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Intrarenal Insulin Replacement Prevents Glucose‐induced Natriuresis in Conscious Rats
Author(s) -
Irsik Debra L.,
Washington Ashley R.,
Alaisami Rabei,
Brands Michael W.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1027.3
Subject(s) - medicine , endocrinology , insulin , natriuresis , postprandial , hyperinsulinemia , diuresis , excretion , kidney , insulin resistance
It has been shown that insulin can alter sodium reabsorption acutely, but its role in the normal physiology of sodium balance has not been elucidated. Previously we reported that the normal, postprandial rise in insulin is necessary to prevent excess salt and water loss after a meal. Rats that were unable to increase insulin in response to an acute glucose load also exhibited increased diuresis and natriuresis. In this study we tested the hypothesis that insulin prevented acute glucose‐induced natriuresis by acting directly through a renal mechanism. Rats were instrumented chronically with artery and vein catheters and an innovative renal artery catheter developed in our laboratory. They were housed in metabolic cages and connected to Instech swivels. Two groups of rats had insulin clamped chronically at normal levels by administering streptozotocin and then infusing insulin iv. 24 hr/day to restore blood glucose levels to normal. In one clamped group, insulin was infused in the renal artery catheter during the glucose challenge (irI), while the other group received intrarenal vehicle (irV). In Control rats (C) the glucose bolus increased plasma insulin significantly, from 19 to 107 uU/ml. The glucose challenge caused no increase in plasma insulin from baseline in either of the clamped groups. During the 4 hrs following the glucose infusion, urinary sodium excretion averaged 0.11±0.02 mmol in C rats and was ~ 3‐fold greater in the clamped irV rats (0.36±0.07 mmol, n=6) similar to our previous report. However, intrarenal insulin replacement completely prevented this, with sodium excretion averaging 0.11±0.03 mmol (n=6) in the irI rats. The urine volume response was similar. These data support our previous results suggesting that physiologic, meal‐induced increases in plasma insulin are a major component of normal sodium homeostasis. Moreover, they suggest that this occurs by direct renal actions of insulin. Support or Funding Information HL056259Intrarenal insulin (irI) replacement abolished the increased Na + excretion evident in intrarenal vehicle (irV) rats following a glucose bolus.