Calcium and sodium transport by the distal convoluted tubule of the rat

Abstract

Calcium and sodium transport were studied in the distal convoluted tubule of the rat by micropuncture and microperfusion techniques. The animals received either control infusions, 0.9% saline at 0.02 ml/min, or chlorothiazide (CTZ), 0.5 mg/min-kg. In free-flow micropuncture, distal calcium reabsorption occurred against an electrochemical gradient; it was 9% of the filtered load in the controls and 13.8% in the CTZ-treated rats. The drug dissociated calcium and sodium transport along the distal tubule. Absolute reabsorptive rates for calcium and sodium, measured in pump perfusion experiments, were proportional to the distal loads. CTZ, acting from the lumen, enhanced net calcium (P less than 0.01) and reduced net sodium (P less than 0.01) reabsorption. In stationary microperfusion experiments, sodium backflux produced rapid establishment of a steady-state concentration of 50 mM. In contrast, net backflux of calcium was negligible. With calcium in the luminal perfusion fluid, there was a concentration-dependent reabsorptive efflux which was not saturated at a luminal calcium concentration of 9.5 mM and which was enhanced by CTZ.

The epithelial calcium channels TRPV5 and TRPV6: regulation and implications for disease

“…Moreover, these drugs concomitantly increase Ca 2+ reabsorption (Costanzo and Windhager 1978). This hypocalciuric effect provides therapeutic opportunities in for instance idiopathic hypercalciuria and nephrolithiasis.…”

“…Furthermore, thiazides have been shown to increase bone mineral density and decrease fracture risk, spiking interest in the favorable long-term effects of these diuretics in counteracting osteoporosis (Reid et al 2000). The decreased Ca 2+ excretion during chronic thiazide administration has been explained by ECV contraction enhancing the paracellular Ca 2+ reabsorption in proximal tubules as well as a direct stimulation of active Ca 2+ reabsorption in the DCT (Costanzo et al 1978;Ellison 2000;Friedman 1998;Friedman and Bushinsky 1999;Loffing et al 2001;Nijenhuis et al 2003).…”

Active Ca2+ reabsorption in the connecting tubule

“…In these segments, Ca 2+ reabsorption is not specifically regulated and depends on gradients established by NaCl and water reabsorption [61]. The final regulation of Ca 2+ excretion, according to physiological needs, appears to occur primarily in two segments of the distal part of the nephron, namely in the late part of the distal convoluted tubule (known as DCT2) and the connecting tubule (CNT; Table 1) [16]. uniform population of principal cells, whereas the CNT contains both principal and two types of intercalated cells [3,16,43,56].…”

Chronic Inhibition of Renal Outer Medullary Potassium Channel Not Only Prevented but Also Reversed Development of Hypertension and End-Organ Damage in Dahl Salt-Sensitive Rats

“…In our studies, the high dose of ROMKi B caused significant urinary loss of Ca 2+ ; in contrast, HCTZ induces hypocalciuria that is suggested to result from enhancement of passive Ca 2+ reabsorption in proximal tubules 21 or stimulation of active Ca 2+ reabsorption in distal convoluted tubules. 22 Because of the concern for the potential effect of increased Ca 2+ loss on bones, we measured femur and lumbar spine BMD by bone dual-energy X-ray absorptiometry, and interestingly, BMD was increased in the prophylactic study and was unaffected in the therapeutic study in ROMKi B 3 mg·kg −1 ·d −1 and 10 mg·kg −1 ·d −1 -treated groups. We hypothesized that ROMK inhibition could improve regional hemodynamics and organ function by decreasing systemic blood pressure; thereby, Ca 2+ reabsorption from the digestive system could be enhanced, and ultimately BMD could be unaffected or even improved.…”