scholarly journals Intrapulmonary Activation of the Angiotensin-Converting Enzyme Type 2/Angiotensin 1-7/G-Protein-Coupled Mas Receptor Axis Attenuates Pulmonary Hypertension in Ren-2 Transgenic Rats Exposed to Chronic Hypoxia

2015 ◽  
pp. 25-38 ◽  
Author(s):  
V. HAMPL ◽  
J. HERGET ◽  
J. BÍBOVÁ ◽  
A. BAŇASOVÁ ◽  
Z. HUSKOVÁ ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pulmonary Hypertension ◽  
Receptor Gene ◽  
Ang Ii ◽  
Transgenic Rats ◽  
Hypoxic Pulmonary Hypertension ◽  
Mas Receptor ◽  
Receptor Gene Expression ◽  
Expression And Activity

The present study was performed to evaluate the role of intrapulmonary activity of the two axes of the renin-angiotensin system (RAS): vasoconstrictor angiotensin-converting enzyme (ACE)/angiotensin II (ANG II)/ANG II type 1 receptor (AT1) axis, and vasodilator ACE type 2 (ACE2)/angiotensin 1-7 (ANG 1-7)/Mas receptor axis, in the development of hypoxic pulmonary hypertension in Ren-2 transgenic rats (TGR). Transgene-negative Hannover Sprague-Dawley (HanSD) rats served as controls. Both TGR and HanSD rats responded to two weeks´ exposure to hypoxia with a significant increase in mean pulmonary arterial pressure (MPAP), however, the increase was much less pronounced in the former. The attenuation of hypoxic pulmonary hypertension in TGR as compared to HanSD rats was associated with inhibition of ACE gene expression and activity, inhibition of AT1 receptor gene expression and suppression of ANG II levels in lung tissue. Simultaneously, there was an increase in lung ACE2 gene expression and activity and, in particular, ANG 1-7 concentrations and Mas receptor gene expression. We propose that a combination of suppression of ACE/ANG II/AT1 receptor axis and activation of ACE2/ANG 1-7/Mas receptor axis of the RAS in the lung tissue is the main mechanism explaining attenuation of hypoxic pulmonary hypertension in TGR as compared with HanSD rats.

scholarly journals Regulation of angiotensin II type 2 receptor gene expression in the adrenal medulla by acute and repeated immobilization stress

2012 ◽  
Vol 215 (2) ◽  
pp. 291-301 ◽  
Author(s):  
Regina Nostramo ◽  
Andrej Tillinger ◽  
Juan M Saavedra ◽  
Ashok Kumar ◽  
Varunkumar Pandey ◽  
...  
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Receptor Gene ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Ang Ii ◽  
Catecholamine Biosynthesis ◽  
Receptor Mrna ◽  
Receptor Gene Expression

While the renin–angiotensin system is important for adrenomedullary responses to stress, the involvement of specific angiotensin II (Ang II) receptor subtypes is unclear. We examined gene expression changes of angiotensin II type 1A (AT1A) and type 2 (AT2) receptors in rat adrenal medulla in response to immobilization stress (IMO). AT2 receptor mRNA levels decreased immediately after a single 2-h IMO. Repeated IMO also decreased AT2 receptor mRNA levels, but the decline was more transient. AT1A receptor mRNA levels were unaltered with either single or repeated IMO, although binding was increased following repeated IMO. These effects of stress on Ang II receptor expression may alter catecholamine biosynthesis, as tyrosine hydroxylase and dopamine β-hydroxylase mRNA levels in PC12 cells are decreased with Ang II treatment in the presence of ZD7155 (AT1 receptor antagonist) or with CGP42112 (AT2 receptor agonist) treatment. Involvement of stress-triggered activation of the hypothalamic–pituitary–adrenocortical or sympathoadrenal axis in AT2 receptor downregulation was examined. Cultured cells treated with the synthetic glucocorticoid dexamethasone displayed a transcriptionally mediated decrease in AT2 receptor mRNA levels. However, glucocorticoids are not required for the immediate stress-triggered decrease in AT2 receptor gene expression, as demonstrated in corticotropin-releasing hormone knockout (Crh KO) mice and hypophysectomized rats, although they can regulate basal gene expression. cAMP and pituitary adenylate cyclase-activating polypeptide also reduced AT2 receptor gene expression and may mediate this response. Overall, the effects of stress on adrenomedullary AT1A and AT2 receptor expression may contribute to allostatic changes, such as regulation of catecholamine biosynthesis.

Selective downregulation of ANP-clearance-receptor gene expression in lung of rats adapted to hypoxia

1995 ◽  
Vol 268 (2) ◽  
pp. L328-L335 ◽  
Author(s):  
H. Li ◽  
S. Oparil ◽  
Q. C. Meng ◽  
T. S. Elton ◽  
Y. F. Chen
Keyword(s):  
Gene Expression ◽  
Pulmonary Hypertension ◽  
Guanylate Cyclase ◽  
Receptor Gene ◽  
Compensatory Mechanism ◽  
Mrna Levels ◽  
Short Term ◽  
Hypoxic Pulmonary Hypertension ◽  
Clearance Receptor ◽  
Receptor Gene Expression

To test the hypothesis that expression of atrial natriuretic peptide (ANP)-receptor genes is modified to provide a compensatory mechanism against hypoxic pulmonary hypertension, steady state mRNA levels for the ANP-A receptor (or guanylate cyclase-A; ANPAR), ANP-B receptor (or guanylate cyclase-B; ANPBR), and ANP-clearance receptor (ANPCR) were quantitated by Northern blot and slot-blot analysis in lung, kidney, spleen, and liver of hypoxia-adapted rats and air controls. Exposure of rats to short-term (48 h) and chronic (4 wk) hypoxia (10% O2, 1 atm) did not affect lung ANPAR-mRNA levels. Lung ANPBR-mRNA levels were unchanged by short-term hypoxia but selectively increased (approximately twofold) by chronic hypoxia. ANPCR-mRNA levels were selectively and significantly downregulated by 48-h and 4-wk hypoxia in lung but were unchanged or upregulated in other tissues. Lung ANPCR gene transcription, assessed by nuclear-runoff analysis, was decreased by hypoxia. These data support the conclusion that altered pulmonary ANP-receptor gene expression modulates the development of hypoxic pulmonary hypertension.

scholarly journals Selective Upregulation of Endothelin B Receptor Gene Expression in Severe Pulmonary Hypertension

Circulation ◽  
2002 ◽  
Vol 105 (9) ◽  
pp. 1034-1036 ◽  
Author(s):  
Michael Bauer ◽  
Heinrike Wilkens ◽  
Frank Langer ◽  
Sven O. Schneider ◽  
Henning Lausberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pulmonary Hypertension ◽  
Receptor Gene ◽  
Severe Pulmonary Hypertension ◽  
Endothelin B Receptor ◽  
Endothelin B ◽  
Receptor Gene Expression

Impact of reference gene selection for type 2 cannabinoid receptor gene expression studies in human spermatozoa

Andrologia ◽  
2012 ◽  
Vol 45 (4) ◽  
pp. 278-284 ◽  
Author(s):  
A. A. Amoako ◽  
A. K. Gebeh ◽  
E. L. Marczylo ◽  
J. M. Willets ◽  
J. Elson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Reference Gene ◽  
Gene Selection ◽  
Cannabinoid Receptor ◽  
Receptor Gene ◽  
Expression Studies ◽  
Selection For ◽  
Gene Expression Studies ◽  
Receptor Gene Expression

scholarly journals Type 2 inositol trisphosphate receptor gene expression in hepatocytes is regulated by cyclic AMP

2017 ◽  
Vol 486 (3) ◽  
pp. 659-664 ◽  
Author(s):  
Emma Kruglov ◽  
Meenakshisundaram Ananthanarayanan ◽  
Pedro Sousa ◽  
Jittima Weerachayaphorn ◽  
Mateus T. Guerra ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cyclic Amp ◽  
Receptor Gene ◽  
Inositol Trisphosphate ◽  
Inositol Trisphosphate Receptor ◽  
Trisphosphate Receptor ◽  
Receptor Gene Expression

scholarly journals Serum 25-Hydroxyvitamin D and Adipose Tissue Vitamin D Receptor Gene Expression: Relationship With Obesity and Type 2 Diabetes

2015 ◽  
Vol 100 (4) ◽  
pp. E591-E595 ◽  
Author(s):  
Mercedes Clemente-Postigo ◽  
Araceli Muñoz-Garach ◽  
Marta Serrano ◽  
Lourdes Garrido-Sánchez ◽  
M. Rosa Bernal-López ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type 2 Diabetes ◽  
Vitamin D ◽  
Receptor Gene ◽  
Vitamin D Receptor Gene ◽  
Hydroxyvitamin D ◽  
25 Hydroxyvitamin D ◽  
Receptor Gene Expression ◽  
Tissue Vitamin

Increase of cardiac M2-muscarinic receptor gene expression in type-1 but not in type-2 diabetic rats

2008 ◽  
Vol 441 (2) ◽  
pp. 201-204 ◽  
Author(s):  
Liang-Ming Lee ◽  
Cheng Kuei Chang ◽  
Kai-Chun Cheng ◽  
Dai-Huang Kou ◽  
I-Min Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Muscarinic Receptor ◽  
Receptor Gene ◽  
Diabetic Rats ◽  
M2 Muscarinic Receptor ◽  
Receptor Gene Expression ◽  
Type 2 Diabetic

scholarly journals Down-Regulation by cAMP of Angiotensin II Type 2 Receptor Gene Expression in PC12 Cells.

1996 ◽  
Vol 19 (4) ◽  
pp. 271-279 ◽  
Author(s):  
Satoshi Murasawa ◽  
Hiroaki Matsubara ◽  
Kazuhisa Kijima ◽  
Katsuya Maruyama ◽  
Naohiko Ohkubo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Pc12 Cells ◽  
Receptor Gene ◽  
Down Regulation ◽  
Receptor Gene Expression

Effects of angiotensin II receptor blockade versus angiotensin-converting-enzyme inhibition on ventricular remodelling following myocardial infarction in the mouse

2003 ◽  
Vol 104 (2) ◽  
pp. 109-118 ◽  
Author(s):  
Richard D. PATTEN ◽  
Mark J. ARONOVITZ ◽  
Michael EINSTEIN ◽  
Matthew LAMBERT ◽  
Natesa G. PANDIAN ◽  
...  
Keyword(s):  
Gene Expression ◽  
Collagen Type ◽  
Receptor Gene ◽  
Ace Inhibition ◽  
At1 Receptor ◽  
Ang Ii ◽  
At1a Receptor ◽  
Collagen Type 1 ◽  
Receptor Gene Expression

Left ventricular (LV) remodelling following myocardial infarction (MI) is associated with increased morbidity and mortality. Previous data suggest that angiotensin II (Ang II) plays a central role in the molecular events contributing to LV remodelling. We explored the effects of angiotensin-converting-enzyme (ACE) inhibition versus Ang II (AT1) receptor blockade on LV remodelling in mice post-MI. Mice underwent sham procedure or left coronary artery ligation, and received placebo, the AT1 receptor antagonist, losartan or the ACE inhibitor, enalapril. At 6 weeks, echocardiography and haemodynamic studies were performed. Infarct size and interstitial collagen content were determined. Expression of genes encoding atrial natriuretic peptide (ANP), collagen type I, AT1a and AT1b receptors were measured. The placebo MI group showed increased LV end-diastolic diameter, LV end-systolic diameter with depressed fractional shortening (P<0.01 versus shams), increased LV mass and volume (both P<0.01 versus shams). The placebo MI group also exhibited increased non-infarct zone collagen content (P<0.01), ANP (P<0.01) and collagen type 1 (P<0.01) gene expression, with a non-significant rise in AT1a receptor gene expression. Neither losartan or enalapril prevented LV dilation or improved fractional shortening. Both similarly lowered systolic blood pressure (P<0.01 for each versus placebo). Losartan and enalapril inhibited LV hypertrophy (P<0.01), and decreased ANP (P<0.01) and collagen type 1 gene expression (P<0.05). Levels of AT1a receptor gene expression were higher than shams (P<0.05 for both), but similar to placebo. AT1b receptor gene expression was much lower than that for AT1a receptor and similar in all groups. Thus, in this model, AT1 receptor antagonism and ACE inhibition have equivalent inhibitory effects on myocardial hypertrophy and fibrosis. These results serve as an important basis for planned investigations to evaluate the anti-remodelling effects of these agents on mice in which genetic manipulations are used to disrupt components of the Ang II signalling system.

Laughter modulates prorenin receptor gene expression in patients with type 2 diabetes

2007 ◽  
Vol 62 (6) ◽  
pp. 703-706 ◽  
Author(s):  
Takashi Hayashi ◽  
Osamu Urayama ◽  
Miyo Hori ◽  
Shigeko Sakamoto ◽  
Uddin Mohammad Nasir ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type 2 Diabetes ◽  
Receptor Gene ◽  
Prorenin Receptor ◽  
Receptor Gene Expression
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