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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Angiotensin I (Ang I) (C62H89N17O14), with the sequence H-Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-OH, is formed by the action of renin on angiotensinogen. Renin is produced in the kidneys in response to renal sympathetic activity, decreased intrarenal blood pressure (<90mmHg systolic blood pressure) at the juxtaglomerular cells. Ang I appears to have no biological activity and exists solely as a precursor to angiotensin II (A II). Ang I is cleaved to Ang II by the angiotensin-converting enzyme (ACE). Ang II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates contraction by an IP3-dependent mechanism).
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Ref:
1. Lundequist, A. et al. J. Biol. Chem. 279, 32339 (2004); Olson, S. et al. Am. J. Physiol. Lung. Cell Mol. Physiol. 287, L559 (2004); Sanker, S. et al. J. Biol. Chem. 272, 2963 (1997).
2. Preston RA, Materson BJ, Reda DJ, et al. Age-Race Subgroup Compared With Renin Profile as Predictors of Blood Pressure Response to Antihypertensive Therapy. JAMA. 1998;280(13):1168-1172. doi:10.1001/jama.280.13.1168.
Animal models
Time-dated pregnant ewes (gestational day 125 ± 5, term ~ 145 days)
Dosage form
5 μg/kg
Intracerebroventricular injection
Applications
Intracerebroventricular injection of Ang I significantly increased fetal blood pressure and c-fos expression in the supraoptic nuclei (SON) and the paraventricular nuclei (PVN) in the hypothalamus, accompanied by an increase of fetal plasma arginine vasopressin (AVP). Double labeling experiments showed colocalization of AT1 receptor and c-fos expression in both SON and PVN following Ang I treatment. The results indicate that central angiotensin I increases fetal AVP neuron activity and pressor responses.
Note
The technical data provided above is for reference only.
References:
1. Shi L, Mao C, Zeng F, et al. Central angiotensin I increases fetal AVP neuron activity and pressor responses. American Journal of Physiology - Endocrinology and Metabolism, 2010, 298(6): E1274-1282.
