ArticleAmerican journal of physiology. Renal physiology2008
A role for the thromboxane receptor in L-NAME hypertension.
Article in American journal of physiology. Renal physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 47 citations in OpenAlex.
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Evaluation ofFrontiers in pharmacology · 2023Article
- The thromboxane receptor antagonistFrontiers in cardiovascular medicine · 2022Article
- High-salt intake reduces renal tissue levels of inflammatory cytokines in mice.Physiological reports · 2021Article
- Antagonism of the Thromboxane-Prostanoid Receptor as a Potential Therapy for Cardiomyopathy of Muscular Dystrophy.Journal of the American Heart Association · 2019Article
- Effects of Aspirin on Endothelial Function and Hypertension.Current hypertension reports · 2016Review
- Antagonism of the thromboxane-prostanoid receptor is cardioprotective against right ventricular pressure overload.Pulmonary circulation · 2016Article
- Vascular dysfunctions in the isolated aorta of double-transgenic hypertensive mice developing aortic aneurysm.Pflugers Archiv : European journal of physiology · 2015Article
- Constrictor prostanoids and uridine adenosine tetraphosphate: vascular mediators and therapeutic targets in hypertension and diabetes.British journal of pharmacology · 2015Review
- Chronic Hypertension Leads to Neurodegeneration in the TgSwDI Mouse Model of Alzheimer's Disease.Hypertension (Dallas, Tex. : 1979) · 2015Article
- MaxiK channel and cell signalling.Pflugers Archiv : European journal of physiology · 2014Review
- Impact of hematopoietic cyclooxygenase-1 deficiency on obesity-linked adipose tissue inflammation and metabolic disorders in mice.Metabolism: clinical and experimental · 2013Article
- Thromboxane-induced renal vasoconstriction is mediated by the ADP-ribosyl cyclase CD38 and superoxide anion.American journal of physiology. Renal physiology · 2013Article
- Article
- Endothelium-mediated control of vascular tone: COX-1 and COX-2 products.British journal of pharmacology · 2011Review
- Comment on: Ott et al. Reduction in basal nitric oxide activity causes albuminuria. Diabetes 2011;60:572-576.Diabetes · 2011Article
- Prostaglandins and inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2011Review
- TRPC6 enhances angiotensin II-induced albuminuria.Journal of the American Society of Nephrology : JASN · 2011Article
- Thromboxane and the thromboxane receptor in cardiovascular disease.Clinical lipidology · 2010Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
Actions of the lipid mediator thromboxane (Tx) A2 acting through the TP receptor contribute to the pathogenesis of cardiovascular disease. To further explore the role of TxA2 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 NG-nitro-L-arginine methyl ester (L-NAME) was administered to TP-deficient (Tp-/-) and wild-type (Tp+/+) 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 TxB2 to a similar extent in both Tp+/+ and Tp-/- 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-/- mice throughout the study period (P<0.001). At the end of the study, the wild-type mice developed significant cardiac hypertrophy (23.6+/-2% increase in heart-to-body weight ratio). The severity of cardiac hypertrophy was attenuated in the TP-deficient group (11.1+/-2.6%; P<0.05). In contrast, kidney hypertrophy was exaggerated in the Tp-/- mice compared with controls (37.1+/-5.4 vs. 12.3+/-2.3%; P<0.01). Moreover, the severity of glomerulosclerosis, tubule vacuolization, and interstitial chronic inflammation was also enhanced in the Tp-/- group (P<0.01). Thus, in L-NAME hypertension, TP receptors contribute to elevated blood pressure and cardiac hypertrophy. In this model, TP receptors also provided unexpected protection against kidney injury.
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