ABSTRACT
The failure to respond normally to parathyroid hormone (PTH) administration has been reported in patients with severe hypomagnesemia. A patient with hypoparathyroidism and a markedly decreased serum concentration of magnesium (0.7 mEq/liter), but a normal red blood cell magnesium level, is described who increased serum calcium concentration and decreased per cent renal tubular reabsorption of phosphate when parathyroid extract was given. It is suggested that PTH responsiveness in hypomagnesemic patients may, at least in part, be dependent upon the adequacy of intracellular magnesium stores. This interpretation is supported by the normal cellular (red blood cell) magnesium concentrations observed in this patient and in comparable studies in which PTH responsiveness in the presence of hypomagnesemia was demonstrated. In addition, a failure of optimal renal conservation of magnesium was noted to occur in this patient since, despite hypomagnesemia, urinary magnesium excretion was greater than the 1 mEq/day loss that is seen when magnesium conservation is induced by means such as dietary restriction.
Subject(s)
Hypoparathyroidism/physiopathology , Magnesium/blood , Parathyroid Hormone , Aged , Calcium/blood , Calcium, Dietary , Humans , Hypoparathyroidism/blood , Hypoparathyroidism/drug therapy , Hypoparathyroidism/urine , Magnesium/therapeutic use , Magnesium/urine , Male , Tissue Extracts , Vitamin D/therapeutic useSubject(s)
Alcoholism/metabolism , Fatty Liver/metabolism , Liver Cirrhosis/metabolism , Uric Acid/metabolism , Alcoholism/blood , Alcoholism/urine , Bilirubin/blood , Creatinine/urine , Fatty Liver/blood , Fatty Liver/urine , Humans , Kidney Function Tests , Kidney Tubules/metabolism , Liver Cirrhosis/blood , Liver Cirrhosis/urine , Male , Pyrazinamide , Syndrome , Uric Acid/blood , Uric Acid/urineSubject(s)
Alkalosis/metabolism , Plasma Substitutes/therapeutic use , Serum Albumin/therapeutic use , Water-Electrolyte Balance/drug effects , Alkalosis/blood , Alkalosis/drug therapy , Alkalosis/urine , Animals , Bicarbonates/blood , Bicarbonates/urine , Calcium/blood , Chlorides/urine , Dogs , Glomerular Filtration Rate , Hematocrit , Humans , Natriuresis/drug effects , Phosphates/urine , Potassium/urineSubject(s)
Hyponatremia/physiopathology , Hypothalamo-Hypophyseal System/physiopathology , Water-Electrolyte Balance , Blood , Drinking , Female , Humans , Hyponatremia/drug therapy , Hyponatremia/metabolism , Infusions, Parenteral , Isotonic Solutions , Mineralocorticoids/therapeutic use , Osmolar Concentration , Sodium/blood , Sodium Chloride/administration & dosage , Urine , Vasopressins/metabolism , Water/administration & dosage , Water/metabolismABSTRACT
Parathyroid hormone increased basal adenyl cyclase activity and that increase was inhibited by prostaglandin E(1) (PGE(1)). Tissue cyclic 3',5'-adenosine monophosphate (cyclic AMP) concentrations were increased by parathyroid hormone and that increase was likewise inhibited by PGE(1). Both parathyroid hormone and dibutyryl cyclic AMP increased (32)P incorporation into renal cortical phospholipids. PGE(1) diminished the effect of parathyroid hormone but not dibutyryl cyclic AMP to influence that parameter. PGE(1) likewise modulated the effect of parathyroid hormone but not dibutyryl cyclic AMP to decrease fractional phosphate reabsorption by the renal tubule. It is suggested that PGE(1) inhibits the effect of parathyroid hormone by decreasing its effect on adenyl cyclase. Such interaction may be important in modulating the intracellular action of parathyroid hormone on kidney cortex.
