Renal interstitial Ca²⁺

Renal interstitial fluid Ca²⁺ concentration ([Ca²⁺](isf)) was measured in anesthetized Wistar rats by using in situ microdialysis. During perfusion of 20 cm of the proximal small intestine with Ca²⁺-free buffer, renal [Ca²⁺](isf) was 1.63 ± 0.19 mmol/l in the cortex (n = 6) and 1.93 ± 0.12 mmol/l in the medulla (n = 5, P = 0.223). When Ca²⁺ in the intestinal lumen was increased to 3 mmol/l, no change was seen in total or ionized serum Ca²⁺ (S(Ca)), urinary Ca²⁺ excretion (U(Ca)), or Ca²⁺ in a microdialysate of the kidney cortex. Increasing intestinal Ca²⁺ further, to 6 mmol/l, was without effect on S(Ca) but significantly increased U(Ca) by 38% and microdialysate Ca²⁺ by 36% (1.25 ± 0.0.09 vs. 1.70 ± 0.14 mmol/l, n = 4, P < 0.05). Intravenous infusion of 28 ng · kg^-1 · min^-1 of parathyroid hormone for I h during perfusion of the intestinal lumen with 1 mmol/Ca²⁺caused a 7-10% rise in S(Ca), a 40% fall in U(Ca), and a 32% increase in microdialysate Ca²⁺ (1.32 ± 0.13 vs. 1.74 ± 0.13 mmol/1, n = 6, P < 0.05). Interlobar arteries with a mean diameter of 120 μm were studied by using a wire myograph to determine whether changes in extracellular Ca²⁺ affect muscle tone. When precontracted with 5 μmol/l serotonin, the arteries relaxed in response to cumulative addition of Ca²⁺ (1-5 mmol/l) with an ED₅₀ value for Ca²⁺ of 3.30 ± 0.08 mmol/l, n = 3. These data demonstrate that [Ca²⁺](isf) changes dynamically during manipulation of whole-animal Ca²⁺ homeostasis and that intrarenal arteries relax in response to extracellular Ca²⁺ varied over the range measured in vivo.