EFFECT OF ANTIHYPERTENSIVE TREATMENT ON INTRACELLULAR CALCIUM-CONCENTRATION AND INTRACELLULAR PH IN ESSENTIAL-HYPERTENSION

Citation
E. Poch et al., EFFECT OF ANTIHYPERTENSIVE TREATMENT ON INTRACELLULAR CALCIUM-CONCENTRATION AND INTRACELLULAR PH IN ESSENTIAL-HYPERTENSION, Journal of human hypertension, 8(6), 1994, pp. 461-467
Citations number
NO
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
09509240
Volume
8
Issue
6
Year of publication
1994
Pages
461 - 467
Database
ISI
SICI code
0950-9240(1994)8:6<461:EOATOI>2.0.ZU;2-G
Abstract
The platelet intracellular calcium concentration ([Ca2+]i) and intrace llular pH (pH(i)) were measured by spectro-fluorimetry with the dyes F ura-2 and BCECF, respectively , in 19 patients with essential hyperten sion (10 males), aged 48 +/- 2 years, before and after 12 weeks of ant ihypertensive treatment and in 19 normotensive controls (11 males), ag ed 46 +/- 3 years. [Ca2+]i and pH(i) were measured in the resting stat e and after stimulation in vitro with 0.1 U/ml human thrombin. In pati ents with essential hypertension, both resting [Ca2+]i (61 +/- 4 nmol/ l) and thrombin-induced maximal increase in [Ca2+]i (291 +/- 26 nmol/l ) were significantly (P < 0.01) greater than in the normotensive contr ols (resting 49 +/- 2 nmol/l and thrombin-induced 199 +/- 21 nmol/l). With respect to pH(i), no difference in resting pH(i) between both gro ups was found (7.16 +/- 0.01 vs. 7.16 +/- 0.01). However, pH(i) increm ent at 300 seconds in response to thrombin was higher in the patients with essential hypertension than in the controls (0.131 +/- 0.02 vs. 0 .083 +/- 0.01 pH units, P < 0.05). The increment in pH(i) was blunted by the amiloride derivative EIPA, indicating that it was mediated by t he Na+/H+ exchanger. After antihypertensive therapy in the essential h ypertensive patients, basal [Ca2+]i was significantly reduced (52 +/- 2 nmol/l, P < 0.01) and was not statistically different to the value f ound in the normotensive controls. Resting pH(i) suffered no significa nt modification after treatment (7.17 +/- 0.01, P = NS). However, both thrombin-induced increments in [Ca2+li and in pH(i) were significantl y reduced after antihypertensive treatment (224 +/- 19 nmol/l and 0.08 2 +/- 0.01, respectively, P < 0.05) showing no differences with the va lues displayed by the controls. These data indicate that resting [Ca2]i is higher in patients with essential hypertension compared with nor motensive controls. Thrombin-induced rises in platelet [Ca2+]i and pH( i) are both augmented in untreated patients with essential hypertensio n compared with controls. Antihypertensive treatment seems to 'normali se' these enhanced rises of [Ca2+]i and pH(i) to levels similar to the controls.