Key result
Insulin produced a dose-dependent reduction of renin release in isolated perfused rat kidneys, a process that requires extracellular calcium influx.
Why the study?
Does insulin modulate renin secretion in an isolated perfused rat kidney model, and is this dependent on extracellular calcium?
Does insulin modulate renin secretion in an isolated perfused rat kidney model, and is this dependent on extracellular calcium?
Insulin suppresses renin secretion in a dose-dependent manner that requires the influx of extracellular calcium.
No immediate clinical implications from rat kidney data; leaves open insulin-renin effects in humans.
The isolated perfused rat kidney was used to examine the effect of insulin on renin release (RR). Insulin produced a dose-dependent reduction of RR when added to the perfusate at concentrations between 10 and 1,000 microU/ml. When kidneys were perfused with a calcium-free perfusate, RR increased nearly fivefold. Insulin (1,000 microU/ml) not only failed to suppress RR in calcium-free perfusions but stimulated it. The addition of verapamil (10(-5) M) to the perfusate likewise prevented the insulin inhibition of RR. Perfusion without potassium reduced RR to one-third of control values. The addition of insulin to kidneys perfused without potassium further suppresses RR. We conclude that at concentrations similar to those found in plasma, insulin modulates renin secretion. This process requires the influx of calcium possibly through insulin receptor-operated channels.
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Cohen et al. (1983) studied this question. Insulin vs. Control perfusate was evaluated on Renin release. Insulin produced a dose-dependent reduction of renin release in isolated perfused rat kidneys, a process that requires extracellular calcium influx.
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