Kev piav qhia

Hydrochlorothiazide (HCTZ), ib qho tshuaj diuretic hauv qhov ncauj ntawm chav kawm thiazide, inhibits kev hloov TGF-β/Smad signaling txoj kev. Hydrochlorothiazide muaj cov nyhuv ncaj qha rau vascular relaxant los ntawm kev qhib cov calcium-activated potassium (KCA) channel. Hydrochlorothiazide txhim kho lub plawv ua haujlwm, txo cov fibrosis thiab muaj cov nyhuv antihypertensive.

Keeb kwm

Hydrochlorothiazide yog cov tshuaj diuretic ntawm chav kawm thiazide.

Hauv Vitro

Hydrochlorothiazide belongs rau thiazide chav kawm ntawm diuretics. Nws txo cov ntshav ntim los ntawm kev ua haujlwm ntawm lub raum kom txo cov sodium (Na) reabsorption hauv lub distal convoluted tubule. Qhov chaw loj ntawm kev ua hauv nephron tshwm rau ntawm ib qho electroneutral Na +-Cl co-transporter los ntawm kev sib tw rau qhov chaw chloride ntawm lub thauj khoom. Los ntawm impairing Na thauj nyob rau hauv lub distal convoluted tubule, hydrochlorothiazide induces ib natriuresis thiab concomitant dej poob. Thiazides ua rau kom cov calcium reabsorption nyob rau hauv ntu no nyob rau hauv ib yam uas tsis cuam tshuam rau sodium thauj. Tsis tas li ntawd, los ntawm lwm cov txheej txheem, Hydrochlorothiazide ntseeg tias txo qis peripheral vascular tsis kam.

Hydrochlorothiazide (HCTZ; qhov ncauj bygavage; 12.5 mg / kg / d; 8 lub lis piam) tau txhim kho lub plawv ua haujlwm, txo qis plawv interstitial fibrosis thiab collagen ntim feem, txo qis ntawm AT1, TGF-β thiab Smad2 nyob rau hauv cov ntaub so ntswg plawv hauv cov txiv neej laus Sprague Dawley nas. Tsis tas li ntawd, hydrochlorothiazide txo plasma angiotensin II thiab aldosterone qib. Tsis tas li ntawd, hydrochlorothiazide inhibits angiotensin II-induced TGF-β1 thiab Smad2 protein qhia nyob rau hauv neonatal nas ventricular fibroblasts.

Cov qauv tshuaj