Celecoxib, but not indomethacin, ameliorates the hypertensive and perivascular fibrotic actions of cyclosporine in rats: Role of endothelin signaling

El‐Mas, Mahmoud M.; Helmy, Maged W.; Ali, Rabab M.; El‐Gowelli, Hanan M.

doi:10.1016/j.taap.2015.01.018

Cited by 27 publications

(19 citation statements)

References 36 publications

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“…, BP elevations caused by the combined use of CSA and diclofenac were significantly greater than the pressor responses elicited by individual drug treatments. Together, findings of the current and previous studies indicate that while CSA hypertension is ameliorated by celecoxib in a sex‐independent fashion, it remains unaltered (male rats) or intensifies (female rats, this study) after non‐selective COX inhibition.…”

Section: Discussionsupporting

confidence: 82%

“…In a previous study performed in male rats, we found that the pressor effect of CSA is abolished upon simultaneous administration of the selective COX‐2 inhibitor celecoxib, whereas non‐selective COX inhibition by indomethacin was without effect . The current study provides more insights into this clinically relevant interaction by studying the sex and drug class dependencies of the CSA/NSAIDs haemodynamic interaction.…”

Section: Discussionmentioning

confidence: 58%

“…Several important observations are reported here along this context. Firstly, similar to its effects in male rats , CSA elicits no hypertension in female rats treated concurrently with celecoxib. Secondly, the preservation of the hypertensive effect of CSA in rats treated with the non‐selective COX inhibitor indomethacin was replicated in the present study when diclofenac, another non‐selective NSAID, was employed.…”

Section: Discussionmentioning

confidence: 76%

“…In a recent study, we showed that celecoxib abolishes the hypertensive effect of chronically administered CSA in contrast to no effect for non-selective COX-1/COX-2 inhibition by indomethacin [20]. The ameliorating effect of celecoxib on CSA hypertension was accounted for by its ability to reverse the associated increases and decreases in vascular endothelin ETA and ETB receptor expressions, respectively [20]. We also reported that the decreases in COX-2 expression caused by CSA were ameliorated after concurrent treatment with celecoxib but not indomethacin [21,22].…”

mentioning

confidence: 95%

“…That said, little information is available regarding the haemodynamic consequences of concurrent CSA/NSAIDs exposure. In a recent study, we showed that celecoxib abolishes the hypertensive effect of chronically administered CSA in contrast to no effect for non-selective COX-1/COX-2 inhibition by indomethacin [20]. The ameliorating effect of celecoxib on CSA hypertension was accounted for by its ability to reverse the associated increases and decreases in vascular endothelin ETA and ETB receptor expressions, respectively [20].…”

mentioning

confidence: 99%

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Opposite Modulatory Effects of Selective and Non‐Selective Cyclooxygenase Inhibition on Cardiovascular and Autonomic Consequences of Cyclosporine in Female Rats

Ibrahim

El-Yazbi

El‐Gowelli

et al. 2017

Basic Clin Pharma Tox

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Non-steroidal anti-inflammatory drugs (NSAIDs) and the immunosuppressant drug cyclosporine (CSA) are concurrently administered in arthritis. Here, we investigated whether diclofenac (non-selective inhibitor of cyclooxygenase-1 and 2, COX-1/COX-2), celecoxib (selective COX-2 inhibitor) or SC560 (selective COX-1 inhibitor) interact variably with haemodynamic effects of CSA in conscious female rats. Changes caused by CSA (10 mg/kg i.v.) in blood pressure (BP), heart rate (HR), HR variability (HRV) and myocardial contractility were assessed in the absence and presence of individual NSAIDs (10 mg/kg each). Compared with vehicle values, CSA caused immediate and sustained (i) increases in BP and decreases in pulse pressure index (PPI) and HR, (ii) elevations in left ventricular (LV) contractility (dP/dt ) and isovolumic relaxation constant (Τau) and (iii) increases in the time- and frequency-domain indices of HRV and shifted the cardiac sympathovagal balance towards parasympathetic dominance. CSA hypertension was abolished in rats pre-treated with celecoxib and intensified in the presence of diclofenac or SC560. Alternatively, the CSA-evoked decreases in PPI, increases in HRV indices and cardiac parasympathetic dominance were blunted by celecoxib in contrast to no effect for diclofenac or SC560. Similarly, celecoxib, but not other NSAIDs, eliminated the elevated LV contractility (dP/dt ) and isovolumic relaxation constant (Τau, τ), which reflect cardiac systolic and diastolic function, respectively, that accompanied the CSA-induced pressure load. 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. By contrast, CSA effects are preserved or even exacerbated after COX-1 inhibition.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 76%

mentioning

confidence: 95%

mentioning

confidence: 99%

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Opposite Modulatory Effects of Selective and Non‐Selective Cyclooxygenase Inhibition on Cardiovascular and Autonomic Consequences of Cyclosporine in Female Rats

Ibrahim

El-Yazbi

El‐Gowelli

et al. 2017

Basic Clin Pharma Tox

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Montelukast potentiates the antiinflammatory effect of NSAIDs in the rat paw formalin model and simultaneously minimizes the risk of gastric damage

et al. 2021

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Modulation by antenatal therapies of cardiovascular and renal programming in male and female offspring of preeclamptic rats

Habib

Gowayed

Abdelhady

et al. 2021

Naunyn-Schmiedeberg's Arch Pharmacol

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Morbidity and mortality risks are enhanced in preeclamptic (PE) mothers and their offspring. Here, we asked if sexual dimorphism exists in (i) cardiovascular and renal damage evolved in offspring of PE mothers, and (ii) offspring responsiveness to antenatal therapies. PE was induced by administering N G -nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day, oral gavage) to pregnant rats for 7 days starting from gestational day 14. Three therapies were co-administered orally with L-NAME, atrasentan (endothelin ETA receptor antagonist), terutroban (thromboxane A2 receptor antagonist, TXA2), or α-methyldopa (α-MD, central sympatholytic drug). Cardiovascular and renal profiles were assessed in 3-month-old offspring. Compared with offspring of non-PE rats, PE offspring exhibited elevated systolic blood pressure and proteinuria and reduced heart rate and creatinine clearance (CrCl). Apart from a greater bradycardia in male offspring, similar PE effects were noted in male and female offspring. While terutroban, atrasentan, or α-MD partially and similarly blunted the PE-evoked changes in CrCl and proteinuria, terutroban was the only drug that virtually abolished PE hypertension. Rises in cardiorenal inflammatory (tumor necrosis factor alpha, TNFα) and oxidative (isoprostane) markers were mostly and equally eliminated by all therapies in the two sexes, except for a greater dampening action of atrasentan, compared with α-MD, on tissue TNFα in female offspring only. Histopathologically, antenatal terutroban or atrasentan was more effective than α-MD in rectifying cardiac structural damage, myofiber separation, and cytoplasmic alterations, in PE offspring. The repair by antenatal terutroban or atrasentan of cardiovascular and renal anomalies in PE offspring is mostly sex-independent and surpasses the protection offered by α-MD, the conventional PE therapy.

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Celecoxib, but not indomethacin, ameliorates the hypertensive and perivascular fibrotic actions of cyclosporine in rats: Role of endothelin signaling

Cited by 27 publications

References 36 publications

Opposite Modulatory Effects of Selective and Non‐Selective Cyclooxygenase Inhibition on Cardiovascular and Autonomic Consequences of Cyclosporine in Female Rats

Opposite Modulatory Effects of Selective and Non‐Selective Cyclooxygenase Inhibition on Cardiovascular and Autonomic Consequences of Cyclosporine in Female Rats

Montelukast potentiates the antiinflammatory effect of NSAIDs in the rat paw formalin model and simultaneously minimizes the risk of gastric damage

Modulation by antenatal therapies of cardiovascular and renal programming in male and female offspring of preeclamptic rats

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