Abnormal calcium handling by platelets of spontaneously hypertensive rats.

Oshima, Tetsuya; Young, Eric W.; Bukoski, Richard D.; McCarron, David A.

doi:10.1161/01.hyp.15.6.606

Cited by 54 publications

(32 citation statements)

References 26 publications

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“…Rmax was obtained by lysing the cell with 50 pM digitonin in the presence of 1mM CaCl2 and Rmin was obtained by successive addition of 10 mM EGTA with the addition of Tris base to bring the buffer pH to 8.5. Extracellular dye leakage was corrected for by the use of 10 mM EGTA as described by Oshima et al (20). In 3 subjects (2 hypertensives and 1 normotensive), inadequate hydrolysis of the dye made it impossible to calculate intracellular calcium, so they were omitted from the data.…”

Section: Methodsmentioning

confidence: 99%

Decreased Platelet Free Magnesium with Increased Free Calcium in Mild Essential Hypertension.

et al. 1992

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Intracellular free magnesium and calcium concentrations of platelets from 21 mild essential hypertensive patients and 8 normotensive individuals were measured using mag-fura2, a recently developed fluorescent indicator, and fura2, respectively. Compared with normotensives, intracellular free magnesium concentration was significantly decreased (0.32 ± 0.10 vs. 0.50 ± 0.15 mmol/1, mean ± SD, p < 0.001) and intracellular free calcium concentration was significantly increased (40.2 ± 9.0 vs. 21.7 ± 11.8 nmol/1, p < 0.001) in the hypertensives. In all subjects, mean blood pressure correlated negatively with intracellular free magnesium (r = -0.57, p < 0.001) and positively with intracellular free calcium (r = 0.48, p < 0.02). Furthermore, intracellular free magnesium correlated negatively with intracellular free calcium. In contrast, serum and intraerythrocyte magnesium concentrations did not differ between the two groups. These results suggest that the decreased intracellular free magnesium of platelets concomitant with the increased intracellular free calcium may participate in the pathophysiology of essential hypertension. (Hypertens Res 1992; 15: 105-110)

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Section: Methodsmentioning

confidence: 99%

Decreased Platelet Free Magnesium with Increased Free Calcium in Mild Essential Hypertension.

et al. 1992

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“…5 In brief, blood was collected from the abdominal aorta using the two-syringe method after ether anesthesia had been administered to the rats. Platelets were washed by gel filtration before and after loading with 2 yiM.…”

Section: Methodsmentioning

confidence: 99%

“…A correction for extracellular fura-2 leakage from cells was performed using ethylene glycol bis()3-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). 5 After recording fluorescence in the resting state, thrombin (0.03, 0.1, 0.3, and 1.0 units/ml) or ionomycin (15,50, and 150 nM) were added as agonists. For each animal, the discharge capacity of Ca 2+ from intracellular stores was estimated by the intracellular Ca 2+ response to (5 fiM) ionomycin in Ca 2+ -free medium.…”

Section: Methodsmentioning

confidence: 99%

Rise and fall of agonist-evoked platelet Ca2+ in hypertensive rats.

et al. 1991

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We previously reported an enhanced peak response of intracellular free Ca 2+ to thrombin in platelets of spontaneously hypertensive rats in comparison with normotensive Wistar-Kyoto rats. In the present study, we compared the platelet intracellular Ca 2+ response to the receptor-linked agonist thrombin with the response to the Ca 2+ ionophore ionomycin. Basal intracellular Ca 2+ was higher in hypertensive platelets as was leakage of fura-2. We confirmed the previous finding that the thrombin-induced intracellular Ca 2+ peak is greater in platelets of hypertensive rats and noted that the rate of recovery from peak intracellular Ca 2+ is significantly greater in this model. In contrast, the peak platelet intracellular Ca 2+ response to ionomycin (50 nM and 5 /uM) was not different between the two strains, and the rate of recovery from the peak response was only slightly depressed in hypertensive rats after the low dose of ionomycin. Internal Ca 2+ discharge capacity, assessed by the intracellular Ca 2+ response to a maximal dose of ionomycin in Ca 2+ -free medium, was not different between platelets of the two strains. Thus, activated platelet intracellular Ca 2+ is not altered in the hypertensive rat when the nonphysiological ionophore ionomycin is used as agonist. However, a heightened intracellular Ca 2+ response is observed when the receptor-mediated agonist thrombin is used. These results are consistent with the hypothesis that differences in receptor-linked second messenger pathways underlie the altered intracellular Ca 2+ response in platelets of genetically hypertensive rats and may contribute to differences both in the mobilization of Ca 2+ and in its fall. {Hypertension 1991;18:758-762)

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“…For all blood collections, rats were anesthetized with pentobarbital sodium (50 mg/kg, intramuscular injection). The abdominal aorta was cannulated, and blood was carefully withdrawn and anticoagulated with citric acid (20% by volume) (14).…”

Section: Preparation Of Plateletsmentioning

confidence: 99%

“…[Ca 2 ]i was measured according to the method described by Oshima et al (14). Platelets were incubated with 2 µmol/l fura2/ acetoxymethylester (Dojindo) for 30 min and analyzed with a fluorescence spectrometer using alternating excitation at 340 and 380 nm of ultraviolet light while measuring emission at 500 nm.…”

Section: [Ca 2 ]I Measurementmentioning

confidence: 99%

Troglitazone Reduces Activity of the Na+/H+ Exchanger in Fructose-Fed Borderline Hypertensive Rats.

et al. 2003

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Activation of the Na /H exchanger (NHE) isty also has been associated with the regulation of blood pressure in several models (3,7,8). We previously examined the activities of NHE in fructose-induced metabolic abnormalities (9-11) in borderline hypertensive rats (BHR), WistarKyoto rats (WKY), and spontaneously hypertensive rats (SHR). BHR were originally developed as a model of environmentally induced hypertension (12). We previously demonstrated that BHR fed a fructose diet developed hyperinsulinemia and hypertriglyceridemia, and showed elevations in NHE activity and blood pressure relative to those fed a standard diet (13). In this previous study, although fructose induced an equivalent degree of hyperinsulinemia in BHR, WKY, and SHR, the elevation in NHE occurred only in BHR. These findings suggest that hyperinsulinemia or hy-

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Abnormal calcium handling by platelets of spontaneously hypertensive rats.

Abstract: There is controversy as to whether platelet intracellular free calcium (

Cited by 54 publications

References 26 publications

Decreased Platelet Free Magnesium with Increased Free Calcium in Mild Essential Hypertension.

Decreased Platelet Free Magnesium with Increased Free Calcium in Mild Essential Hypertension.

Rise and fall of agonist-evoked platelet Ca2+ in hypertensive rats.

Troglitazone Reduces Activity of the Na+/H+ Exchanger in Fructose-Fed Borderline Hypertensive Rats.

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