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Crosstalk between angiotensin II and endothelin

Colin A Nurse, Erin M Leonard, Shaima Salman
Mammalian carotid bodies (CB) are chemosensory organs that mediate compensatory cardiorespiratory reflexes in response to low blood PO2 (hypoxemia) and elevated CO2 /H+ (acid hypercapnia). The chemoreceptors are glomus or type I cells that occur in clusters enveloped by neighboring glial-like type II cells. During chemoexcitation type I cells depolarize, leading to Ca2+ -dependent release of several neurotransmitters, some excitatory and others inhibitory, that help shape the afferent carotid sinus nerve (CSN) discharge...
April 1, 2018: Physiological Genomics
Stefan Wanderer, Jan Mrosek, Hartmut Vatter, Volker Seifert, Juergen Konczalla
Under physiologic conditions, losartan showed a dose-dependent antagonistic effect to the endothelin-1 (ET-1)-mediated vasoconstriction. This reduced vasoconstriction was abolished after preincubation with an endothelin B1 receptor (ET(B1 )-receptor) antagonist. Also, an increased ET(B1 )-receptor-dependent relaxation to sarafotoxin S6c (S6c; an ET(B1 )-receptor agonist) was detected by preincubation with losartan. Investigations after experimental induced subarachnoid hemorrhage (SAH) are still missing. Therefore, we analyzed losartan in a further pathological setup...
April 2018: Neurosurgical Review
Xinyu Weng, Liming Yu, Peng Liang, Luyang Li, Xin Dai, Bisheng Zhou, Xiaoyan Wu, Huihui Xu, Mingming Fang, Qi Chen, Yong Xu
Angiotensin II (Ang II) induces cardiac hypertrophy and fibrosis in part by stimulating endothelin (ET-1) transcription. The involvement of the epigenetic machinery in this process is largely undefined. In the present study, we examined the epigenetic maneuvering underlying cardiac hypertrophy and fibrosis following ET-1 transactivation by Ang II. In response to Ang II stimulation, core components of the mammalian chromatin remodeling complex (Brahma-related gene 1, or Brg1, and Brahma or Brm) and histone H3K4 methylation complex (Ash2, absent, small, or homeotic discs 2, or Ash2 and WD domain repeat 5, or Wdr5) were recruited to the ET-1 promoter region in endothelial cells...
May 2015: Journal of Molecular and Cellular Cardiology
Juergen Konczalla, Stefan Wanderer, Jan Mrosek, Patrick Schuss, Johannes Platz, Erdem Güresir, Volker Seifert, Hartmut Vatter
Investigations have shown a multifactorial process as cause for the poor outcome after subarachnoid hemorrhage (SAH), including inflammation, early brain injury, cortical spreading depression, lack of cerebral autoregulation and the cerebral vasospasm (CVS) itself. Losartan may have a beneficial effect after SAH - preventing CVS, restoring cerebral autoregulation, reducing inflammation and early brain injury. Also some data is available for an AT1-receptor-upregulation and upregulated gene expression after subarachnoid hemorrhage, but the functional role of angiotensin on the cerebrovascular contractility is still not completely understood...
November 2013: Current Neurovascular Research
Chao He, Xiongying Miao, Jiequn Li, Haizhi Qi
BACKGROUND: Both angiotensin (Ang)-II and endothelin-1 (ET-1) are involved in the pathogenesis of liver fibrosis. Activated hepatic stellate cells (HSCs) are considered a key effector of liver fibrosis. AIMS: To explore the effect of Ang-II on ET-1 expression in cultured human HSCs and the underlying mechanisms. METHODS: Human HSCs were treated with Ang-II in different concentrations (0.1, 0.5, 1, 5, or 10 nM) for different lengths of time (0...
September 2013: Digestive Diseases and Sciences
Claudia Grossmann, Michael Gekle
The mineralocorticoid receptor (MR) is a steroid receptor that physiologically regulates water and electrolyte homeostasis but that can also induce pathophysiological effects in the renocardiovascular system. Classically, the MR acts as a transcription factor at glucocorticoid response elements but additional protein-protein interactions with other signaling cascades have been described. Of these, the crosstalk with EGFR signaling is especially interesting because various vasoactive substances like angiotensin II and endothelin-1 also mediate their pathophysiological effects via the EGFR...
March 24, 2012: Molecular and Cellular Endocrinology
R L Webb, M de Gasparo
Despite an enormous amount of research carried out in the past 10 to 20 years, the role of the renin-angiotensin system in the development of heart failure is still not very well understood. This review looks at preclinical data on the role of angiotensin II as a circulating and local hormone, and the effects of stimulation of the respective receptors in heart tissue. Recent large scale clinical trials have begun to furnish evidence of the effects of blocking the renin-angiotensin system in patients with heart failure using angiotensin-converting enzyme inhibitors or, more recently, angiotensin II receptor blockers that act directly at the receptor level, independent of pathways for angiotensin II generation...
2001: Experimental and Clinical Cardiology
A P Fontes-Sousa, A L Pires, V F Monteiro-Cardoso, A F Leite-Moreira
Endogenous regulators, such as angiotensin-II (AngII), endothelin-1 (ET-1) and urotensin-II (U-II) are released from various cell types and their plasma levels are elevated in several cardiovascular diseases. The present study evaluated a potential crosstalk between these systems by investigating if the myocardial effects of U-II are modulated by AngII or ET-1. Effects of U-II (10(-8), 10(-7), 10(-6) M) were tested in rabbit papillary muscles in the absence and in the presence of losartan (selective AT(1) receptor antagonist), PD-145065 (nonselective ET-1 receptors antagonist), losartan plus PD-145065, AngII or ET-1...
2009: Physiological Research
Susana López-Ongil, M-Luisa Díez-Marqués, Mercedes Griera, Manuel Rodríguez-Puyol, Diego Rodríguez-Puyol
OBJECTIVE: Since mesangial and endothelial cells interact in the kidney, the present experiments were designed to analyze the ability of human mesangial cells (HMC) to modulate endothelin-1 (ET-1) synthesis by human umbilical vein endothelial cells (HuVEC). METHODS AND RESULTS: The supernatants of HuVEC/HMC contained significantly lower amounts of ET-1 than those of HuVEC alone. This effect was not due to a decreased prepro-ET-1 mRNA expression and was only partially the consequence of HMC-dependent ET-1 degradation...
2005: Cellular Physiology and Biochemistry
Y Iwanaga, Y Kihara, K Inagaki, Y Onozawa, T Yoneda, K Kataoka, S Sasayama
BACKGROUND: In view of their mutual crosstalk, the roles of angiotensin II (Ang II) and endothelin-1 (ET-1) in the myocardium are assumed to be synergistic and supplemental. METHODS AND RESULTS: In the phase of compensated left ventricular (LV) hypertrophy of Dahl salt-sensitive rats, Ang II peptide and the ACE mRNA in the LV were increased by 1.6- and 3.8-fold, respectively. In contrast, ET-1 peptide and the preproET-1 mRNA remained unchanged. In subsequent congestive heart failure (CHF), Ang II and ACE mRNA did not show further increases...
July 31, 2001: Circulation
M Lavallée, M Takamura, R Parent, E Thorin
Several lines of evidence indicate that nitric oxide (NO) impairs endothelin (ET) production/action in vitro. Acute pressor responses caused by the blockade of NO formation with arginine analogues in vivo are blunted by selective ET(A) or dual ET(A)/ET(B) receptor blockade whereas blockade of NO formation magnifies ET-induced constriction of various vascular territories. Given that ET receptor blockade has normally limited effects on mean arterial pressure, the reversal of pressor responses caused by the blockade of NO formation with ET receptor blockade most likely reflects a significant crosstalk between NO and ET...
December 2001: Heart Failure Reviews
M Harada, Y Saito, O Nakagawa, Y Miyamoto, M Ishikawa, K Kuwahara, E Ogawa, M Nakayama, S Kamitani, I Hamanaka, N Kajiyama, I Masuda, H Itoh, I Tanaka, K Nakao
In cardiac hypertrophy or ventricular remodeling, not only the enlargement of myocytes but also interstitial or perivascular fibrosis are observed simultaneously, which suggests an interaction between cardiac myocytes and fibroblasts. In this study, we examined the mechanism of cyclic mechanical stretch-induced myocyte hypertrophy, highlighting the interaction between myocytes and cardiac nonmyocytes, mostly fibroblasts. Ventricular myocytes (MC) and cardiac nonmyocytes (NMC) were separately extracted from neonatal rat ventricles by the discontinuous Percoll gradient method and primary cultures of cardiac cells were prepared...
1997: Heart and Vessels
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