title: Effects of calcitonin on the renal concentrating mechanism.
abstract: The effects of salmon calcitonin on the renal concentrating mechanism were investigated in homozygous DI Brattleboro rats. The levels of peptide hormones believed to produce the same physiological responses as antidiuretic hormone on the thick ascending limb (glucagon, parathyroid hormone, and calcitonin) and the cortical collecting ducts (calcitonin) were reduced by acute thyroparathyroidectomy and somatostatin administration. In these hormone-deprived animals, the corticomedullary concentration gradient was almost abolished; the (F/P)osmol at the tip of the juxtamedullary nephrons was 1.19 +/- 0.05. Calcitonin administration restored the gradient [(F/P)osmol = 1.85 +/- 0.14] and simultaneously absolute and fractional water excretion fell significantly despite the concomitant rise in the glomerular filtration rate. It is concluded that 1) in the hormone-deprived animal, calcitonin administration consistently enhances the corticomedullary concentration gradient, and 2) the effects of hormone deprivation and calcitonin administration on the urinary concentrating mechanism are compatible with direct stimulation by calcitonin of electrolyte reabsorption along the thick ascending limb and/or of the water permeability of the cortical collecting ducts.
mesh_terms: D000818:Animals; D002116:Calcitonin / Q000494:pharmacology*; D003919:Diabetes Insipidus / Q000503:physiopathology*; D004573:Electrolytes / Q000378:metabolism; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology*; D008297:Male; D010280:Parathyroid Glands / Q000503:physiopathology; D051381:Rats; D011910:Rats, Brattleboro; D012474:Salmon; D013965:Thyroidectomy
chemical_list: D004573:Electrolytes; D002116:Calcitonin