Increased basal and thrombin-induced free calcium in platelets of essential hypertensive patients.
Author(s) -
Alessandro Lechi,
C Lechi,
Giovanni Bonadonna,
D Sinigaglia,
Paolo Corradini,
Roberto Polignano,
Enrico Arosio,
G Covi,
P. De Togni
Publication year - 1987
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.9.3.230
Subject(s) - medicine , endocrinology , calcium , platelet , extracellular , epinephrine , essential hypertension , ouabain , thrombin , calcium in biology , chemistry , angiotensin ii , basal (medicine) , fura 2 , stimulation , biochemistry , blood pressure , sodium , enzyme , organic chemistry , insulin , cytosol
Intracellular free calcium, [Ca2+]i, was studied in platelets of essential hypertensive subjects and normotensive controls under basal conditions and after stimulation with epinephrine, norepinephrine, angiotensin II, ouabain, and thrombin, using the fluorescent calcium indicator quin 2. Basal [Ca2+]i was significantly higher in hypertensive subjects (n = 32) than in normotensive controls (n = 30; 167.4 +/- 5.0 vs 143.2 +/- 3.1 nmol/L; p less than 0.001). Epinephrine, norepinephrine, angiotensin II, and ouabain had no effect on platelet calcium, whereas thrombin induced a dose-dependent increase in [Ca2+]i in both the presence and absence of extracellular calcium. This [Ca2+]i increase in the presence of extracellular calcium, which depends mainly on calcium influx, was significantly higher (p less than 0.05) in platelets of hypertensive subjects at all thrombin concentrations (ranging from 0.025-0.1 U/ml), while the [Ca2+]i increase in the absence of extracellular calcium, which depends only on release from intracellular stores, was similar in hypertensive subjects and controls. These results suggest that, in essential hypertension, there is not only increased platelet resting [Ca2+]i but also an increase in agonist-mediated calcium influx, which appears to indicate a cell membrane abnormality in the platelets of subjects with essential hypertension.
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