title: Effects of insulin on Na and K transporters in the rat CCD.
abstract: We tested the effects of insulin (2 nM, 30-60 min) on principal cells of isolated split-open rat cortical collecting ducts (CCD) using whole-cell current measurements. Insulin addition to the superfusate of the tubules enhanced Na pump (ouabain-sensitive) current from 18 ± 3 to 31 ± 3 pA/cell in control and from 74 ± 9 to 126 ± 11 pA/cell in high K-fed animals. It also more than doubled ROMK (tertiapin-Q-sensitive) K(+) currents in control CCD from 320 ± 40 to 700 ± 80 pA/cell, although it did not affect this current in tubules from K-loaded rats. Insulin did not induce the appearance of amiloride-sensitive Na(+) current in control animals, while in high K-fed animals the currents were similar in the presence (140 ± 30) and the absence (180 ± 70 pA/cell) of insulin. Intraperitoneal injection of insulin plus hypertonic dextrose decreased Na excretion, as previously reported. However, injection of dextrose alone, or the nonmetabolized sugar mannose, had similar effects, suggesting that they were largely the result of vascular volume depletion rather than specific actions of the hormone. In summary, we find no evidence for acute upregulation of the epithelial Na channel (ENaC) by physiological concentrations of insulin in the mammalian CCD. However, the hormone does activate both the Na/K pump and apical K(+) channels and could, under some conditions, enhance renal K(+) secretion.
authors.affiliation: Dept. of Physiology and Biophysics, Weill Medical College of Cornell Univ., 1300 York Ave., New York, NY 10065, USA.
authors.forename: Gustavo
authors.initials: G
authors.lastname: Frindt
authors.forename: Lawrence G
authors.initials: LG
authors.lastname: Palmer
mesh_terms: D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D004231:Diuresis / Q000187:drug effects / Q000502:physiology; D053503:Epithelial Sodium Channels / Q000502:physiology*; D005260:Female; D005950:Glucose Solution, Hypertonic / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000378:metabolism / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism* / Q000494:pharmacology; D007685:Kidney Tubules, Collecting / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008358:Mannose / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000493:pharmacokinetics; D024661:Potassium Channels, Inwardly Rectifying / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000493:pharmacokinetics; D026941:Sodium Channel Blockers / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology*
chemical_list: D053503:Epithelial Sodium Channels; D005950:Glucose Solution, Hypertonic; D007004:Hypoglycemic Agents; D007328:Insulin; C510692:Kcnj1 protein, rat; D024661:Potassium Channels, Inwardly Rectifying; D026941:Sodium Channel Blockers; D000584:Amiloride; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D008358:Mannose; D011188:Potassium