Alkalosis and renal p-aminohippurate transport in dog: relation to lactate uptake

¹ Department of Physiology, University of Rochester School of Medicine and Dentistry, Rochester, New York

Does alkalosis per se or does the associated lactacidemia determine the rate of PAH or Diodrast transport? How is net renal uptake of lactate related to Tm_pah? Tm_pah, renal extraction of I¹³¹-Diodrast (E_diod) and net renal lactate uptake were studied in anesthetized (pentobarbital) dogs. In clearance experiments, Tm_pah is elevated (facilitated) by isohydric increases in blood [lactate]; alkalosis has no further effect on the facilitated (by lactate) Tm_pah. In contrast to the effects of alkalosis on Tm_pah, no rise in E_diod occurs during alkalosis. However, when E_diod is depressed by [PAH] sufficiently high to achieve Tm_pah, a rise in blood lactate does enhance E_diod. Thus, lactate enhances E_diod when the transport mechanism common to it and PAH is saturated. Net renal uptake of endogenous lactate is decreased during alkalosis; no net renal production of lactate has been observed. Therefore, the increases in Tm_pah and E_diod are not related to a rise in net renal uptake of lactate but are probably more related to the blood [lactate]. It is postulated that Tm_pah and E_diod may be more dependent on the metabolic mixture presented to the kidney, and thus on extrarenal metabolism, than on intrarenal distribution of blood flow or rate of renal blood flow.

Key Words: lactacidemia • Diodrast transport • acid-base • tubular secretion • tubular function • lactate metabolism • renal extraction of Diodrast metabolism • renal metabolism • renal blood flow

Submitted on February 18, 1963