Renal Ca²⁺ wasting, hyperabsorption, and reduced bone thickness in mice lacking TRPV5
J. Clin. Invest. Joost G.J. Hoenderop, et al. 112:1906 doi:10.1172/JCI19826 [Go to this article.]

Figure 3
Renal and duodenal Ca²⁺ transport assays. (a) Fractional Ca²⁺ delivery to the LPT, to the distal convolution (DC), and to urine (U), measured by micropuncture experiments in TRPV5^+/+ and TRPV5^–/– mice. (b) Relation between K⁺ concentration in tubular fluid of the distal convolution and fractional Ca²⁺ delivery to these sites. Low K⁺ concentrations indicate early puncture sites and high K⁺ concentrations late aspects of distal convolution (2). Values are means ± SEM of six mice per group for urine data and of 19–24 nephrons per group for LPT and distal convolution collections. *P < 0.05 versus TRPV5^+/+. (c) Changes in serum Ca²⁺ (ΔμM) within 10 minutes of administration of ⁴⁵Ca²⁺ by oral gavage in TRPV5^+/+ and TRPV5^–/– mice (n = 12). Data are averaged values ± SEM from mice 8 weeks old. *P < 0.05, significant difference from wild-type mice. (d) Expression of calbindin-D_28K and NCX1 mRNA in kidney cortexes of TRPV5^+/+ and TRPV5^–/– mice (n = 9), assessed by quantitative real-time PCR analysis and calculated as a ratio to HPRT RNA. (e) Expression of TRPV6 and calbindin-D_9K mRNA in duodenums of TRPV5^+/+ and TRPV5^–/– mice, assessed by quantitative real-time PCR analysis and calculated as a ratio to the HPRT RNA (n = 9).