Thromboxane A receptor antagonist (ONO-8809) attenuates renal disorders caused by salt overload in stroke-prone spontaneously hypertensive rats.

Epidemiological and clinical studies have demonstrated that excessive salt intake causes severe hypertension and exacerbates organ derangement, such as in chronic kidney disease (CKD). In this study, we focused on evaluating the histological and gene expression effects in the kidneys of stroke-prone spontaneously hypertensive rats (SHRSP) with a high salt intake and the thromboxane A / prostaglandin H receptor (TPR) blocker ONO-8809. Six-week-old SHRSPs were divided into three groups and were fed normal chow containing 0.

Involvement of thromboxane A2 receptor in the cerebrovascular damage of salt-loaded, stroke-prone rats.

Background: Inflammatory processes may play a pivotal role in the pathogenesis of cerebrovascular injury in salt-loaded, stroke-prone, spontaneously hypertensive rats (SHRSP). Thromboxane A2 (TP) receptor stimulation by 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) is involved in the process of vascular inflammation.

Objective: In the present study, we examined the involvement of TP receptor in the development of cerebrovascular damage in salt-loaded SHRSP.

Eccentric dosing of nitrates does not increase cardiac events in patients with healed myocardial infarction.

This study was performed to investigate the risk of cardiac events by eccentric or continuous dosing of nitrates in patients with healed myocardial infarction. A total of 573 patients with healed myocardial infarction were assigned to one of two groups: a nitrate-treatment (n =239) and a nontreatment (n =334) group. The nitrate-treatment group was further subdivided into a group receiving eccentric dosing of nitrates (n =153) and a group receiving continuous dosing of nitrates (n =86).