11/1/2022 0 Comments Taurine blood pressure![]() ![]() Oral taurine has been shown to significantly lower blood pressure and protect vascular function and responsiveness in clinical hypertensive patients. Taurine supplementation can decrease blood pressure in various hypertensive animal models, including L-NAME-induced hypertensive rats, stroke-prone spontaneously hypertensive rats, cyclosporine A-induced hypertensive rats, and DOCA-salt rats. Taurine has a variety of biological effects, including the inhibition of RAAS activation, antioxidant stress, and vasodilation, promotion of water and sodium metabolism, and suppression of sympathetic nerve excitation. Taurine blood pressure free#Taurine is a nonprotein free amino acid produced endogenously from cysteine by the oxidation of cysteine dioxygenase (CDO) and decarboxylation of cysteine sulfinic acid decarboxylase (CSAD). However, the mechanism for endogenous regulation of salt-sensitive hypertensive renal injury has not been fully elucidated. ![]() The activation of the renin-angiotensin-aldosterone system (RAAS), oxidative stress, and inflammation are all related to high salt-induced renal damage. High salt intake also directly causes renal damage. Notably, salt-sensitive hypertensive patients are more likely to develop end-stage renal disease compared with salt-resistant hypertensive patients. Up to 50% of patients with essential hypertension have high salt-induced hypertension, also known as salt-sensitive hypertension. Dietary habits are closely related to the incidence of hypertension. However, the pathogenesis of hypertensive renal injury is still poorly understood. Chronic kidney disease, which is caused by hypertension, is a powerful independent risk factor for adverse cardiovascular outcomes. A chronic increase in arterial pressure leads to a decrease in the glomerular filtration rate, proteinuria, and ultimately renal failure. The kidney is the main target of organ damage due to hypertension. This decrease subsequently promoted renin-angiotensin-aldosterone system (RAAS) activation and oxidative stress in the kidney, ultimately contributing to renal injury in salt-sensitive Dahl rats. In conclusion, the downregulation of endogenous taurine production resulted in a decrease in the renal CBS/H 2S pathway. Pretreatment with the CBS inhibitor HA or renal CBS knockdown inhibited H 2S generation and subsequently blocked the effect of taurine on renin, superoxide dismutase 1 (SOD1), and superoxide dismutase 2 (SOD2) levels in high-salt-stimulated Dahl renal slices. However, taurine failed to achieve this effect in the renal tissue of SS-13BN rats fed a high-salt diet. Taurine reduced the renin, angiotensin II, and aldosterone contents and the levels of oxidative stress indices in Dahl rat renal tissues but increased antioxidant capacity, antioxidant enzyme activity, and protein expression. Taurine intervention increased the renal H 2S content and enhanced cystathionine- β-synthase (CBS) expression and activity in Dahl rats fed a high-salt diet. In contrast, taurine did not affect SS-13BN SBP and renal function and structure. ![]() However, taurine supplementation and the resulting increase in renal taurine content reduced the increased SBP and improved renal function and structural damage in high-salt diet-fed Dahl rats. Taurine content and mRNA and protein levels of taurine synthases, cysteine dioxygenase type 1 (CDO1) and cysteine sulfinic acid decarboxylase (CSAD), were decreased in Dahl rats fed a high-salt diet. Kidney ultrastructure was observed under an electron microscope. Rat systolic blood pressure (SBP) was measured by the tail-cuff method and artery catheterization. To reveal the role of endogenous taurine in renal injury formation during salt-sensitive hypertension and clarify its mechanisms, both salt-sensitive Dahl rats and salt-resistant SS-13BN rats were fed a high-salt diet (8% NaCl) and given 2% taurine for 6 weeks. Although taurine is known to exert an antihypertensive effect, it is unclear whether it is involved in the mechanism for hypertension-related target organ injury. ![]()
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