Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2001;37:1129-1135

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Li, Y.
Right arrow Articles by Cohen, R. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Li, Y.
Right arrow Articles by Cohen, R. A.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*CALCIUM COMPOUNDS
*CALCIUM, ELEMENTAL
*HYDRALAZINE HYDROCHLORIDE
*NITRIC OXIDE
*RESERPINE
Medline Plus Health Information
*Dietary Sodium
*High Blood Pressure
Related Collections
Right arrow Animal models of human disease
Right arrow Hypertension - basic studies
Right arrow Ion channels/membrane transport
Right arrow Signal transduction
Right arrow Platelets

(Hypertension. 2001;37:1129.)
© 2001 American Heart Association, Inc.


Scientific Contributions

Abnormal Platelet Function and Calcium Handling in Dahl Salt-Hypertensive Rats

Yun Li; Takeshi Adachi; Victoria M. Bolotina; Cathy Knowles; Kenneth A. Ault; Richard A. Cohen

From the Vascular Biology Unit, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Mass (Y.L., T.A., V.M.B., R.A.C); and Maine Medical Center Research Institute, South Portland, Maine (C.K., K.A.A.).

Correspondence to Dr Richard A. Cohen, Vascular Biology Unit, EBRC 7, Boston University School of Medicine, 650 Albany St, Boston, MA 02118. E-mail racohen{at}medicine.bu.edu

Abstract—The effect of dietary salt on platelet function and Ca2+ 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 Ca2+ homeostasis were measured. The high-salt diet increased blood pressure and markedly increased the amount of ionomycin (IM)-releasable Ca2+ in platelet intracellular stores (Ca2+/IM). The alteration in Ca2+ stores was not prevented when the hypertension was prevented by treatment with hydralazine and reserpine. The Ca2+ store filling during platelet exposure to 1 mmol/L Ca2+ for 5 minutes and the rate of sarcoplasmic/endoplasmic Ca2+ ATPase–dependent Ca45 uptake were higher in DSHS compared with that in DSLS. There was a decrease in thrombin-induced Ca2+ influx in platelets from DSHS; consistent with this, agonist-induced P-selectin expression was decreased. In DSLS, nitric oxide accelerated reloading of platelet Ca2+ 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 Ca2+ ATPase activity and the Ca2+/IM but decreases the reuptake of Ca2+ caused by nitric oxide. Decreases in Ca2+ influx and platelet P-selectin expression might be explained by changes in intracellular Ca2+ stores in DSHS rats, which apparently is a heritable response to a high-salt diet.


Key Words: salt • calcium • diet • nitric oxide • rats, Dahl • platelets