scholarly journals Enrichment of (pro)renin receptor promoter with activating histone codes in the kidneys of spontaneously hypertensive rats

2011 ◽  
Vol 13 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Hae-Ahm Lee ◽  
Dong-Youb Lee ◽  
Hyo-Jung Lee ◽  
Hyung Soo Han ◽  
InKyeom Kim
Keyword(s):  
Real Time ◽  
Spontaneously Hypertensive Rats ◽  
Methylation Status ◽  
Histone H3 ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Spontaneously Hypertensive ◽  
Mrna And Protein Expression ◽  
Wistar Kyoto ◽  
Histone Codes

Background: The (pro)renin receptor [(P)RR] non-proteolytically, through conformational change, activates prorenin which can convert angiotensinogen to angiotensin I in addition to the classic conversion of angiotensinogen to angiotensin I by circulating renin. Since renal (P)RR is upregulated in hypertension and implicated in the pathogenesis of malignant hypertension, we hypothesized that (pro)renin receptor promoter is enriched with activating histone codes in the kidney of spontaneously hypertensive rats (SHR). Methods: The mRNA and protein expression levels were measured by real-time polymerase chain reaction (PCR) and western blot, respectively. The DNA methylation status of (P)RR promoter region was analyzed by bisulfite sequencing. The histone modifications were determined by chromatin immunoprecipitation followed by real-time PCR. Results: The (P)RR mRNA expression in the kidney was about six times greater in SHR than in Wistar–Kyoto (WKY) rats. The (P)RR promoter was little methylated in the kidneys of both WKY and SHR. Acetylated histone H3 (H3Ac) and di-methylated histone H3 at lysine 4 (H3K4me2), activating histone codes, were about 25 and three times higher in SHR than in WKY, respectively. On the other hand, di-methylated histone H3 at lysine 9 (H3K9me2), a suppressive histone code, was 50 times lower in SHR than in WKY. Conclusion: These results suggest that the (P)RR promoter is enriched with activating histone codes in the kidneys of SHR.

scholarly journals Pioglitazone Attenuates Vascular Fibrosis in Spontaneously Hypertensive Rats

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Dengfeng Gao ◽  
Ning Ning ◽  
Guanghua Hao ◽  
Xiaolin Niu
Keyword(s):  
Real Time ◽  
Immunohistochemical Staining ◽  
Spontaneously Hypertensive Rats ◽  
Pcr Analysis ◽  
Rt Pcr ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ppar Γ ◽  
Collagen Iii ◽  
Wistar Kyoto

Objective. We sought to investigate whether the peroxisome proliferator-activated receptor-γ (PPAR-γ) ligand pioglitazone can attenuate vascular fibrosis in spontaneously hypertensive rats (SHRs) and explore the possible molecular mechanisms.Methods. SHRs (8-week-old males) were randomly divided into 3 groups (n=8each) for treatment: pioglitazone (10 mg/kg/day), hydralazine (25 mg/kg/day), or saline. Normal male Wistar Kyoto (WKY) rats (n=8) served as normal controls. Twelve weeks later, we evaluated the effect of pioglitazone on vascular fibrosis by Masson’s trichrome and immunohistochemical staining of collagen III and real-time RT-PCR analysis of collagen I, III and fibronectin mRNA.Vascular expression of PPAR-γ and connective tissue growth factor (CTGF) and transforming growth factor-β (TGF-β) expression were evaluated by immunohistochemical staining, western blot analysis, and real-time RT-PCR.Results. Pioglitazone and hydralazine treatment significantly decreased systolic blood pressure in SHRs. Masson’s trichrome staining for collagen III and real-time RT-PCR analysis of collagen I, III and fibronectin mRNA indicated that pioglitazone significantly inhibited extracellular matrix production in the aorta. Compared with Wistar Kyoto rats, SHRs showed significantly increased vascular CTGF expression. Pioglitazone treatment significantly increased PPAR-γ expression and inhibited CTGF expression but had no effect on TGF-β expression.Conclusions. The results indicate that pioglitazone attenuated vascular fibrosis in SHRs by inhibiting CTGF expression in a TGF-β-independent mechanism.

Disposition of biogenic amines and angiotensin I by lungs of spontaneously hypertensive rats

1980 ◽  
Vol 239 (6) ◽  
pp. H736-H741
Author(s):  
R. A. Roth ◽  
K. B. Wallace
Keyword(s):  
Biogenic Amines ◽  
Spontaneously Hypertensive Rats ◽  
Pulmonary Vasculature ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Spontaneously Hypertensive ◽  
Hydroxyindoleacetic Acid ◽  
Wistar Kyoto ◽  
Pass Through ◽  
Isolated Lungs

Recent studies have suggested that the lung plays an important role in modifying concentrations of circulating vasoactive compounds. Isolated lungs of spontaneously hypertensive rats (SHR) were examined for their ability to modify concentrations of perfused norepinephrine, 5-hydroxytryptamine, or angiotensin I. Lungs from 4- or 14-wk-old SHR removed significantly more perfused 0.1 microM norepinephrine (NE) than lungs of normotensive controls (Wistar-Kyoto rats, WKY) of the same age. For example, lungs of 14-wk-old WKY removed 18.5 +/- 1.8% of perfused NE in a single pass through the pulmonary vasculature, whereas lungs from SHR removed 31.7 +/- 1.0%. Lungs of 14-wk-old SHR also produced more O-methylated NE metabolite than did lungs of WKY. Conversely, lungs of 14-wk-old SHR removed slightly less perfused 5-hydroxytryptamine and produced less 5-hydroxyindoleacetic acid metabolite than those of WKY. Monoamine oxidase activity, determined in 600 g supernatant fractions of lung homogenates, was the same in SHR and WKY. In addition, no difference in the ability of lungs of WKY and SHR to remove perfused angiotensin I was found either in animals 4 or 14 wk of age. These results suggest that lung may contribute to differences in concentrations of circulating biogenic amines observed in SHR and WKY.

scholarly journals PET-CT and RNA sequencing reveal novel targets for acupuncture-induced lowering of blood pressure in spontaneously hypertensive rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jing Li ◽  
Chong Peng ◽  
Dongjian Lai ◽  
Yajing Fang ◽  
Daihong Luo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Negative Control ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Pet Ct ◽  
Lower Blood ◽  
Mrna And Protein Expression ◽  
Wistar Kyoto ◽  
Control Sham

AbstractManual acupuncture (MA) can be used to manage high blood pressure; however, the underlying molecular mechanism remains unknown. To explore the mechanism of acupuncture in the treatment of hypertension, Wistar Kyoto rats (WKYs) and spontaneously hypertensive rats (SHRs) were subjected to either MA stimulation or the corresponding sham procedure as a negative control (Sham-MA) for 1 week. PET-CT scans, transcriptomics and molecular biology were used to evaluate the effect of MA. The results show that MA can regulate blood pressure in SHRs, change the glucose metabolism of the paraventricular hypothalamus (PVH), and affect the mRNA and protein expression levels of differentially expressed genes in the PVH. These genes may lower blood pressure by regulating angiotensin, endothelial function and inflammation. These findings reveal that MA regulates multiple biological processes and genes/proteins of the PVH, and provide a solid theoretical basis for exploring the mechanisms by which MA regulates hypertension.

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

scholarly journals Aging Additively Influences Insulin- and Insulin-Like Growth Factor-1-Mediated Endothelial Dysfunction and Antioxidant Deficiency in Spontaneously Hypertensive Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 676
Author(s):  
Kunanya Masodsai ◽  
Yi-Yuan Lin ◽  
Sih-Yin Lin ◽  
Chia-Ting Su ◽  
Shin-Da Lee ◽  
...  
Keyword(s):  
Growth Factor ◽  
Endothelial Dysfunction ◽  
Spontaneously Hypertensive Rats ◽  
No Production ◽  
Organ Bath ◽  
Insulin Like Growth Factor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Nos Inhibitors ◽  
Wistar Kyoto

This study aimed to investigate the aging-related endothelial dysfunction mediated by insulin and insulin-like growth factor-1 (IGF-1) and antioxidant deficiency in hypertension. Male spontaneously hypertensive rats (SHRs) and age-matched normotensive Wistar–Kyoto rats (WKYs) were randomly divided into 24-week-old (younger) and 48-week-old (older) groups, respectively. The endothelial function was evaluated by the insulin- and IGF-1-mediated vasorelaxation of aortic rings via the organ bath system. Serum levels of nitric oxide (NO), malondialdehyde (MDA), catalase, and total antioxidant capacity (TAC) were examined. The insulin- and IGF-1-mediated vasorelaxation was significantly impaired in both 24- and 48-week-old SHRs compared with age-matched WKYs and was significantly worse in the 48-week-old SHR than the 24-week-old SHR. After pretreatments of phosphoinositide 3-kinase (PI3K) or NO synthase (NOS) inhibitors, the insulin- and IGF-1-mediated vasorelaxation became similar among four groups. The serum level of MDA was significantly increased, while the NO, catalase, and TAC were significantly reduced in the 48-week-old SHR compared with the 24-week-old SHR. This study demonstrated that the process of aging additively affected insulin- and IGF-1-mediated endothelial dysfunction in SHRs, which could be partly attributed to the reduced NO production and antioxidant deficiency.

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