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.
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