Effects of Calcium Intake and Renal Function on Plasma Immunoreactive Parathyroid Hormone Levels in Rats
W. Grubenmann, U. Binswanger, W. Hunziker, Jan A. Fischer
Abstract
W. Grubenmann, U. Binswanger, W. Hunziker, Jan A. Fischer
Abstract
Parathyroid hormone (PTH) was estimated with a radioimmunoassay system which recognised presumably intact rat PTH as the major circulating species. A low calcium diet was found to increase PTH levels in shamoperated and in 5/6-nephrectomized rats. In rats with normal renal function, a low calcium intake resulted in a significant mean increase of PTH levels, while changes in plasma calcium, magnesium, phosphate and protein concentrations were not detectable; at the same time the ability of the duodenum to transport calcium in vitro was accelerated. In 5/6-nephrectomized rats, on the other hand, PTH levels were dramatically increased in hypocalcemic animals kept on a calcium deficient diet, while intestinal calcium transport was impaired. These data support the concept that hypocalcemia is the most important stimulus for increased PTH release. Since increased PTH levels can be seen in situations where increased 1,25-dihydroxy-cholecalciferol synthesis is known to occur, it appears that this metabolite cannot inhibit a rise in plasma PTH levels.
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Parathyroid hormone (PTH) was estimated with a radioimmunoassay system which recognised presumably intact rat PTH as the major circulating species. A low calcium diet was found to increase PTH levels in shamoperated and in 5/6-nephrectomized rats. In rats with normal renal function, a low calcium intake resulted in a significant mean increase of PTH levels, while changes in plasma calcium, magnesium, phosphate and protein concentrations were not detectable; at the same time the ability of the duodenum to transport calcium in vitro was accelerated. In 5/6-nephrectomized rats, on the other hand, PTH levels were dramatically increased in hypocalcemic animals kept on a calcium deficient diet, while intestinal calcium transport was impaired. These data support the concept that hypocalcemia is the most important stimulus for increased PTH release. Since increased PTH levels can be seen in situations where increased 1,25-dihydroxy-cholecalciferol synthesis is known to occur, it appears that this metabolite cannot inhibit a rise in plasma PTH levels.
Key concepts: Endocrinology, Internal medicine, Parathyroid hormone, Calcium, Chemistry, Radioimmunoassay, Calcium metabolism, Medicine