[tyr(p)4] angiotensin ii

[Tyr(P)4] Angiotensin II is a peptide that affects vascular smooth muscle by causing contraction in normal arteries and inducing hypertrophy or hyperplasia in cultured cells or diseased vessels.

Angiotensin II human (Ang II) is a biologically active peptide, a vasoconstrictor. Angiotensin II interacts with AT1R and AT2R to regulate blood pressure, stimulate sympathetic nerves, and increase aldosterone biosynthesis and renal activity in humans.

Angiotensin II 5-valine TFA is an agonist of angiotensin receptor.

Angiotensin I/II (1-5) is a peptide (ASP-ARG-VAL-TYR-ILE) that contains the amino acids 1-5 and is converted from Angiotensin I/II.

[Sar1, Ile8]-Angiotensin II acetate activates both the NADPH and NADH oxidases, and stimulates superoxide anion formation in vascular smooth muscle cells. [Sar1, Ile8]-Angiotensin II acetate has multiple effects on vascular smooth muscle, including contra

[Sar1, Ile8]-Angiotensin II 3TFA ([Sar1, Ile8]-Angiotensin II 3TFA (37827-06-8(free base))) is a peptide that has multiple effects on vascular smooth muscle.

Angiotensin I/II (1-6) is a peptide (ASP-ARG-VAL-TYR-ILE-HIS) that contains the amino acids 1-6 and is converted from Angiotensin I/II peptide.

Angiotensin II human acetate (DRVYIHPF acetate) is a vasoconstrictor that mainly acts on the AT1 receptor.

[Sar1, Ile8]-Angiotensin II(3TFA) is a peptide that has multiple effects on vascular smooth muscle.

Angiotensin II (5-8) is an endogenous C-terminal fragment of the peptide vasoconstrictor angiotensin II

[Sar1, Ile8]-Angiotensin II (TFA) is a peptide compound that affects vascular smooth muscle by causing contraction of normal arteries and inducing hypertrophy or hyperplasia in cultured cells or diseased vessels.

[D-Pro4,D-Trp7,9] Substance P (4-11) acts as a potent Substance P antagonist, significantly reducing plasma aldosterone (ALDO) concentrations[1].

Tyr-(D-Dab4,Arg5,D-Trp8)-cyclo-Somatostatin-14 (4-11) is a somatostatin agonist used in cancer research [1].

Angiotensin II is a potent direct vasoconstrictor, causing arteries and veins to constrict, so leading to an increase in blood pressure. Angiotensin also potentiates the release of norepinephrine by a direct action on postganglionic sympathetic fibers.

[D-Pro4,D-Trp7,9,10] Substance P (4-11) is a potent antagonist of the tachykinin family of neuropeptides [1].

[Sar4] Substance P (4-11) is a Substance P agonist and an analog of the C-terminus fragment of Substance P known as Substance P (4-11) [1].

Substance P (4-11), a C-terminal fragment of Substance P, acts as a highly selective agonist for NK1 receptors, demonstrating specificity in its interaction.

(p-Iodo-Phe7)-ACTH (4-10), a derivative of adrenocorticotrophic hormone (ACTH) produced by the anterior pituitary gland, functions as a melanocortin (MC) receptor antagonist and effectively inhibits α-melanocyte-stimulating hormone (α-MSH)-induced excessive grooming behavior in rats [1].

Angiotensin II (3-8), human, is a less effective agonist at the angiotensin AT1 receptor.

Angiotensin II human TFA, a potent vasoconstrictor within the renin/angiotensin system, plays a pivotal role in human blood pressure regulation primarily through interactions with the G-protein-coupled receptors Angiotensin II type 1 receptor (AT1R) and Angiotensin II type 2 receptor (AT2R). It not only prompts sympathetic nervous stimulation, aldosterone biosynthesis, and renal effects but also fosters growth in vascular smooth muscle cells and boosts collagen type I and III synthesis in fibroblasts. This action results in the thickening of the vascular wall and myocardium, alongside fibrosis. Additionally, Angiotensin II human TFA triggers apoptosis and encourages capillary formation from endothelial cells through the LOX-1 dependent redox-sensitive pathway [1] [2] [3] [4].

[DAla4] Substance P (4-11), an analog of Substance P (Substance P), effectively inhibits the binding of 125I-Bolton Hunter-conjugated Eledoisin (Eledoisin) and 125I-Bolton Hunter-conjugated Substance P to rat brain cortex membranes, with IC50 values of 0.5 μM and 0.15 μM, respectively [1].

(Sar1,Ile4,8)-Angiotensin II is a functionally selective agonist for the angiotensin II type 1 receptor (AT1R), enhancing insulin-stimulated signaling of the insulin receptor (IR) and glycogen synthesis, and boosting the insulin-induced phosphorylation of Akt and GSK3α β [1].

Angiotensin II is a potent direct vasoconstrictor, causing arteries and veins to constrict, so leading to an increase in blood pressure.

Substance P(1-4) acts as a potent antagonist of neurokinin receptors (NK-R) and regulates normal hematopoiesis, additionally inhibiting the formation of endogenous erythroid colonies (EEC) [1].

Tyr-ACTH(4-9) is a behaviorally active peptide utilized in research on learned behavior extinction in rats [1].

Angiotensin I II (1-6) TFA is a chemical compound comprising amino acids 1-6, derived from the Angiotensin I II peptide. This peptide is formed by the cleavage of angiotensinogen by renin, with Angiotensin I subsequently hydrolyzed by angiotensin-converting enzyme (ACE) to produce biologically active Angiotensin II. Angiotensin II has been extensively studied for its potential applications in the treatment of Hypertension, Renin Angiotensin System, and Idiopathic Membranous Nephropathy[1][2][3].

The substitution with Sar at position 1 of angiotensin II resulted in a partial agonistic activity.

[D-Pro4,D-Trp7,9,Nle11] Substance P (4-11) is a potent neurokinin NK1 antagonist that effectively inhibits the actions of gold-protein-substance P (GPSP) and substance P (SP), demonstrating its efficacy in neutralizing their effects [1].

Pentasarcosyl angiotensin II is a synthetic analog of angiotensin II.

ngiotensin II 5-valine is an angiotensin II analog which is an agonist at angiotensin receptors.