Influence of Parathyroidectomy and Calcium on Rat Renal Function

Parathyroid hormone (PTH) has multiple effects on water and electrolyte transport along the nephron. However, the influences of PTH and calcium on the urinary concentration ability are not fully understood. In this study, clearance and microperfusion studies were performed in thyroparathyroidectomized (TPTX) rats either supplemented (TPTX+Ca2+) or not with calcium added to the ingested food as CaCl2 (1.6 g/100 g). Acid-base data and renal functional parameters were measured in TPTX and TPTX+Ca2+ rats. Additional studies were performed in the isolated inner medullary collecting tubules of intact and TPTX rats to evaluate the osmotic permeability of this segment in the presence of 10–6M PTH added to the bath. In these experiments the possible influence of PTH on antidiuretic hormone induced changes of the osmotic permeability in TPTX and TPTX+Ca2+ rats was also investigated. In the TPTX+Ca+ group, the glomerular filtration rate increased significantly when compared to the TPTX group (6.04 ± 0.42 vs. 4.88 ± 0.20 ml·min–1·kg–1; p < 0.05), but the U/P inulin ratio remained lower than control values (30.8 ± 1.48 vs. 54.0 ± 3.5; p < 0.05), which suggests that normal levels of PTH are necessary to maintain the concentrating ability. In a group of TPTX rats, an acute infusion of PTH (0.5 µg·min–1·kg–1) significantly decreased the urinary flow and increased the renal plasma flow, results that agree with the vasomodulator action of this hormone on the renal vasculature. A significant increase in the fractional K+ excretion observed in the TPTX+Ca2+ group as compared with both control and TPTX, groups suggests that the excreted load of Ca2+ may interfere with tubular K+ handling in the absence of PTH. PTH (10–6M) added to the bath of the isolated inner medullary collecting tubules did not change the osmotic permeability, of intact, TPTX, and TPTX+Ca2+ rats. Furthermore, it did not modify the antidiuretic hormone induced changes in the osmotic permeability. These results suggest that this segment of the nephron is PTH insensitive as far as water and ion transport are concerned.

[1]  J. Chow,et al.  Role for parathyroid hormone in mechanical responsiveness of rat bone. , 1998, American journal of physiology. Endocrinology and metabolism.

[2]  E. Brown,et al.  Localization of the extracellular Ca(2+)-sensing receptor and PTH/PTHrP receptor in rat kidney. , 1996, The American journal of physiology.

[3]  S. Carney,et al.  Mechanism of lithium-induced polyuria in the rat. , 1996, Kidney international.

[4]  P. Welling Cross-talk and the role of KATP channels in the proximal tubule. , 1995, Kidney international.

[5]  S. Carney,et al.  Acute effect of parathyroid hormone on urine concentration in the rat. , 1995, Clinical science.

[6]  G. Giebisch,et al.  Role of Ca2+/CaMK II in Ca(2+)-induced K+ channel inhibition in rat CCD principal cell. , 1995, The American journal of physiology.

[7]  G. Segre,et al.  Parathyroid hormone induces sequential c-fos expression in bone cells in vivo: in situ localization of its receptor and c-fos messenger ribonucleic acids. , 1994, Endocrinology.

[8]  V. Briner,et al.  Parathyroid hormone inhibition of vasopressin-induced vascular smooth muscle contraction. , 1993, The American journal of physiology.

[9]  F. Z. Gil,et al.  Effects of parathyroid hormone and calcium and their interrelationship on urinary acidification in the rat. , 1992, Clinical science.

[10]  F. Z. Gil,et al.  Effect of aluminium on urinary acidification in the rat: influence of parathyroid hormone. , 1991, Clinical science.

[11]  A. Werner,et al.  Cellular mechanisms in proximal tubular reabsorption of inorganic phosphate. , 1991, The American journal of physiology.

[12]  E. Brown,et al.  Extracellular Ca2+ sensing, regulation of parathyroid cell function, and role of Ca2+ and other ions as extracellular (first) messengers. , 1991, Physiological reviews.

[13]  G. Malnic,et al.  Effects of parathyroid hormone on urinary acidification in the rat. , 1991, Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas.

[14]  M. G. Cogan,et al.  Effects of intracellular calcium on proximal bicarbonate absorption. , 1990, The American journal of physiology.

[15]  M. Paillard,et al.  Peptide hormone effects on urinary acidification and acid-base balance: PTH, ADH, and glucagon. , 1989, The American journal of physiology.

[16]  E. Windhager,et al.  Effect of peritubular [Ca] or ionomycin on hydrosmotic response of CCTs to ADH or cAMP. , 1988, The American journal of physiology.

[17]  S. Carney,et al.  Effect of parathyroid and antidiuretic hormone on water and calcium permeability in the rat collecting duct. , 1988, Mineral and electrolyte metabolism.

[18]  L. Palmer,et al.  Ca-activated K channels in apical membrane of mammalian CCT, and their role in K secretion. , 1987, The American journal of physiology.

[19]  S. Goldfarb,et al.  Mechanism of the polyuria of hypercalcemia. , 1984, American journal of nephrology.

[20]  F. Morel,et al.  Multiple hormonal control of adenylate cyclase in distal segments of the rat kidney. , 1982, Kidney international. Supplement.

[21]  E. Slatopolsky,et al.  Alterations in renal tubular water transport induced by parathyroid hormone: evidence for both antidiuretic hormone-mediated and independent effects. , 1982, The Journal of laboratory and clinical medicine.

[22]  F. Morel Sites of hormone action in the mammalian nephron. , 1981, The American journal of physiology.

[23]  G. Malnic,et al.  Effects of furosemide on urinary acidification during alterations of acid-base equilibrium in the rat , 1979 .

[24]  R. du Bois,et al.  Computation of the osmotic water permeability of perfused tubule segments. , 1976, Kidney international.

[25]  J. Kokko,et al.  Permeability of medullary nephron segments to urea and water: Effect of vasopressin. , 1974, Kidney international.

[26]  H. W. Smith,et al.  THE RENAL CLEARANCES OF SUBSTITUTED HIPPURIC ACID DERIVATIVES AND OTHER AROMATIC ACIDS IN DOG AND MAN. , 1945, The Journal of clinical investigation.