Role of Intrarenal Endothelin 1, Endothelin 3, and Angiotensin II Expression in Chronic Cyclosporin A Nephrotoxicity in Rats

2000 ◽  
Vol 8 (3) ◽  
pp. 161-172 ◽  
Author(s):  
César Ramírez ◽  
Asunción Olmo ◽  
Francisco O’Valle ◽  
Marco Masseroli ◽  
Mariano Aguilar ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cyclosporin A ◽  
Endothelin 1 ◽  
Endothelin 3

scholarly journals Role of Histone Demethylases in Cardiomyocytes Induced to Hypertrophy

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Wendy Rosales ◽  
Juan Carulla ◽  
Jeison García ◽  
Diana Vargas ◽  
Fernando Lizcano
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Transient Transfection ◽  
Cardiac Cells ◽  
Pcr Analysis ◽  
Histone Demethylases ◽  
Rat Cardiomyocytes ◽  
Endothelin 1 ◽  
Cardiac Gene

Epigenetic changes induced by histone demethylases play an important role in differentiation and pathological changes in cardiac cells. However, the role of the jumonji family of demethylases in the development of cardiac hypertrophy remains elusive. In this study, the presence of different histone demethylases in cardiac cells was evaluated after hypertrophy was induced with neurohormones. A cell line from rat cardiomyocytes was used as a biological model. The phenotypic profiles of the cells, as well as the expression of histone demethylases, were studied through immunofluorescence, transient transfection, western blot, and qRT-PCR analysis after inducing hypertrophy by angiotensin II and endothelin-1. An increase in fetal gene expression (ANP, BNP, andβ-MHC) was observed in cardiomyocytes after treatment with angiotensin II and endothelin-1. A significant increase in JMJD2A expression, but not in UTX or JMJD2C expression, was observed. When JMJD2A was overexpressed in cardiomyocytes through transient transfection, the effect of neurohormones on fetal cardiac gene expression was increased. We conclude that JMJD2A plays a principal role in the regulation of fetal cardiac genes, which increase in expression during the pathological hypertrophic process.

Endothelin receptors in human placenta: relationship to vascular resistance and thromboxane release

1990 ◽  
Vol 258 (5) ◽  
pp. E864-E870
Author(s):  
B. M. Wilkes ◽  
P. F. Mento ◽  
A. M. Hollander ◽  
M. E. Maita ◽  
S. Sung ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Human Placenta ◽  
Competitive Inhibition ◽  
Scatchard Analysis ◽  
Binding Studies ◽  
Single Class ◽  
Endothelin 1 ◽  
Binding Data ◽  
Endothelin 3

This investigation was performed to study the potential role of endothelin in the modulation of fetoplacental vascular resistance in the human placenta. Full-term placentas from uncomplicated pregnancies were studied within 30 min of delivery. The umbilical artery and vein to a single placental cotyledon were cannulated and the artery perfused with RPMI media (0.82 ml/min). Endothelin 1 caused a sustained dose-dependent increase in perfusion pressure. Infused endothelin 1 (50 nM) stimulated thromboxane release 2.3-fold compared with basal values. Thromboxane release persisted for 15 min after discontinuation of endothelin. Properties of human placental endothelin 1 receptors were defined in binding studies performed on a crude membrane fraction of placental cotyledons. Binding was saturable, reached steady state by 3 h at 25 degrees C, and was linear with protein concentration. Scatchard analysis of binding data indicated a single class of high-affinity binding sites with a Kd of 36.1 +/- 9.7 pM and a density of 185.4 +/- 9.6 fmol/mg protein (n = 5). The potency order for competitive inhibition of the binding of 125I-labeled endothelin 1 was endothelin 1 greater than endothelin 2 = endothelin 3 = sarafotoxin S6b greater than big endothelin (human) = big endothelin (porcine). Phenylephrine, bradykinin, norepinephrine, atrial natriuretic factor, diltiazem, U46619, and angiotensin II did not displace 125I-endothelin 1 from its receptors. These experiments demonstrate that endothelin 1 is a potent pressor substance in the human fetoplacental cotyledon. Pressor effects of endothelin may be mediated by a combination of direct effects and stimulation of vasoconstrictor prostanoids.

Role of angiotensin II in the response to endothelin-1 of goat cerebral arteries after ischemia–reperfusion

2009 ◽  
Vol 50 (5-6) ◽  
pp. 160-165 ◽  
Author(s):  
Adely Salcedo ◽  
Nuria Fernández ◽  
Angel Luis García Villalón ◽  
Luis Monge ◽  
Raúl Narváez Sánchez ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Ischemia Reperfusion ◽  
Cerebral Arteries ◽  
Endothelin 1

Role of endothelin-1 in microvascular dysfunction caused by cyclosporin a

2003 ◽  
Vol 196 (4) ◽  
pp. 584-591 ◽  
Author(s):  
Chumpon Wilasrusmee ◽  
Monica Da Silva ◽  
Josephine Siddiqui ◽  
David Bruch ◽  
Smita Kittur ◽  
...  
Keyword(s):  
Cyclosporin A ◽  
Microvascular Dysfunction ◽  
Endothelin 1

scholarly journals Role of endothelin-1 and thromboxane A2 in renal vasoconstriction induced by angiotensin II in diabetes and hypertension

2002 ◽  
Vol 62 ◽  
pp. S2-S7 ◽  
Author(s):  
Eva Cediel ◽  
Beatriz Vázquez-Cruz ◽  
Josefa Navarro-Cid ◽  
Natalia De Las Heras ◽  
David Sanz-Rosa ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Thromboxane A2 ◽  
Renal Vasoconstriction ◽  
Endothelin 1

ANGIOTENSIN-II-INDUCED ENDOTHELIN-1 PRODUCTION CONTRIBUTES TO THE INCREASED COX-2 EXPRESSION IN HYPERTENSIVE RATS. ROLE OF PPAR: PP.24.478

2010 ◽  
Vol 28 ◽  
pp. e389
Author(s):  
R Palacios ◽  
JV V-Girón ◽  
A Martín ◽  
R Hernanz ◽  
AM Briones ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Hypertensive Rats ◽  
Endothelin 1 ◽  
Cox 2

scholarly journals Trophic effect of angiotensin II in neonatal rat cardiomyocytes: role of endothelin-1 and non-myocyte cells

1997 ◽  
Vol 121 (1) ◽  
pp. 118-124 ◽  
Author(s):  
Klaus Pönicke ◽  
Ingrid Heinroth-Hoffmann ◽  
Karin Becker ◽  
Otto-Erich Brodde
Keyword(s):  
Angiotensin Ii ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Trophic Effect ◽  
Endothelin 1 ◽  
Neonatal Rat Cardiomyocytes

Receptor externalization determines sustained contractile responses to endothelin-1 in the rat aorta

1993 ◽  
Vol 264 (3) ◽  
pp. C687-C693 ◽  
Author(s):  
R. Marsault ◽  
E. Feolde ◽  
C. Frelin
Keyword(s):  
Angiotensin Ii ◽  
Cell Surface ◽  
Dissociation Constant ◽  
Rat Aorta ◽  
Receptor Internalization ◽  
Contractile Responses ◽  
Endothelin 1 ◽  
Receptor Sites

The role of receptor internalization and recycling in the vasoconstrictor action of endothelin-1 (ET-1) is investigated using a combination of biochemical and physiological experiments. The binding of 125I-ET-1 to cultured aortic myocytes is first defined. Binding is rapidly followed by an internalization of the peptide. Part of the receptor sites then slowly reappears at the cell surface via a cycloheximide-insensitive mechanism. Evidence that externalizing receptors are functional and can trigger contractions is presented. Finally, the actions of cyclo[D-Trp-D-Asp-Pro-D-Val-Leu] (BQ-123), an antagonist of ETA receptors, are investigated. BQ-123 prevents 125I-ET-1 binding to aortic myocytes (dissociation constant, 10 nM). It prevents the constricting action of ET-1 but not that of angiotensin II. BQ-123 also relaxes almost completely aortic strips that have been precontracted by ET-1 irrespective of the time of its addition. It is concluded that a recycling of internalized ET-1 receptors occurs in ET-1-treated aortic myocytes. This process amplifies the action of the peptide and is probably responsible for the unique contractile action of ET-1.

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