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Dietary calcium attenuates platelet aggregation and intracellular Ca2+ mobilization in spontaneously hypertensive
1Department of Medicine, Oregon Health Sciences University, Portland 97201-3098, USA.
Insights
Dietary calcium supplementation reduced blood pressure and platelet aggregation in spontaneously hypertensive rats. This effect is linked to decreased intracellular calcium mobilization in platelets.
Area of Science:
- Cardiovascular Physiology
- Nutritional Science
- Biochemistry
Background:
- Spontaneously hypertensive rats (SHR) exhibit blood pressure sensitivity to dietary calcium.
- Calcium plays a crucial role in regulating vascular tone and platelet function.
Purpose of the Study:
- To investigate the impact of dietary calcium on platelet aggregation and intracellular calcium ([Ca2+]i) mobilization in SHR.
- To explore the relationship between systolic blood pressure (SBP) and platelet activity in response to calcium intake.
Main Methods:
- Assessment of platelet aggregation using turbidimetric methods.
- Measurement of intracellular calcium ([Ca2+]i) mobilization with fura-2 in washed platelets.
- Analysis of Ca2+-ATPase activity in aortic membrane fractions.
Main Results:
- Dietary calcium supplementation significantly attenuated the rise in SBP and thrombin-induced platelet aggregation.
- Calcium supplementation decreased ionomycin-induced [Ca2+]i peak and thrombin-evoked [Ca2+]i release, indicating reduced intracellular calcium storage and release.
- SBP was positively correlated with platelet aggregation and [Ca2+]i mobilization.
Conclusions:
- Dietary calcium supplementation exerts beneficial effects on SHR platelets by reducing intracellular calcium ([Ca2+]i) mobilization.
- The hypotensive effect of dietary calcium in SHR may be associated with attenuated intracellular calcium ([Ca2+]i) mobilization.
Abstract:
Spontaneously hypertensive rats (SHR) are known to be blood pressure sensitive to dietary calcium. The effects of dietary calcium on platelet aggregation and intracellular Ca2+ mobilization were assessed by turbidimetric methods and fura-2 methods, respectively, in washed platelets of SHR. Ca2+ ATPase activity was examined in aortic membrane fractions. Six weeks of dietary calcium supplementation attenuated the increase of systolic blood pressure (SBP 199 +/- 16 v 170 +/- 9 mm Hg, P < .001) and thrombin-induced platelet aggregation (84.5 +/- 3.7 v 73.7 +/- 7.4%, P < .004) at 9 weeks of age. The ionomycin-induced intracellular calcium ([Ca2+]i) peak in the absence of external Ca2+, which reflects [Ca2+]i storage size, and thrombin-evoked [Ca2+]i release from [Ca2+]i storage were decreased by 2.0% Ca diet (472 +/- 55 v 370 +/- 23 nmol/L, P < .001, 339 +/- 29 v 278 +/- 33 nmol/L, P < .002). In addition, SBP was positively correlated with platelet aggregation (r = 0.703, P = .0088), thrombin-evoked [Ca2+]i (r = 0.739, P = .0044), and ionomycin-induced [Ca2+]i (r = 0.591, P = .0415), respectively. However, there was no significant effect of dietary calcium on Ca2+-ATPase activity in aortic membranes. These results suggest that dietary calcium supplementation had a beneficial effect on platelets of SHR by attenuating [Ca2+]i mobilization from [Ca2+]i storage. The hypotensive effect of dietary calcium might be associated with attenuated [Ca2+]i mobilization in SHR.