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Changes in Ca2+ mobilization in platelets from stroke-prone spontaneously hypertensive rats
1Department of Pharmacology, Kinki University School of Medicine, Osaka-Sayama, Japan.
Clinical and Experimental Hypertension (New York, N.Y. : 1993)
|January 1, 1994
Summary
Platelets from stroke-prone rats show higher intracellular calcium levels due to increased membrane permeability and impaired calcium uptake. Protein kinase C activity may also contribute to sustained calcium levels in these hypertensive models.
Area of Science:
- Cardiovascular Research
- Cell Physiology
- Hypertension Studies
Background:
- Elevated intracellular calcium ([Ca2+]i) is implicated in hypertension.
- Platelet function is sensitive to calcium levels.
- Stroke-prone spontaneously hypertensive rats (SHRSP) serve as a model for studying hypertension-related cardiovascular changes.
Purpose of the Study:
- To investigate intracellular calcium levels and handling in platelets of SHRSP compared to normotensive Wistar-Kyoto rats (WKY).
- To explore the mechanisms underlying altered calcium homeostasis in SHRSP platelets.
Main Methods:
- Measurement of intracellular free Ca2+ ([Ca2+]i) using fura-2AM in platelets from SHRSP and WKY rats of different ages (2 and 9 months).
- Assessment of calcium levels under basal conditions and in response to extracellular calcium.
- Evaluation of receptor-linked calcium influxes stimulated by thrombin or collagen.
- Investigation of the effect of phorbol 12-myristate 13-acetate (TPA) on calcium influx.
Main Results:
- Unstimulated platelets from both young and old SHRSP exhibited significantly higher [Ca2+]i than age-matched WKY rats, even without extracellular calcium in older rats.
- Receptor-stimulated calcium influxes were reduced in platelets from older SHRSP.
- TPA-induced calcium influx was more pronounced in older SHRSP platelets compared to older WKY platelets.
Conclusions:
- SHRSP platelets demonstrate increased plasma membrane calcium permeability.
- Elevated resting [Ca2+]i in SHRSP platelets is sustained by impaired calcium uptake mechanisms.
- Enhanced protein kinase C activity may contribute to the altered calcium homeostasis in SHRSP platelets.
