ABSTRACT

Hypertension and diabetes development had been characterized as idiopathic disorders tightly interconnected, and therefore it is essential to understand how the functionality of neurohormonal pathways are involved in both diseases. Hypertensive and diabetic patients have shown increased systolic blood pressure (SBP), oxidative stress, vascular hypertrophy, and remodeling. It is well established that the long-term consumption of red wine and/or polyphenol-stilbene causes cardioprotective and antihypertensive effects; however, some functions remain unrevealed. Downstream pathways such as reactive oxygen species (ROS), sympathoadrenal axis represented by β₁-adrenoceptors, and renin–angiotensin system via angiotensin-II receptors critically contribute to hypertension development.

Aims

This raised the issue of whether in vivo long-term red wine treatment can act as a modulator of these targets.

Main methods

We monitored SBP, glucose tolerance, oxidative stress, and cardiovascular function. Aortic and atrial tissues from normotensive-WKY, hypertensive-SHR, and diabetic-STZ animals, chronically exposed to red wine (3.715 ml/kg/v.o/day) or alcohol (12%) for 21-days, were used to measure contractile/relaxation responses by force transducers. Key findings: red wine, but not alcohol, prevented the increase of SBP and hyperglycemic peak. Additionally, was observed prevention of oxidative stress metabolites formation and an improvement in ROS scavenging antioxidant capacity of SHR. We also revealed that red wine intake enhances the endothelium-dependent relaxation, decreases the hypercontractile mediated by angiotensin-II in the aorta, and via β₁-adrenoceptors in the atrium.

Significance

The long-term consumption of red wine can improve oxidative stress and the functionality of angiotensin-II and β₁-adrenoceptors, inspiring new pharmacologic and dietetic therapeutic approaches for the treatment of hypertension and diabetes.

Abbreviation Acronyms and/or abbreviations: [Ca²⁺]_cyt = Cytosolic Ca²⁺ Concentration; ACh = Acetylcholine; ANG II = Angiotensin II; AT1 = ANG II type 1 receptor; AUC = Area Under the Curve; Ca²⁺ = Calcium; Endo + = Endothelium Intact; Fen = Phenylephrine (1 μM); GTT = Glucose Tolerance Test; ISO = Isoprenaline (isoproterenol); KHN = Krebs-Henseleit Nutrient; LA = Left Atria; LH = Lipid Hydroperoxide; NO = Nitric Oxide; RA = Right Atria; RAS = Renin-Angiotensin System; ROS = Reactive Oxygen Species; SBP = Systolic Blood Pressure; SHR = Spontaneously Hypertensive Rats; STZ = Streptozotocin; WKY = Normotensive Wistar Kyoto Rats.

中文翻译：

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红酒而非饮酒可改善高血压-SHR 和糖尿病-STZ 大鼠的心血管功能和氧化应激

摘要

高血压和糖尿病的发展已被描述为紧密相连的特发性疾病，因此了解神经激素通路的功能如何参与这两种疾病至关重要。高血压和糖尿病患者表现出收缩压 (SBP) 升高、氧化应激、血管肥大和重塑。众所周知，长期饮用红酒和/或多酚-芪会导致心脏保护和抗高血压作用；但是，某些功能仍未公开。下游通路，如活性氧 (ROS)、以 β ₁肾上腺素受体为代表的交感肾上腺轴，以及通过血管紧张素-II 受体的肾素-血管紧张素系统，对高血压的发展至关重要。

目标

这提出了体内长期红酒治疗是否可以作为这些目标的调节剂的问题。

主要方法

我们监测 SBP、葡萄糖耐量、氧化应激和心血管功能。来自正常血压-WKY、高血压-SHR 和糖尿病-STZ 动物的主动脉和心房组织，长期暴露于红酒（3.715 ml/kg/vo/天）或酒精（12%）21 天，用于测量收缩力/力传感器的松弛反应。主要发现：红酒（而非酒精）可防止 SBP 升高和高血糖峰值。此外，观察到 SHR 的氧化应激代谢物形成的预防和 ROS 清除抗氧化能力的改善。我们还发现，红葡萄酒的摄入增强了内皮依赖性舒张，降低了由主动脉中血管紧张素-II 和心房中β _{1肾上腺素受体介导的高收缩性。}

意义

长期饮用红酒可以改善氧化应激和血管紧张素-II 和β1-肾上腺素受体的功能，_为治疗高血压和糖尿病提供新的药理和饮食治疗方法。

缩写词和/或缩写词：[Ca ²⁺ ] _cyt = Cytosolic Ca ²⁺浓度；ACh =乙酰胆碱；ANG II =血管紧张素 II；AT1 = ANG II 1 型受体；AUC =曲线下面积；Ca ²⁺ =钙；Endo + =内皮完整；Fen =去氧肾上腺素 (1 μM)；GTT =葡萄糖耐量测试；ISO =异丙肾上腺素（异丙肾上腺素）；KHN = Krebs-Henseleit 营养素；LA =左心房；LH =脂质过氧化氢；NO =一氧化氮；RA =右心房；RAS =肾素-血管紧张素系统；ROS =活性氧；SBP =收缩压；SHR =自发性高血压大鼠；STZ =链脲佐菌素；WKY =血压正常的 Wistar 京都大鼠。