1. PI3K/Akt/mTOR Immunology/Inflammation GPCR/G Protein Membrane Transporter/Ion Channel
  2. PI3K Akt NO Synthase Guanylate Cyclase Potassium Channel
  3. Antihypertensive agent 7

Antihypertensive agent 7 is a vasodilator. Antihypertensive agent 7 acts on vascular endothelial cells to activate the PI3K/AKT signaling axis, increase phosphorylated eNOS, release NO, activate the sGC/cGMP pathway in smooth muscle cells, and synergistically activate multiple K+ channels in vascular smooth muscle (Kir/Kv/KCa/KATP, thereby inducing endothelium-dependent vasodilation. Antihypertensive agent 7 can be used in the research of hypertension.

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Antihypertensive agent 7

Antihypertensive agent 7 Chemical Structure

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Description

Antihypertensive agent 7 is a vasodilator. Antihypertensive agent 7 acts on vascular endothelial cells to activate the PI3K/AKT signaling axis, increase phosphorylated eNOS, release NO, activate the sGC/cGMP pathway in smooth muscle cells, and synergistically activate multiple K+ channels in vascular smooth muscle (Kir/Kv/KCa/KATP, thereby inducing endothelium-dependent vasodilation. Antihypertensive agent 7 can be used in the research of hypertension[1].

In Vitro

Antihypertensive agent 7 (Compound A24) at concentrations of 3.75-60 μM induces potent, concentration-dependent relaxation in endothelium-intact rat thoracic aortic rings, with an EC50 of 21.47 μM and a maximum relaxation rate of 97.24%[1].
The vasodilatory effect of Antihypertensive agent 7 (3.75-60 μM) is mainly endothelium-dependent, as the maximum relaxation amplitude of endothelium-denuded rat thoracic aortic rings is significantly reduced to 38.49%[1].
The vasodilatory effect of Antihypertensive agent 7 (3.75-60 μM; 20 min) on intact endothelium rat thoracic aortic rings is mediated by the PI3K/AKT signaling pathway, as pretreatment with pathway inhibitors significantly attenuates this response[1].
The vasodilatory effect of Antihypertensive agent 7 (3.75-60 μM; 20 min) on rat thoracic aortic rings with intact endothelium involves the eNOS/NO/sGC signaling pathway, as pretreatment with pathway inhibitors significantly attenuates this response[1].
Antihypertensive agent 7 (60 μM; 15-60 min) activates AKT in a time-dependent manner in human umbilical vein endothelial cells, with the maximum phosphorylation level observed after treatment with 60 μM for 30 min[1].
Antihypertensive agent 7 (15-60 μM; 30 min) increases the phosphorylation levels of AKT and eNOS in human umbilical vein endothelial cells in a concentration-dependent manner[1].
The vasodilatory effect of Antihypertensive agent 7 (3.75-60 μM; 20 min) on endothelium-intact rat thoracic aortic rings is independent of the activation of muscarinic receptors and β-adrenergic receptors[1].
Antihypertensive agent 7 (3.75-60 μM; 20 min) exerts vasodilatory effects on rat thoracic aortic rings with intact endothelium independent of the PGI2 signaling pathway[1].
The vasodilatory effect of Antihypertensive agent 7 (3.75-60 μM; 20 min) on endothelium-intact rat thoracic aortic rings involves the activation of multiple potassium channel subtypes, including KATP, KCa, KV and KIR channels[1].
Antihypertensive agent 7 (60 μM) does not affect ROCCs- or VDCCs-mediated vasoconstriction in rat thoracic aortic rings[1].
Antihypertensive agent 7 (60 μM) does not affect vasoconstriction mediated by sarcoplasmic reticulum Ca2+ release in rat thoracic aortic rings[1].
Antihypertensive agent 7 (2.5-80 μM; 24 h) exhibits no significant cytotoxicity against human umbilical vein endothelial cells at concentrations up to 80 μM following 24 h of treatment[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Antihypertensive agent 7 (Compound A24) (20-60 mg/kg; i.p.; daily; 5 weeks) dose-dependently lowers systolic and diastolic blood pressure in L-NAME (HY-18729)-induced hypertensive rats, while also improving body weight gain and reducing multi-organ pathological damage[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Sprague-Dawley (SD) (male, 250-300 g, L-NAME-induced hypertension)[1]
Dosage: 20 mg/kg; 40 mg/kg; 60 mg/kg
Administration: i.p.; daily; 5 weeks
Result: Reduced systolic blood pressure (SBP) to ~115 mmHg by week 9 in the 60 mg/kg group, with SBP significantly lower than the L-NAME model group at all measured time points.
Exerted dose-dependent reductions in diastolic blood pressure (DBP), with the 60 mg/kg group showing effects comparable to positive control CPT (10 mg/kg, i.p. daily).
Attenuated reduced body weight gain impairment and improved growth status at 20, 40, or 60 mg/kg doses.
Showed dose-dependent protective effects against multi-organ pathological damage: 20 mg/kg group showed partial improvement in heart, liver, spleen, and kidney tissue morphology; 40 mg/kg and 60 mg/kg progressively restored tissue structural integrity; 60 mg/kg group had histological outcomes comparable to CPT (10 mg/kg, i.p. daily) group.
Molecular Weight

371.41

Formula

C20H22FN3O3

SMILES

CC(N1CCC(CC1)NC(C2=CC(C3=C(OC)C=C(F)C=C3)=CC=N2)=O)=O

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Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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Product Name:
Antihypertensive agent 7
Cat. No.:
HY-184303
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