|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
This work also warrants an evaluation of high-dose aspirin and COX-2 inhibitor therapy in sufferers of inflammatory conditions who are already at increased risk for cardiovascular disease.-Khan, S. I., Shihata, W. A., Andrews, K. L., Lee, M. K. S., Moore, X.-L., Jefferis, A.-M., Vinh, A., Gaspari, T., Dragoljevic, D., Jennings, G. L., Murphy, A. J., Chin-Dusting, J. P. F. Effects of high- and low-dose aspirin on adaptive immunity and hypertension in the stroke-prone spontaneously hypertensive rat.
|
30156911 |
2019 |
|
Hypertensive disease
|
0.600 |
AlteredExpression
|
group |
BEFREE |
Hence, overexpression of YAP in endothelial cells enhanced the mRNA and protein levels of COX-2 and mPGES-1 and reversed the endothelial dysfunction and hypertension in <i>Tie2Cre-Raptor</i><sup>
|
31378107 |
2019 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
These results showed that LMAE prevents Ang II-induced hypertension and vascular dysfunction through a reduction of oxidative stress linked to COX-2 and NOX-2 pathway and inhibition of calcium entry.
|
31183001 |
2019 |
|
Hypertensive disease
|
0.600 |
GeneticVariation
|
group |
BEFREE |
The risk of hypertension increased by 45% overall (RR 1.45, 95% CI 1.01-2.10; I<sup>2</sup> = 25%); however, when rofecoxib was removed from the analysis the risk of hypertension in the COX-2 inhibitor group was no longer significant (RR 1.21, 95% CI 0.80-1.83; I<sup>2</sup> = 20%).
|
31073922 |
2019 |
|
Hypertensive disease
|
0.600 |
AlteredExpression
|
group |
BEFREE |
Mercury exposure accelerated the natural course of hypertension in young SHRs and increased oxidative stress associated with reduced participation of antioxidant enzymes, an activated COX-2 pathway, thereby producing endothelial dysfunction, which is a risk factor in prehypertensive individuals.
|
31745719 |
2019 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
We conducted a cohort study of patients with hypertension who initiated COX-2-selective or nonselective NSAIDs in a population-based Taiwanese database.
|
29468706 |
2018 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
Renal Medullary Interstitial COX-2 (Cyclooxygenase-2) Is Essential in Preventing Salt-Sensitive Hypertension and Maintaining Renal Inner Medulla/Papilla Structural Integrity.
|
30354807 |
2018 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
These findings support oxylipins, particularly the ARA LOX-derived, in blood pressure control and indicate that pharmacologic inhibition of COX-2 has effects on LOX and CYP450 ARA metabolism that contribute to hypertension in some patients.
|
29698447 |
2018 |
|
Hypertensive disease
|
0.600 |
GeneticVariation
|
group |
BEFREE |
In PRECISION-ABPM, allocation to the non-selective NSAID ibuprofen, compared with the COX-2 selective inhibitor celecoxib was associated with a significant increase of SBP, and a higher incidence of new-onset hypertension.
|
29020251 |
2017 |
|
Hypertensive disease
|
0.600 |
GeneticVariation
|
group |
BEFREE |
However, selective COX-2 inhibitors may increase the risk of hypertension due to inhibiting 6-keto PGF<sub>1α</sub>, the vasodilator product of COX-2.
|
29201221 |
2017 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
The data underscore the preferential capacity of selective COX-2 inhibition by celecoxib to mitigate CSA hypertension and consequent alterations in cardiac performance and autonomic balance.
|
28054752 |
2017 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
In contrast, the peripheral artery dysfunction associated with increased cyclooxygenase-2-derived production of vasoconstrictor prostanoids could underlie the increased blood pressure in male O-DR.
|
28556994 |
2017 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
Site-specific inhibition of COX-2 in the renal medulla of Sprague-Dawley rats causes sodium retention and salt-sensitive hypertension.
|
27814606 |
2017 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
However, the simultaneous inhibition of COX-2 in the vasculature translates into a prothrombotic phenotype and promotes hypertension and heart failure.
|
28569569 |
2017 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
Inhibition of COX-2 may modulate high blood pressure but controversy still exists.
|
25846103 |
2015 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
However, the inhibition of COX-1 in cells of the gastrointestinal (GI) system and COX-2 in vascular cells translates into increased risk of serious GI adverse events and atherothrombosis and hypertension, respectively.
|
23953622 |
2014 |
|
Hypertensive disease
|
0.600 |
Therapeutic
|
group |
CTD_human |
Overexpression of HIF-1α transgene in the renal medulla attenuated salt sensitive hypertension in Dahl S rats.
|
22349312 |
2012 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
CTD_human |
Overexpression of HIF-1α transgene in the renal medulla attenuated salt sensitive hypertension in Dahl S rats.
|
22349312 |
2012 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
This BMP4/ROS/COX-2 cascade is important in the maintenance of endothelial dysfunction in hypertension.
|
20724703 |
2010 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
CTD_human |
Induction of hemeoxygenase-1 attenuates the hypertension and renal inflammation in spontaneously hypertensive rats.
|
20667508 |
2010 |
|
Hypertensive disease
|
0.600 |
Therapeutic
|
group |
CTD_human |
Induction of hemeoxygenase-1 attenuates the hypertension and renal inflammation in spontaneously hypertensive rats.
|
20667508 |
2010 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
BEFREE |
These findings suggest that selective inhibition of COX-2 may have detrimental pulmonary vascular consequences in patients with preexisting pulmonary hypertension or underlying hypoxemic lung diseases.
|
19577709 |
2009 |
|
Hypertensive disease
|
0.600 |
AlteredExpression
|
group |
BEFREE |
Pulmonary and cardiorenal cyclooxygenase-1 (COX-1), -2 (COX-2), and microsomal prostaglandin E synthase-1 (mPGES-1) and -2 (mPGES-2) expression in a hypertension model.
|
17641732 |
2007 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
RGD |
We have tested the hypothesis that in hypertension elevated ROS levels may modify the expression of NOS1 and COX-2 in the JGA, thereby interacting with juxtaglomerular signaling.
|
16467505 |
2006 |
|
Hypertensive disease
|
0.600 |
Biomarker
|
group |
RGD |
Hypertension increases the participation of vasoconstrictor prostanoids from cyclooxygenase-2 in phenylephrine responses.
|
15775781 |
2005 |