Nifedipine Improves Kidney Function after 24h Cold Storage in a High Sodium UW Solution

Abstract

In a previous study using the isolated perfused rat kidney model (IPK), we have shown that a high Na — low K (Na=125, K = 30 mmol/L) version of Belzer UW cold-storage solution (Na-UW) seemed to be less deleterious than the standard high K — low Na UW (K-UW) (K= 125, Na=30 mmol/L). Intracellular-type cold-storage solutions have been shown to induce vasoconstriction when flushed into the organ. On the other hand, calcium channel blockers (CCB) have been shown to improve the ischemia — reperfusion syndrome. In this study, we used the IPK model to assess the effects of the CCB nifedipine on the vasoconstriction induced by K-UW and on the function of the IPK after 24h cold-storage. Infusion of K-UW into the IPK at increasing rates induces a dose-dependent increase in perfusion pressure, whereas Na-UW infusion had no effect on renal vascular resistances (RVR). Infusion of nifedipine (10⁻⁴ mol/L) with K-UW prevents the increase in perfusion pressure. In another series of experiments, K-UW or Na-UW cooled at +4°C was flushed into the kidney without (−) or with nifedipine (+) (10⁻⁴ mol/L). After 24h cold storage at +4°C in the same solution with or without nifedipine, kidneys were reperfused at 37°C with Krebs—Henseleit—bicarbonate—albumin with or without nifedipine (10⁻⁶ mol/L). GFR (inulin clearance, µl/min/g) and fractional Na reabsorption (FRNa %) were measured during 60 min after normothermic reperfusion and were compared to values obtained in a control group in which renal function was measured immediately after the kidneys had been harvested. Results were as follows (mean ± SEM):

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