Carvedilol protects the peritubular capillaries and kidney structure in spontaneously hypertensive rats

Cao, Gabriel; Llambí, Hernán Gómez; Ottaviano, G; Müller, Angélica; Milei, José

doi:10.1016/j.ijcard.2014.12.049

Cited by 3 publications

(3 citation statements)

References 10 publications

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“…The severity of these pathological changes was less in the carvedilol and nebivolol pre-treated rats. This agree with Nakamoto et al [3] , Cao et al [9] , Moningka et al [32] Despite extensive research, the precise roles of different MAPKs in renal pathology, especially in hypoxic/ischemic nephropathy, are still not well understood, and there are major controversies. For example, some studies showed that, activation of ERK1/2 in the human kidney with glomerulopathies correlated with cell proliferation, histologic lesions, renal fibrosis [33] , while other work suggests that apoptosis in diabetic rat kidneys is likely related to a decrease in pERK1/2 levels.…”

Section: Discussionsupporting

confidence: 85%

“…Experimental design: Rats were randomly divided into five groups, each containing (7) rats: Group (I): Sham-operated, received 1% DMSO; Group (II): Untreated renal hypertensive, received 1% DMSO; Group (III): Carvedilol pre-treated (20 mg/kg, dissolved in 1% DMSO) [9] ; Group (IV): Nebivolol pre-treated (10 mg/kg, dissolved in 1% DMSO) [10] ; Group (V): Nadolol pre-treated (50 mg/kg, dissolved in distilled water) [11] . Hypertension was induced in rats by persistent complete left renal artery ligation.…”

Section: Materials and Methods Animalsmentioning

confidence: 99%

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Carvedilol and nebivolol protect the kidney against renal ischemia in Wistar rats.

Abdelhamid¹,

Moustafa²,

Sekinah³

et al. 2019

Zagazig University Medical Journal

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Background: Classical β-blockers usually reduce renal blood flow thus, worsening renal function in hypertensive patients with renal impairment. However, vasodilator -blockers with biased agonist activity on -arrestin, at least theoretically, could protect the kidney against ischemia. Objectives: To compare the effect of prophylactic administration of carvedilol, nebivolol, nadolol on the kidneys. Materials & Methods: Rats were divided into five groups: Group1: shamoperated; Group2: Untreated hypertensive; Group3: Carvedilol pre-treated; Group4: Nebivolol pre-treated; Group5: Nadolol pre-treated. MABP, serum urea, creatinine, renal level of TNFα, BAX and pERK1/2 to non-pERK1/2 ratio were measured, besides renal histopathology and Bax immunohistochemistry. Results: In carvedilol and nebivolol groups, MABP, Bax, TNFα and pERK1/2 to non-pERK1/2 ratio were not only significantly (P<0.05) lower than that of the untreated group; but also, not significantly different from that of the sham; except significantly higher pERK1/2 to non-pERK1/2 ratio. In the nadolol pre-treated rats, MABP and the pERK1/2 to non-pERK1/2 ratio were significantly lower than that of the untreated hypertensive rats, however, they were significantly higher than that of the carvedilol, nebivolol pre-treated groups and the sham-operated group. Furthermore, Bax and TNFα were not significantly different from that of the untreated hypertensive group; in the meantime, they were significantly higher compared to sham, carvedilol and nebivolol pretreated groups. Serum urea& creatinine levels were significantly higher in nadolol pretreated group compared to other groups. Conclusion: Carvedilol and nebivolol have renal protective effect which is nearly equal in contrast to the deterioration caused by nadolol.

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Section: Discussionsupporting

confidence: 85%

Section: Materials and Methods Animalsmentioning

confidence: 99%

Carvedilol and nebivolol protect the kidney against renal ischemia in Wistar rats.

Abdelhamid¹,

Moustafa²,

Sekinah³

et al. 2019

Zagazig University Medical Journal

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“…Carvedilol is a novel NSBB with additional anti-α 1 -adrenergic activity and is more effective than traditional NSBBs (propranolol and nadolol) for the primary prophylaxis of variceal bleeding [18]. Recently, several studies in the cardiovascular field found that carvedilol could improve vascular structural remodeling [19–21]. Our previous study confirmed that carvedilol inhibited angiogenesis in vitro [22].…”

Section: Introductionmentioning

confidence: 66%

Carvedilol Ameliorates Intrahepatic Angiogenesis, Sinusoidal Remodeling and Portal Pressure in Cirrhotic Rats

Ling

Meng

et al. 2018

Med Sci Monit

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BackgroundCarvedilol is the first-line drug for the primary prophylaxis of variceal bleeding due to portal hypertension (PHT) in liver cirrhosis. This study aimed to investigate the effects of carvedilol on intrahepatic angiogenesis and sinusoidal remodeling in cirrhotic rats and explore the underlying mechanisms of carvedilol in PHT.Materials/MethodsFor in vivo experiments, carbon tetrachloride was used to induce liver cirrhosis in rats, and carvedilol was simultaneously administered by gavage. The portal pressure was measured in rats, and liver tissues were examined by immunohistochemistry. Sinusoidal remodeling was observed by transmission electron microscopy. For in vitro experiments, the effects of carvedilol on fibronectin (FN) synthesis in human umbilical vein endothelial cells (HUVECs) were explored by quantitative real-time polymerase chain reaction and western blot analysis.ResultsPortal vein pressure measurements showed that carvedilol reduced portal pressure in cirrhotic rats. Immunohistochemistry assays indicated that carvedilol ameliorated intrahepatic angiogenesis. Transmission electron microscopy examination demonstrated that carvedilol improved sinusoidal remodeling. In the in vitro experiments, carvedilol suppressed transforming growth factor β1 (TGFβ1)-induced FN synthesis in HUVECs by inhibition of the TGFβ1/Smads pathway.ConclusionsCarvedilol ameliorated intrahepatic angiogenesis, sinusoidal remodeling and portal pressure in cirrhotic rats. Carvedilol improved sinusoidal remodeling by suppressing FN synthesis in endothelial cells. Carvedilol has potential utility for treating early-stage liver cirrhosis.

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Negotiating renal dysfunction when treating patients with heart failure

Carubelli

Metra

Lund

2018

Expert Review of Cardiovascular Therapy

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Chronic kidney disease (CKD) is one of the most prevalent comorbidities in HF, and no specific treatment is still available for the so-called cardiorenal syndrome. Areas covered: The aim of this review is to describe the interaction of heart and kidney function and the consequences of cardiorenal syndrome, focusing on the use of available therapeutics. Expert commentary: The presence of CKD has been associated with adverse outcomes in HF regardless of ejection fraction. On the other hand, cardiovascular events are the most common causes of morbidity and mortality among CKD patients, reflecting the close pathophysiological crosstalk between these organs. Multiple mechanisms are involved in the development of cardiorenal syndrome, including hemodynamic, neurohormonal and inflammatory mediators. The management of several HF drugs is a challenge in the presence of CKD mainly due to blunted diuretic response and increased risk of worsening of kidney function. Therefore, finding a balance between the optimization of cardiac and renal outcomes is a real negotiation in the everyday clinical practice.

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Carvedilol protects the peritubular capillaries and kidney structure in spontaneously hypertensive rats

Cited by 3 publications

References 10 publications

Carvedilol and nebivolol protect the kidney against renal ischemia in Wistar rats.

Carvedilol and nebivolol protect the kidney against renal ischemia in Wistar rats.

Carvedilol Ameliorates Intrahepatic Angiogenesis, Sinusoidal Remodeling and Portal Pressure in Cirrhotic Rats

Negotiating renal dysfunction when treating patients with heart failure

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