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CHRONIC CALCITONIN ADMINISTRATION AND RENAL CALCIUM TRANSPORT IN THE RAT
Author(s) -
Carney Shane L,
Thompson Lisa
Publication year - 1998
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1998.t01-12-.x
Subject(s) - parathyroid hormone , calcitonin , medicine , endocrinology , excretion , bolus (digestion) , renal physiology , hormone , renal function , chemistry , calcium , kidney
1. While calcitonin (CT) has now been clearly demonstrated to be a renal Ca 2+ ‐conserving hormone and may share similar transport mechanisms with parathyroid hormone (PTH), the effect of prolonged CT exposure on renal Ca 2+ transport has not been evaluated. 2. Consequently, a submaximal and maximal Ca 2+ ‐conserving concentration of human CT was infused into groups of anaesthetized acutely thyroparathyroidectomized rats that had been treated with twice daily subcutaneous human (h) CT at a low or high dose or vehicle for 12 days. 3. The maximal hCT infusion (10 μg bolus and per hour) produced a marked inhibitory effect on renal Ca 2+ excretion in vehicle‐treated rats, with the fractional excretion rate of Ca 2+ being reduced from 4.49±0.31 to 1.39±0.23% ( P <0.001). However, in rats pretreated with high concentrations of hormone (0.25 μg hCT) twice daily for 12 days, marked Ca 2+ conservation was measured (fractional excretion 1.09±0.18%), which was not altered by the additional intravenous administration of maximal hCT. 4. Renal Mg 2+ transport was similarly altered by hCT administration, without any evidence that prolonged CT inhibited renal Mg 2+ transport. The increase in glomerular filtration rate caused by hCT also appeared to persist with repeated hormone administration. The fractional excretion of Na + and PO 4 was significantly increased by high‐ but not low‐dose hCT treatment and was not altered by the addition of a maximal hormone dose at day 12. 5. The present study failed to demonstrate any down‐ regulation of the response to prolonged hCT administration when renal Ca 2+ and Mg 2+ transport was measured. If renal escape does occur with CT, as has been suggested but not proven with PTH, other mechanisms, such as hormone production or release, may be responsible.