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Abnormal platelet function and calcium handling in Dahl salt-hypertensive rats
1Vascular Biology Unit, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Insights
A high-salt diet in Dahl rats alters platelet calcium handling and reduces P-selectin expression, impacting blood pressure regulation. These changes in platelet function appear to be a heritable response to dietary salt.
Area of Science:
- Cardiovascular Physiology
- Cellular Biology
- Hypertension Research
Background:
- Dietary salt intake is a major factor in hypertension development.
- Platelet function and calcium (Ca2+) homeostasis are crucial in cardiovascular health.
- Dahl salt-sensitive (DS) rats are a genetic model for studying salt-induced hypertension.
Purpose of the Study:
- To investigate the impact of a high-salt diet on platelet function and Ca2+ homeostasis in DS rats.
- To determine if salt-induced alterations in platelet Ca2+ handling are linked to hypertension.
- To explore the role of nitric oxide in modulating platelet Ca2+ dynamics under high-salt conditions.
Main Methods:
- DS rats were fed high-salt (DSHS) or low-salt (DSLS) diets for up to 4 weeks.
- Systolic blood pressure, platelet P-selectin expression, and intracellular Ca2+ stores were measured.
- Platelet Ca2+ influx, sarcoplasmic/endoplasmic Ca2+ ATPase activity, and nitric oxide effects were analyzed.
Main Results:
- High-salt diet increased blood pressure and significantly elevated ionomycin-releasable Ca2+ in platelet stores (Ca2+/IM).
- Increased Ca2+ store filling and sarcoplasmic/endoplasmic Ca2+ ATPase activity were observed in DSHS rats.
- Thrombin-induced Ca2+ influx and agonist-induced P-selectin expression decreased in DSHS rats, with impaired nitric oxide-mediated Ca2+ store reuptake.
Conclusions:
- High-salt diet in DS rats enhances sarcoplasmic/endoplasmic Ca2+ ATPase activity and Ca2+ store capacity.
- Altered intracellular Ca2+ handling in platelets may explain decreased Ca2+ influx and P-selectin expression.
- These salt-induced platelet changes are potentially heritable and contribute to salt-sensitive hypertension.
Abstract:
The effect of dietary salt on platelet function and Ca(2+) homeostasis was studied in Dahl (DS) rats, a genetic model of salt-sensitive hypertension. DS rats were fed a high-salt (DSHS) or a low-salt diet (DSLS) for up to 4 weeks, and the effects of salt loading on systolic blood pressure, platelet P-selectin expression, and platelet Ca(2+) homeostasis were measured. The high-salt diet increased blood pressure and markedly increased the amount of ionomycin (IM)-releasable Ca(2+) in platelet intracellular stores (Ca(2+)/IM). The alteration in Ca(2+) stores was not prevented when the hypertension was prevented by treatment with hydralazine and reserpine. The Ca(2+) store filling during platelet exposure to 1 mmol/L Ca(2+) for 5 minutes and the rate of sarcoplasmic/endoplasmic Ca(2+) ATPase-dependent Ca(45) uptake were higher in DSHS compared with that in DSLS. There was a decrease in thrombin-induced Ca(2+) influx in platelets from DSHS; consistent with this, agonist-induced P-selectin expression was decreased. In DSLS, nitric oxide accelerated reloading of platelet Ca(2+) stores after their emptying by thrombin but failed to do so in DSHS. These results indicate that in DS rats, a high-salt diet increases sarcoplasmic/endoplasmic Ca(2+) ATPase activity and the Ca(2+)/IM but decreases the reuptake of Ca(2+) caused by nitric oxide. Decreases in Ca(2+) influx and platelet P-selectin expression might be explained by changes in intracellular Ca(2+) stores in DSHS rats, which apparently is a heritable response to a high-salt diet.
