Rat Angiotensinogen ELISA Kit
Activation of the renin-angiotensin system in excessive fructose-induced metabolic syndrome
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Excessive fructose consumption induces hyperglycemia and hypertension. Nevertheless, the mechanism by which fructose induces metabolic syndrome is essentially unknown. We hypothesized that top fructose consumption induces activation of the renin-angiotensin system (RAS), leading to hypertension and metabolic syndrome.
Human Angiotensinogen (AGT) ELISA Package | Mouse Angiotensinogen, Agt ELISA KIT
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We supplied 11-week-old Sprague-Dawley rats with ingesting water, with or with out 20% fructose, for 2 weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) utilizing ELISA kits. The expression of RAS genes was decided by quantitative reverse transcription polymerase chain response.
Sdhaf1 3’UTR Luciferase Secure Cell Line | Serpinf2 3’UTR Luciferase Secure Cell Line
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Excessive fructose consumption elevated physique weight and water retention, no matter meals consumption or urine quantity. After two weeks, fructose consumption induced glucose intolerance and hypertension. Excessive fructose consumption elevated serum renin, Ang II, triglyceride, and levels of cholesterol, however not Aldo ranges.
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Excessive fructose consumption elevated the expression of angiotensinogen within the liver; angiotensin-converting enzyme within the lungs; and renin, angiotensin II sort 1a receptor (AT1aR), and angiotensin II sort 1b receptor (AT1bR) within the kidneys. Nevertheless, expression of AT1aR and AT1bR within the adrenal glands didn’t enhance in rats given fructose. Taken collectively, these outcomes point out that top fructose consumption induces activation of RAS, leading to hypertension and metabolic syndrome.Key phrases: Fructose; Hypertension; Metabolic syndrome; Weight problems; Renin-angiotensin system.
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Up-regulation of intrarenal renin-angiotensin system contributes to renal harm in high-salt induced hypertension rats.
OBJECTIVE
To check the speculation that in a high-salt induced hypertension in regular rats, whether or not the modifications of intrarenal renin-agiotensin system (RAS) play a crucial position in renal harm and might be mirrored by urinary angiotensinogen (AGT).
METHODS
Within the research, 27 normotensive male Wistar-Kyoto rats had been divided into management group [0.3% (mass faction) NaCl in chow, n=9, NS], high-salt food plan group [8% (mass faction) NaCl in chow, n=9, HS] and high-salt food plan with Losartan group [8% (mass faction) NaCl in chow and 20 mg/(kg×d) Losartan in gavages, n=9, HS+L)], and had been fed for six weeks.
The blood stress was monitored and urine samples had been collected each 2 weeks. AGTs in plasma, kidney and urine had been measured by ELISA kits. The renal cortex expression of mRNA and protein of AGT had been measured by Actual-time PCR and immunohistochemistry (IHC). The renin exercise and ANG II had been measured by radioimmunoassay (RIA) kits.
Mouse Angiotensinogen (AGT) ELISA Package
RESULTS
In contrast with NS, the systolic blood stress (SBP) [(156 ± 2) mmHg vs. (133 ± 3) mmHg, P<0.05] elevated considerably on the finish of the 2nd week, and the urinary protein [(14.07 ± 2.84) mg/24 h vs. (7.62 ± 3.02) mg/24 h, P<0.05] elevated considerably on the finish of the sixth week in HS.
In contrast with HS, there was no important distinction in SBP (P>0.05) however the proteinuria [(9.69 ± 2.73) mg/24 h vs. (14.07 ± 2.84) mg/24 h, P<0.01] decreased considerably in HS+L. In contrast with NS, there was no important distinction within the plasma renin exercise, angiotensinogen and ANG II degree in HS (P>0.05), however the renal cortex renin content material [(8.72 ± 1.98) ng/(mL × h) vs. (4.37 ± 1.26) ng/(mL × h), P<0.05], AGT formation [(4.02 ± 0.60) ng/mg vs. (2.59 ± 0.42) ng/mg, P<0.01], ANG II degree [(313.8 ± 48.76) pmol/L vs. (188.9 ± 46.95) pmol/L, P<0.05] had been elevated considerably in HS, and the urinary AGT and ANG II excretion charges elevated considerably (P<0.05). In contrast with HS, the plasma renin exercise, angiotensinogen and ANG II degree had been considerably elevated (P<0.05), however the renal cortex renin content material, AGT formation, ANG II degree considerably decreased (P<0.05), and the urinary AGT and ANG II excretion charges decreased considerably in HS+L (P<0.05). The urinary AGT excretion charges had been positively correlated with the AGT degree within the renal cortex (P<0.05).
CONCLUSIONS
Up-regulation of intarenal RAS might contribute to renal harm in high-salt induced hypertension rats. Urinary AGT might replicate the standing of intrarenal RAS.
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Mouse angiotensinogen(aGT)ELISA Kit |
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| GA-E0649MS-48T | GenAsia Biotech | 48T | EUR 403.2 |
Mouse angiotensinogen(aGT)ELISA Kit |
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| GA-E0649MS-96T | GenAsia Biotech | 96T | EUR 640.8 |
Human angiotensinogen(aGT)ELISA Kit |
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| GA-E1243HM-48T | GenAsia Biotech | 48T | EUR 346.8 |
Human angiotensinogen(aGT)ELISA Kit |
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| GA-E1243HM-96T | GenAsia Biotech | 96T | EUR 559.2 |
Human Angiotensinogen, AGT ELISA KIT |
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| ELI-02698h | Lifescience Market | 96 Tests | EUR 988.8 |
Mouse Angiotensinogen, Agt ELISA KIT |
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| ELI-02699m | Lifescience Market | 96 Tests | EUR 1038 |
Human Angiotensinogen (AGT) ELISA Kit |
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| RD-AGT-Hu-48Tests | Reddot Biotech | 48 Tests | EUR 501.6 |
Human Angiotensinogen (AGT) ELISA Kit |
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| RD-AGT-Hu-96Tests | Reddot Biotech | 96 Tests | EUR 690 |