Metabolic support of collecting duct transport

Abstract

The present studies address the metabolic processes that support the reabsorption of sodium and the secretion of bicarbonate in the interspersed but distinct principal and intercalated cells of the cortical collecting duct (CCD). In microperfused rabbit CCD, sodium reabsorption was measured by lumen-to-bath 22Na flux, and bicarbonate transport was assayed by microcalorimetry. Flux measurements were made before and after metabolic substrate changes or application of metabolic inhibitors. Both sodium reabsorption and bicarbonate secretion were dependent on oxidative metabolism (inhibited by antimycin A) and appeared to have no special dependence on glycolysis or the hexose-monophosphate shunt pathways. Endogenous substrates (in the absence of exogenous metabolic substrates) supported a small component of sodium transport; in contrast, bicarbonate reabsorption in the outer medullary collecting duct, which was studied for comparison, was fully supported by endogenous substrates. In the CCD, sodium reabsorption was supported best by a mixture of basolateral metabolic substrates (glucose and acetate, as a fatty acid), whereas bicarbonate secretion was fully supported by either glucose or acetate. Alanine, as a representative amino acid, was not an effective metabolic substrate. Another contrasting feature of the two transport processes was that bicarbonate secretion, and not sodium transport, was supported to some extent by luminal glucose. In sum, principal cells and intercalated cells differ not only in their morphology and function, but also in their metabolism.