title: Platelet calcium handling is different in rats with salt-dependent and spontaneous forms of genetic hypertension.
abstract: Increased platelet cytosolic free calcium concentration ([Ca2+]i) has been demonstrated in both human essential hypertension and spontaneous hypertension of the rat. The present study was designed to extend the investigation on platelet Ca2+ handling to two models of salt-dependent genetic hypertension (Sabra and Dahl rat strains). No major [Ca2+]i elevation was seen in salt hypertensive SBH Sabra or SS/Jr Dahl rats. This contrasts with the data obtained in Lyon hypertensive rats (a spontaneous form of genetic hypertension) in which basal platelet [Ca2+]i was clearly increased and correlated positively with diastolic blood pressure. In these two strains, basal platelet [Ca2+]i correlated with pulse pressure but not with diastolic pressure. The absence of a significant relationship between platelet [Ca2+]i and diastolic pressure in both Sabra and Dahl rats indicates that, at least in young rats with developing salt hypertension, platelet cytosolic calcium need not reflect calcium changes occurring in the vascular smooth muscle or resistance arterioles. In contrast to the high values seen in Lyon hypertensive rats, the [Ca2+]i rise induced by thrombin was unchanged in salt-sensitive SS/Jr Dahl rats and substantially reduced in hypertension-prone SBH rats (irrespective of salt intake). The initial rate of thrombin-induced Mn2+ entry through receptor-operated Ca2+ channels was similar in SBN and SBH as well as in SR/Jr and SS/Jr rats kept on a low-salt diet but was reduced by high salt intake in platelets of salt-resistant (SBN and SR/Jr) animals only. Since platelets of Lyon hypertensive rats are also characterized by greater initial rate of thrombin-induced Mn2+ entry, this parameter was always higher in rats with established hypertension compared to their respective normotensive controls. Our study demonstrated that alterations of platelet Ca2+ handling are different in salt-dependent than in spontaneous forms of genetic hypertension.
authors.affiliation: Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
authors.forename: J
authors.initials: J
authors.lastname: Zicha
authors.forename: J
authors.initials: J
authors.lastname: Kunes
authors.forename: M A
authors.initials: MA
authors.lastname: Devynck
mesh_terms: D000818:Animals; D001792:Blood Platelets / Q000378:metabolism*; D001794:Blood Pressure / Q000502:physiology; D002118:Calcium / Q000097:blood*; D003600:Cytosol / Q000378:metabolism; D006973:Hypertension / Q000097:blood* / Q000139:chemically induced / Q000235:genetics; D008297:Male; D008345:Manganese / Q000097:blood; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*; D013045:Species Specificity; D013917:Thrombin / Q000494:pharmacology
chemical_list: D017673:Sodium Chloride, Dietary; D008345:Manganese; D013917:Thrombin; D002118:Calcium