{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T11:21:12Z","timestamp":1790767272778,"version":"4.1.0"},"reference-count":43,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2008,10]]},"abstract":"<jats:p> Actions of the lipid mediator thromboxane (Tx) A<jats:sub>2<\/jats:sub> acting through the TP receptor contribute to the pathogenesis of cardiovascular disease. To further explore the role of TxA<jats:sub>2<\/jats:sub> in hypertension, we examined the consequences of deficiency of the TP receptor on the course of hypertension associated with endothelial dysfunction and salt sensitivity. To this end, the nitric oxide synthase inhibitor N<jats:sup>G<\/jats:sup>-nitro-l-arginine methyl ester (l-NAME) was administered to TP-deficient ( Tp<jats:sup>\u2212\/\u2212<\/jats:sup>) and wild-type ( Tp<jats:sup>+\/+<\/jats:sup>) control mice in drinking water for 21 wk along with a high-salt (HS; 6% NaCl) diet. Administration of l-NAME increased urinary excretion of TxB<jats:sub>2<\/jats:sub> to a similar extent in both Tp<jats:sup>+\/+<\/jats:sup> and Tp<jats:sup>\u2212\/\u2212<\/jats:sup> animals. l-NAME also caused significant and sustained elevations in blood pressure that reached a maximum between weeks 3 and 6. However, the severity of hypertension was attenuated in the Tp<jats:sup>\u2212\/\u2212<\/jats:sup> mice throughout the study period ( P &lt; 0.001). At the end of the study, the wild-type mice developed significant cardiac hypertrophy (23.6 \u00b1 2% increase in heart-to-body weight ratio). The severity of cardiac hypertrophy was attenuated in the TP-deficient group (11.1 \u00b1 2.6%; P &lt; 0.05). In contrast, kidney hypertrophy was exaggerated in the Tp<jats:sup>\u2212\/\u2212<\/jats:sup> mice compared with controls (37.1 \u00b1 5.4 vs. 12.3 \u00b1 2.3%; P &lt; 0.01). Moreover, the severity of glomerulosclerosis, tubule vacuolization, and interstitial chronic inflammation was also enhanced in the Tp<jats:sup>\u2212\/\u2212<\/jats:sup> group ( P &lt; 0.01). Thus, in l-NAME hypertension, TP receptors contribute to elevated blood pressure and cardiac hypertrophy. 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