Testosterone depletion contributes to cyclosporine-induced chronic impairment of acetylcholine renovascular relaxations

El‐Mas, Mahmoud M.; Afify, Elham A.; Omar, Abdelsattar M.; El-Din, Mahmoud M. Mohy; Sharabi, Fouad M.

doi:10.1016/s0014-2999(03)01720-5

Cited by 40 publications

(34 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rats were randomly assigned to receive one of the following treatments: (i) cremophor (40%, 1 mg kg −1 day −1 ), (ii) CSA (20 mg kg −1 day −1 ) (El-Mas et al, 2003, (iii) indomethacin (5 mg kg − 1 day −1 ) (Kamalutheen et al, 2009), (iv) CSA + indomethacin, (v) atrasentan (ET A receptor blocker, 5 mg kg − 1 day − 1 ) (Lima, 2010), (vi) CSA + atrasentan, (vii) indomethacin + atrasentan, or (viii) CSA + indomethacin + atrasentan. All drugs were administered once daily via oral gavage for 10 consecutive days.…”

Section: Csa-indomethacin Hemodynamic Interactionmentioning

confidence: 99%

“…The mechanisms of the hypertensive effect of CSA include sympathoexcitation (Zhang and Victor, 2000), enhanced reninangiotensin activity (Nishiyama et al, 2003), arterial baroreflex impairment (El-Mas et al, 2002, 2012b, oxidative stress (El-Mas et al, 2012b), vascular endothelium dysfunction (El-Mas et al, 2003, and interruption of brainstem nitric oxide synthase/heme oxygenase pathway and downstream guanylate cyclase activity (El-Mas et al, 2012c). Moreover, experimental (Nasser et al, 2014) and clinical (Cauduro et al, 2005) studies suggest the involvement of endothelin (ET) in the pathogenesis of CSA hypertension.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

El‐Mas

Helmy

Ali

et al. 2015

Toxicology and Applied Pharmacology

Self Cite

View full text Add to dashboard Cite

Section: Csa-indomethacin Hemodynamic Interactionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

El‐Mas

Helmy

Ali

et al. 2015

Toxicology and Applied Pharmacology

Self Cite

View full text Add to dashboard Cite

“…Increases and decreases in the endothelium-derived vasoconstrictor (e.g., endothelin) and vasodilator (e.g., nitric oxide and prostanoids) factors, respectively, also play a considerable role in the renal vascular spasm induced by CyA (Perico et al 1986;Zoja et al 1986;Gossmann et al 2001). Recent reports from our laboratory implicated the male gonadal hormone testosterone in the deleterious cardiovascular and renal effects of CyA (El-Mas et al 2002, 2003 and suggested differential contributions of endothelial-relaxing factors in CyA nephrotoxicity (El-Mas et al 2004a, 2004b.…”

Section: Introductionmentioning

confidence: 93%

“…The rat kidney was isolated and perfused according to the method described in our previous studies (El-Mas et al 2003, 2004a, 2004b. Briefly, rats were anesthetized with thiopental sodium (50 mg/kg, i.p.…”

Section: Rat Isolated Perfused Kidneymentioning

confidence: 99%

“…To standardize the vasodilator responses to SKF38393 or nitroprusside, a bolus dose of papaverine (50 nmol) was injected, and the effects of SKF38393 or nitroprusside were expressed as a percentage of the papaverine vasodilation (El-Mas et al 2003, 2004a, 2004b. This dose of papaverine caused an approximately 80% reduction in phenylephrineinduced tone.…”

Section: Effect Of Cya On Vasodilatory Responses To Skf38393 or Sodiumentioning

confidence: 99%

See 1 more Smart Citation

The α₁-adrenergic receptor not the DA₁-dopaminergic receptor mediates cyclosporine–SKF38393 renovascular interaction

El‐Mas

El-Din

El‐Gowilly

et al. 2005

Can. J. Physiol. Pharmacol.

Self Cite

View full text Add to dashboard Cite

In this study, we investigated the effect of acute exposure to cyclosporine A (CyA) on renal vasodilations evoked by the DA(1) dopaminergic agonist SKF38393 and whether dopamine DA(1) receptors are directly involved in the interaction. Changes evoked by CyA in SKF38393 vasodilations were evaluated in phenylephrine-preconstricted isolated perfused rat kidneys in the absence and presence of SCH23390, a DA(1) receptor antagonist. SKF38393 (3 x 10(-8) to 3 x 10(-6) mol) produced dose-dependent reductions in the renal perfusion pressure that were significantly attenuated in tissues pretreated with SCH23390 or CyA. Unlike SKF38393, the vasodilatory action of sodium nitroprusside, a nitrovasodilator, was not altered by CyA. The attenuating effect of CyA on SKF38393 vasodilations was preserved in preparations pretreated with SCH23390, suggesting that sites other than DA(1) receptors may be involved in CyA-SKF38393 interaction. The study was then extended to investigate the possible involvement of renal alpha1-adrenoceptors in the interaction. Blockade of alpha(1)-adrenoceptors by prazosin (30 nmol/L) significantly reduced the vasodilatory effect of SKF38393 and virtually abolished the CyA-induced attenuation of SKF38393 responses. Further, CyA failed to alter SKF38393 vasodilations when the renal tone was raised with prostaglandin F2alpha (PGF2alpha), a vasoconstrictor whose effect is independent of alpha(1)-adenoceptors. Together, these findings support earlier reports that both DA(1) and alpha(1)-receptors mediate the renal vasodilatory action of SKF38393 and suggest that CyA interacts selectively with the alpha(1)-receptor component to compromise SKF38393 responses.

show abstract

Male hypogonadism in cirrhosis and after liver transplantation

Foresta

Schipilliti

Ciarleglio

et al. 2008

J Endocrinol Invest

View full text Add to dashboard Cite

Liver is deeply involved in the metabolism of proteins, hormones, enzymes, cytokines, as well as in sex hormones catabolism. Gonadal function requires a normal liver function, and it is well known that clinical signs of hypogonadism are common in patients with liver cirrhosis. Few studies have focused on hypothalamic- pituitary-gonadal alterations in male cirrhotic patients or after orthotopic liver transplantation (OLT). The pathogenesis of hypogonadism in cirrhotic patients is complex and not well explained. It involves both a gonadal and a hypothalamic- pituitary dysfunction. After OLT the hypothalamic-pituitary-gonadal function partially improves, showing that the hepatic dysfunction before OLT is deeply involved in its pathogenesis. After OLT some alterations persist in some patients, both because of pre-existing gonadal alterations (toxic-metabolic damage) and immunosuppressive pharmacological side effects. Further studies will explain the relationship between hypogonadism and OLT outcome, and the role of androgen therapy in hypogonadism after OLT, in the early months and in the long term.

show abstract

Testosterone depletion contributes to cyclosporine-induced chronic impairment of acetylcholine renovascular relaxations

Cited by 40 publications

References 30 publications

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

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

The α₁-adrenergic receptor not the DA₁-dopaminergic receptor mediates cyclosporine–SKF38393 renovascular interaction

Male hypogonadism in cirrhosis and after liver transplantation

Contact Info

Product

Resources

About

Testosterone depletion contributes to cyclosporine-induced chronic impairment of acetylcholine renovascular relaxations

Cited by 40 publications

References 30 publications

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

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

The α1-adrenergic receptor not the DA1-dopaminergic receptor mediates cyclosporine–SKF38393 renovascular interaction

Male hypogonadism in cirrhosis and after liver transplantation

Contact Info

Product

Resources

About

The α₁-adrenergic receptor not the DA₁-dopaminergic receptor mediates cyclosporine–SKF38393 renovascular interaction