Determinants of Platelet Intracellular Free Calcium in Essential Hypertension and Effect of Stimulation by Arginine Vasopressin

1993 ◽  
Keyword(s):  
Essential Hypertension ◽  
Arginine Vasopressin ◽  
Intracellular Free Calcium ◽  
Free Calcium

Platelet Cytosolic Free Calcium in Essential Hypertension: Responses to Vasopressin

1989 ◽  
Vol 77 (2) ◽  
pp. 183-188 ◽  
Author(s):  
A. F. Dominiczak ◽  
J. J. Morton ◽  
G. Murray ◽  
P. F. Semple
Keyword(s):  
Essential Hypertension ◽  
Arginine Vasopressin ◽  
Calcium Concentration ◽  
Systolic Pressure ◽  
Extracellular Calcium ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Hypertensive Patients ◽  
Free Calcium Concentration ◽  
The Difference

1. Resting and stimulated free calcium concentrations have been measured in platelets loaded with the fluorescent probe quin2 from 30 patients with essential hypertension and from 30 age-matched controls. 2. Cytosolic free calcium concentrations were 94.6 ± 2.7 (mean ± sem) in the hypertensive group and 91.7 ± 2.8 nmol/l in the normotensive group, the difference was not significant. 3. Arginine vasopressin caused a transient increase in platelet free calcium concentration in all subjects. In the presence of extracellular calcium the increase was significantly higher in the control subjects than in the hypertensive patients (P = 0.005). In the absence of extracellular calcium, arginine vasopressin caused much smaller increases, and there was then no difference between the responses of the two groups. 4. Platelet free calcium concentrations were measured again in 13 patients after 8 weeks treatment with either verapamil (n = 6) or atenolol (n = 7). The reductions in systolic pressure after drug treatment were correlated with the changes in cytosolic free calcium concentrations (r = 0.75, P < 0.01).

Platelet intracellular free calcium response to arginine vasopressin is similar in preeclampsia and normal pregnancy

1995 ◽  
Vol 172 (2) ◽  
pp. 654-660 ◽  
Author(s):  
Phillipa M. Kyle ◽  
Michael C. Jackson ◽  
Davina C. Buckley ◽  
Michael de Swiet ◽  
Christopher W.G. Redman
Keyword(s):  
Arginine Vasopressin ◽  
Normal Pregnancy ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Calcium Response

The adrenaline -α2-adrenoceptor-mediated vasoconstrictor axis

1985 ◽  
Vol 68 (s10) ◽  
pp. 141s-146s ◽  
Author(s):  
Peter Bolli ◽  
Paul Erne ◽  
Wolfgang Kiowski ◽  
Franz W. Amman ◽  
Fritz R. Bühler
Keyword(s):  
Essential Hypertension ◽  
Calcium Concentration ◽  
Smooth Muscle Contraction ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Plasma Adrenaline ◽  
Α2 Adrenoceptor ◽  
Intracellular Free Calcium Concentration ◽  
Free Calcium Concentration ◽  
Normotensive Subjects

1. In patients with essential hypertension plasma adrenaline concentrations have been found to be higher than in normotensive subjects and this may represent increased adrenergic activity. Adrenaline released into the circulation can be taken up by the sympathetic nerve ending and as it is re-released as a co-transmitter it enhances exocytotic noradrenaline release by stimulating prejunctional β-adrenoceptors and as a consequence it contributes to postjunctional α1-adrenoceptor-induced vasoconstriction. Adrenaline may also induce vasoconstriction via post- and extra-junctional (α2-adrenoceptors, as shown by a decrease in the forearm blood flow during adrenaline infusions in the postjunctional α1- and β-blocked forearm vasculature, an effect that could be antagonized by α2-adrenoceptor blockade with yohimbine. 2. α2-Adrenoceptor stimulation in platelets showed an increased sensitivity to adrenaline, as determined by sensitivity in counteracting the inhibitor effect of PGI2 on intracellular free calcium concentration in untreated patients with essential hypertension, when compared with treated patients or normotensive subjects. As these effects can be normalized by antihypertensive treatment this suggests that the increased hormone sensitivity may be related to the elevated intracellular free calcium concentration. 3. Thus adrenaline, via pre- and post-junctional adrenoceptors, may contribute to enhanced vascular smooth muscle contraction, which most likely is sensitized by the elevated intracellular calcium concentration.

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