Role of endothelin ETB receptor in the pathogenesis of monocrotaline-induced pulmonary hypertension in rats

Nishida, Masahiro; Okada, Yoshinori; Akiyoshi, Kenji; Eshiro, Keiko; Takaoka, Masanori; Gariepy, Cheryl E.; Yanagisawa, Masashi; Matsumura, Yasuo

doi:10.1016/j.ejphar.2004.06.028

Cited by 27 publications

(28 citation statements)

References 30 publications

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“…This result is in accordance with the findings of previous studies (Mei et al, 2011;Nishida et al, 2004). In addition, different groups which received barberry extract alone or plus monocrotaline and also sildenafil plus monocrotaline group did not show significant changes in systemic arterial pressure.…”

Section: Discussionsupporting

confidence: 83%

“…In agreement with previous studies (Mei et al, 2011;Nishida et al, 2004), we observed a significant increase in RVSP, as an equivalent parameter of pulmonary arterial pressure, and the RVH in the M group. In addition, monocrotaline increased the medial wall thickness of the pulmonary arterioles, which is consistent with previous studies (Mei et al, 2011;Nishida et al, 2004;Todd et al, 1985).…”

Section: Discussionsupporting

confidence: 81%

“…In addition, monocrotaline increased the medial wall thickness of the pulmonary arterioles, which is consistent with previous studies (Mei et al, 2011;Nishida et al, 2004;Todd et al, 1985). Barberry extract significantly decreased the monocrotaline-induced pulmonary arterial hypertension, the RVH, and also the medial wall thickness of pulmonary arterioles.…”

Section: Discussionsupporting

confidence: 81%

“…The right ventricular hypertrophy (RVH) index was calculated using the following formula: ''RVH ¼ 2 Â (RVFWT)/(LVFWT + IST)'', where RVFWT is the right ventricular free wall thickness, LVFWT is the left ventricular free wall thickness and IST is the interventricular septum thickness (Nishida et al, 2004).…”

Section: Right Ventricular Hypertrophy Indexmentioning

confidence: 99%

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The promising effect of barberry (Zereshk) extract against experimental pulmonary microvascular remodeling and hypertension: A comparison with sildenafil

Mahdavi

Joukar

Najafipour

et al. 2015

Pharmaceutical Biology

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Context: Despite the beneficial effects of barberry (Berberis integerrima Berberidaceae) on decreasing systemic hypertension, its influence has not been investigated on pulmonary hypertension. Objective: The objective of this study is to examine the effect of barberry fruit, on monocrotaline-induced pulmonary hypertension. Materials and methods: Nine groups were arranged as follows: the control group, the monocrotaline (M) group, the barberry groups with doses of 50, 100, and 200 (mg/kg), the M plus barberry groups, and the M plus sildenafil group. Two weeks after a single injection of monocrotaline (60 mg/kg, s.c.), barberry water extracts or sildenafil (30 mg/kg/d) were gavaged daily for 2 weeks. At the end of the 4th week, hemodynamic, biochemical, and histopathological parameters were assessed. Results: In comparison with the M group, barberry (200 mg/kg) or sildenafil significantly reduced the right ventricular systolic pressure (RVSP) (22.95 ± 1.78 mm Hg and 30.71 ± 1.64 mm Hg, versus 41.28 ± 1.5 mm Hg), right ventricular hypertrophy (RVH) (0.39 ± 0.03 and 0.42 ± 0.02, versus 0.57 ± 0.02), and the medial wall thickness (MWT) (4.56 ± 0.15 mm and 5.97 ± 0.19 mm, versus 7.02 ± 0.43 mm). Barberry or sildenafil had no significant effect on the plasma level of endothelin-1, glutathione peroxidase, and the malondialdehide of lung. Conclusion: 200 mg/kg of barberry has an improving effect on the monocrotaline-induced pulmonary hypertension. This effect was stronger than that of the sildenafil's and may have been mediated through mechanisms other than the modulation of the endothelin-1 or redox system.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 81%

Section: Discussionsupporting

confidence: 81%

Section: Right Ventricular Hypertrophy Indexmentioning

confidence: 99%

See 2 more Smart Citations

The promising effect of barberry (Zereshk) extract against experimental pulmonary microvascular remodeling and hypertension: A comparison with sildenafil

Mahdavi

Joukar

Najafipour

et al. 2015

Pharmaceutical Biology

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“…Pulmonary ET B clears endothelin-1 from the plasma, limiting the ET A-mediated vasoconstrictor (38). In rats, ET B deficiency exacerbates monocrotaline (39) and hypoxia-induced PH (40). Impaired extracellular ET B-mediated NO/prostaglandin 2 release from pulmonary resistance vessels during hypoxia may have contributed to the development of PAH (41).…”

Section: E C -S O D a N D T R E A T M E N T O F P U L M O N A R Y H Ymentioning

confidence: 99%

Extracellular Superoxide Dismutase Overexpression Can Reverse the Course of Hypoxia-Induced Pulmonary Hypertension

Ahmed

Zhang

Codipilly

et al. 2011

Mol Med

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Hypoxia leads to free radical production, which has a pivotal role in the pathophysiology of pulmonary hypertension (PH). We hypothesized that treatment with extracellular superoxide dismutase (EC-SOD) could ameliorate the development of PH induced by hypoxia. In vitro studies using pulmonary microvascular endothelial cells showed that cells transfected with EC-SOD had significantly less accumulation of xanthine oxidase and reactive oxygen species than nontransfected cells after hypoxia exposure for 24 h. To study the prophylactic role of EC-SOD, adult male wild-type (WT) and transgenic (TG) mice, with lung-specific overexpression of human EC-SOD (hEC-SOD), were exposed to fraction of inspired oxygen (FiO 2 ) 10% for 10 d. After exposure, right ventricular systolic pressure (RVSP), right ventricular mass (RV/S + LV), pulmonary vascular wall thickness (PVWT) and pulmonary artery contraction/relaxation were assessed. TG mice were protected against PH compared with WT mice with significantly lower RVSP (23.9 ± 1.24 versus 47.2 ± 3.4), RV/S + LV (0.287 ± 0.015 versus 0.335 ± 0.022) and vascular remodeling, indicated by PVWT (14.324 ± 1.107 versus 18.885 ± 1.529). Functional studies using pulmonary arteries isolated from mice indicated that EC-SOD prevents hypoxia-mediated attenuation of nitric oxide-induced relaxation. Therapeutic potential was assessed by exposing WT mice to FiO 2 10% for 10 d. Half of the group was transfected with plasmid containing cDNA encoding human EC-SOD. The remaining animals were transfected with empty vector. Both groups were exposed to FiO 2 10% for a further 10 d. Transfected mice had significantly reduced RVSP (18.97 ± 1.12 versus 41.3 ± 1.5), RV/S + LV (0.293 ± 0.012 versus 0.372 ± 0.014) and PVWT (12.51 ± 0.72 versus 18.98 ± 1.24). On the basis of these findings, we concluded that overexpression of EC-SOD prevents the development of PH and ameliorates established PH.

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Pulmonary Hypertension: Pathophysiology and Signaling Pathways

Maron¹,

Loscalzo²

2013

Handbook of Experimental Pharmacology

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Pulmonary hypertension (PH) is characterized by pathological changes to cell signaling pathways within the alveolar-pulmonary arteriole-right ventricular axis that results in increases in pulmonary vascular resistance and, ultimately, the development of right ventricular (RV) dysfunction. Cornerstone histopathological features of the PH vasculopathy include intimal thickening, concentric hypertrophy, and perivascular fibrosis of distal pulmonary arterioles. The presence of plexogenic lesions is pathognomonic of pulmonary arterial hypertension (PAH); when present, this severe form of remodeling is associated with subtotal obliteration of the blood vessel lumen. The extent of RV remodeling in PH correlates with clinical symptom severity and portends a poor outcome. Currently available PH-specific pharmacotherapies that aim to improve symptom burden by targeting pulmonary vasodilatory/vasoconstrictor cell signaling pathways do not fully reverse pulmonary vascular remodeling and, thus, are largely unsuccessful at maintaining normal cardiopulmonary hemodynamics long term. Thus, determining the molecular mechanisms that are responsible for pulmonary vascular remodeling in PH is of great potential therapeutic value, particularly pathways that promote apoptosis-resistant cellular proliferation, disrupt normal cellular bioenergetics to alter cell function, and/or modulate severely abnormal responses to pulmonary vascular injury. This chapter reviews current insights into PH pathophysiology and disease mechanisms, and discusses novel cell signaling pathways that implicate microRNAs and mitochondrial dysfunction in the development of the PH phenotype.

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Role of endothelin ETB receptor in the pathogenesis of monocrotaline-induced pulmonary hypertension in rats

Cited by 27 publications

References 30 publications

The promising effect of barberry (Zereshk) extract against experimental pulmonary microvascular remodeling and hypertension: A comparison with sildenafil

The promising effect of barberry (Zereshk) extract against experimental pulmonary microvascular remodeling and hypertension: A comparison with sildenafil

Extracellular Superoxide Dismutase Overexpression Can Reverse the Course of Hypoxia-Induced Pulmonary Hypertension

Pulmonary Hypertension: Pathophysiology and Signaling Pathways

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