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MedChemExpress - Model Hydrochlorothiazide - 58-93-5
Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[1][2][3].MCE products for research use only. We do not sell to patients.
Hydrochlorothiazide
MCE China:Hydrochlorothiazide
Brand:MedChemExpress (MCE)
Cat. No.HY-B0252
CAS:58-93-5
Synonyms:HCTZ
Purity:99.51%
Storage:Powder -20°C 3 years 4°C 2 years *The compound is unstable in solutions, freshly prepared is recommended.
Shipping:Room temperature in continental US; may vary elsewhere.
Description:Hydrochlorothiazide (HCTZ), an orally active diuretic agent of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect.
In Vitro:Hydrochlorothiazide belongs to thiazide class of diuretics. It reduces blood volume by acting on the kidneys to reduce sodium (Na) reabsorption in the distal convoluted tubule. The major site of action in the nephron appears on an electroneutral Na+-Cl co-transporter by competing for the chloride site on the transporter. By impairing Na transport in the distal convoluted tubule, hydrochlorothiazide induces a natriuresis and concomitant water loss. Thiazides increase the reabsorption of calcium in this segment in a manner unrelated to sodium transport. Additionally, by other mechanisms, Hydrochlorothiazide is believed to lower peripheral vascular resistance[1].
In Vivo:Hydrochlorothiazide (HCTZ; orally bygavage; 12.5 mg/kg/d; 8 weeks) has improved cardiac function, reduced cardiac interstitial fibrosis and collagen volume fraction, decreased expression of AT1, TGF-β and Smad2 in the cardiac tissues in adult male Sprague Dawley rats. In addition, hydrochlorothiazide reduces plasma angiotensin II and aldosterone levels. Furthermore, hydrochlorothiazide inhibits angiotensin II-induced TGF-β1 and Smad2 protein expression in the neonatal rat ventricular fibroblasts[2].
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References:
[1]. Duarte, J.D. and R.M. Cooper-DeHoff, Mechanisms for blood pressure lowering and metabolic effects of thiazide and thiazide-like diuretics. Expert Rev Cardiovasc Ther, 2010. 8(6): p. 793-802. [Content Brief]
[2]. Jinghong Luo, et al. Hydrochlorothiazide modulates ischemic heart failure-induced cardiac remodeling via inhibiting angiotensin II type 1 receptor pathway in rats. Cardiovasc Ther. 2017 Apr;35(2). [Content Brief]
[3]. Magdy M Abdelquader, et al. Inhibition of Co-Crystallization of Olmesartan Medoxomil and Hydrochlorothiazide for Enhanced Dissolution Rate in Their Fixed Dose Combination. AAPS PharmSciTech. 2018 Dec 17;20(1):3. [Content Brief]
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