Increased internal calcium mobilization in platelets of patients with chronic renal failure

• Published in: Hormone and metabolic research Vol. 24; no. 12; p. 588
• Main Authors: Tokumoto, A, Uemasu, J, Kawasaki, H
• Format: Journal Article
• Language: English
• Published: Germany 01.12.1992
• Subjects: Adenosine Diphosphate - pharmacology; Adult; Blood Platelets - drug effects; Blood Platelets - metabolism; Calcium - antagonists & inhibitors; Calcium - blood; Gallic Acid - analogs & derivatives; Gallic Acid - pharmacology; Glomerulonephritis - blood; Humans; Kidney Failure, Chronic - blood; Middle Aged; Thrombin - pharmacology
• ISSN: 0018-5043
• DOI: 10.1055/s-2007-1003397

Platelet free calcium concentrations ([Ca2+]i) were measured with Fura-2 to elucidate the intracellular calcium kinetics in patients with renal disease. There were no significant differences of the resting [Ca2+]i among the control subjects (C) (n = 12), patients with chronic glomerulonephritis (CGN) (n = 8), and patients with chronic renal failure (CRF) (n = 12). In all groups, platelets [Ca2+]i were significantly increased by agonists (thrombin, adenosine diphosphate) compared with their respective basal level. Thrombin-induced [Ca2+]i rise was significantly higher in CRF (840 +/- 265 nM) than in C (600 +/- 163) and CGN (562 +/- 137). Also adenosine diphosphate elicited similar responses. In the presence of calcium chelator in the incubation buffer, the elevation of [Ca2+]i after thrombin stimulation was statistically higher in CRF (469 +/- 85 nM) than in C (275 +/- 60) and CGN (301 +/- 41). These findings suggest that platelets of CRF were capable of increasing [Ca2+]i in response to agonists, through further mobilization of calcium from the intracellular pool rather than the elevation of transmembrane calcium influx.