca²⁺ uptake system which is two to three times more active in accumulating Ca²⁺ than are the microsomes prepared from the outer medulla or papilla of the cat kidney. The microsomal Ca²⁺ uptake system was unaffected by sodium azide, and electron microscopy confirmed the absence of intact mitochondria. Ca²⁺ accumulating activity was significantly increased by 13 per cent in cortical microsomes prepared from kidneys which had been perfused with isoproterenol (2 × 10^?7 M), whereas medullary or papillary microsomal Ca²⁺ accumulation was unaffected. Perfusate containing a higher isoproterenol concentration (2 × 10^?6 M) stimulated cortical as well as papillary microsomal Ca²⁺ uptake by 13 and 31 per cent respectively, but had no effect on medullary microsomal Ca²⁺ accumulation. A lower isoproterenol concentration (2 × 10^?8 M) did not change the Ca²⁺ uptake activity of microsomes isolated from either region of the cat kidney. The isoproterenol concentrations (2 × 10^?7 and 2 × 10^?6 M) which activated Ca²⁺ uptake in microsomes produced graded increases in renin secretion, whereas 2 × 10^?8 M isoproterenol was relatively inactive in eliciting renin secretion. Renal cortical tissue exposed to cyclic AMP (cAMP) and 5'-AMP during subcellular fractionation showed significant increases in microsomal Ca²⁺ uptake. However, microsomes exposed to cAMP or 5'-AMP in the Ca²⁺ uptake medium were not stimulated. Isoproterenol also activated Ca²⁺ uptake by microsomes prepared from isolated glomeruli, and this stimulation was blocked by propranolol. We conclude that the cat renal cortex possesses specific receptors for isoproterenol which activate Ca²⁺ transport through a nucleotide mediated mechanism.