Effect of parathyroid hormone and uremic sera on the autoagglutination and sedimentation of human red blood cells.
Parathyroid hormone (PTH) caused a dramatic acceleration of erythrocyte sedimentation rate (ESR). This effect was calcium dependent and was partially reversed by verapamil. It was not mimicked by 5 mumol/l calcium ionophore A-23187. Following the removal of PTH from the cell suspension the ESR returned to normal. PTH also caused haemagglutination, the reaction was Ca2+ dependent, pH dependent and was partially reversed by verapamil. High levels of Ca2+ ionophore A-23187 mimicked this phenomenon. Magnesium ions even at concentrations of 5 mmol/l did not replace Ca2+, while Ca2+ at concentrations of 3 mmol/l and above caused haemagglutination. The glycolytic inhibitor NaF at levels of 1 mmol/l did not inhibit haemagglutination. The polyamines pertusin and spermidin, prostaglandins PGE2 and PGF, and the calcium hormone calcitonin, did not reproduce the PTH effect. Dialysate from serum of patients with chronic renal failure and hyperparathyroidism caused haemagglutination, while dialysate from patients with chronic renal failure following parathyroidectomy and normal individuals did not cause this phenomenon. It seems that abnormal erythrocyte behaviour seen in patients with chronic renal failure is caused by PTH which leads to modified Ca2+ metabolism in these cells.
D001799:Blood Sedimentation; D002118:Calcium / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006384:Hemagglutination / Q000187:drug effects*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006961:Hyperparathyroidism / Q000097:blood; D010281:Parathyroid Hormone / Q000494:pharmacology*; D014511:Uremia / Q000097:blood*; D014700:Verapamil / Q000494:pharmacology
D010281:Parathyroid Hormone; D014700:Verapamil; D002118:Calcium