The AT1 receptor is involved in the classical physiological actions of Ang II: regulation of blood pressure, electrolyte and water balance, thirst, hormone secretion, and renal function. The AT1 receptor belongs to the G protein-coupled receptor (GPCR) superfamily, typically activates phospholipase C (PLC) through the heterotrimeric Gq protein and lacks intrinsic tyrosine kinase activity[1]. Angiotensin II (3-8), human is a less effective agonist at the angiotensin AT1 receptor. Human Angiotensin II (3-8) causes endothelium-dependent renal cortical vasodilatation, in anaesthetized rats. At doses up to 125 pmol/kg, human Angiotensin II (3-8) is without any cardiovascular effects, but with doses of 1.25 and 12.5 nmol/kg there are dose-dependent increases in mean arterial blood pressure and reductions in renal and mesenteric flows and vascular conductances[2]. Angiotensin II-(3-8)-hexapeptide, at the dose of 1 nmol given intracerebroventricularly, only slightly less than angiotensin II (the same dose and route) stimulated exploratory locomotor behaviour in an open field and electromagnetic motimeter. Equimolar doses of angiotensin II-(3-8)-hexapeptide and angiotensin II in improving processes related to learning and memory in rats, the effectiveness is almost identical. So it must be independent of specific angiotensin receptors in brain , which the hexapeptide binds with about 1000 times lower affinity than angiotensin II[3].
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Angiotensin II (3-8), human | Angiotensin Receptor | AmBeed-信号通路专用抑制剂
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