Acute effect of calcium and insulin on hyperfiltration of early diabetes

1987 ◽  
Vol 252 (1) ◽  
pp. E13-E20 ◽  
Author(s):  
N. Bank ◽  
M. A. Lahorra ◽  
H. S. Aynedjian

We examined the effect of calcium administration on renal hyperfiltration in streptozotocin-treated diabetic rats. Rats were studied 7–10 days after streptozotocin injection. Intrarenal infusion of CaSO4 in Ringer's solution had no effect on the hyperfiltration of the diabetic kidney. Infusion of insulin in a dose that did not effect hyperglycemia also had no effect on the hyperfiltration. However, when insulin and calcium were infused together, a rapid decrease in glomerular filtration rate, single-nephron filtration rate, glomerular hydraulic pressure, and renal plasma flow occurred. The contralateral control kidney was unaffected. Verapamil infusion had no significant effect in untreated diabetic rats, but immediately reversed the vasoconstriction induced by insulin plus calcium. Similar intrarenal insulin and calcium infusions had no effect in euvolemic or chronically salt-loaded nondiabetic rats. The observations indicate that renal vascular cells (probably preglomerular) are hyperresponsive to calcium in early insulin-dependent diabetes mellitus and that this response requires insulin. We suggest that decreased renal vascular tone in early insulin-dependent diabetes mellitus may be due in part to defective transmembrane calcium flux across vascular smooth muscle cells. Insulin appears to be required for calcium entry or mobilization, to initiate renal vascular smooth muscle contraction in diabetes.

1997 ◽  
Vol 8 (5) ◽  
pp. 749-755 ◽  
Author(s):  
J A Miller

Increased GFR and decreased renal vascular resistance are common renal hemodynamic changes in persons with early, uncomplicated, insulin-dependent diabetes mellitus. It has been hypothesized that excess total-body sodium in patients with diabetes contributes to the renal vasodilation, possibly by suppressing vasoconstricting neurohormonal systems. This study was undertaken to examine whether sodium restriction could normalize these renal abnormalities. Subjects were 12 male patients with uncomplicated insulin-dependent diabetes mellitus (duration, < 5 yr). Results were compared with those of an age- and gender-matched control group. All subjects received either a high-sodium diet (200 mmol/day) or a sodium-restricted diet (20 mmol/day) for 7 days, according to a randomized crossover protocol. GFR and RPF were measured using inulin and para-aminohippurate clearance techniques, respectively. Subjects with diabetes were maintained euglycemic during the clearance measurements. GFR was significantly higher in the diabetic group than in the control group with sodium repletion (124 +/- 4 versus 107 +/- 8 mL/min/1.73 m2; P = 0.03), and renal vascular resistance was significantly reduced (94 +/- 6 versus 107 +/- 17 mm Hg/L/min; P = 0.05). In response to sodium restriction, the hematocrit increased significantly in both groups, as did PRA and aldosterone, although responses in the diabetic group were somewhat blunted, indicating persisting volume expansion. Despite this humoral activation, sodium restriction had little effect on renal hemodynamic function in control subjects. In the diabetic subjects, this maneuver appeared to exacerbate the underlying renal abnormalities, with the GFR increasing to 131 +/- 4 mL/min/1.73 m2 (P = 0.05) and the renal vascular resistance declining to 73 +/- 5 mm Hg/L/min (P = 0.001). These data indicate that, rather than correcting renal hyperperfusion, sodium restriction exacerbates these characteristic abnormalities, suggesting that mechanisms other than suppression of vasoconstrictor activity are operative in the underlying renal hemodynamic abnormalities of early, uncomplicated, insulin-dependent diabetes mellitus.


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