Arterial Baroreflex Control of Blood Pressure (Exercise)

动脉压力反射控制血压（运动）

• 批准号: 6897303
• 负责人: PETER Bernard RAVEN
• 金额: $ 39.24万
• 依托单位: UNIVERSITY OF NORTH TEXAS HLTH SCI CTR
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-06-01 至 2007-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6897303
• 关键词: aerobic exercise; baroreceptors; baroreflex; blood chemistry; blood pressure; blood volume; cardiac output; cardiovascular pharmacology; carotid body; clinical research; heart rate; human subject; metformin; muscle metabolism; noninsulin dependent diabetes mellitus; physical fitness; potassium channel; vascular smooth muscle nervous control; vasoconstriction

DESCRIPTION (provided by applicant): A number of investigations have demonstrated that arterial baroreflex (CBR) control of blood pressure has a primary role in providing the necessary regulation of the sympathetic neural outflow to active and inactive tissue beds associated with dynamic exercise. In addition, we have documented a reduced vasoconstrictive response to hypotension of the highly trained endurance athlete despite an augmented CBR mediated increase in MSNA. A growing body of evidence suggests that the regulatory role of sympathetic neural outflow to the vasculature is modulated by metabolic by-products released within the active tissue and involve mechanisms of functional sympatholysis. A suggested mechanism of functional sympatholysis is that contraction induced metabolites within the active muscle open ATP-sensitive potassium (KATP) channels and thereby partially inhibit sympathetic vasoconstriction. However, it has recently been demonstrated that the CBR mediated vasoconstriction within the active muscle provides the greatest reflex vasoconstrictor response to hypotension during exercise. Therefore, we hypothesize that the CBR has a fundamental role in the control of MSNA and skeletal muscle vasculature at rest and during exercise. Furthermore, we contend that the CBR regulation of vasomotor function in exercising muscle is altered by local metabolic by-products and their interaction with other vasoactive substances and the KATP channels of the vascular smooth muscle within the active tissue. In addition, these mechanisms of CBR control of the vasculature are modulated by endurance exercise training. To address these hypotheses: Comparisons of carotid baroreflex function curves of blood pressure (BP), MSNA and leg vascular conductance (LVC) will be made between rest, the non-exercising leg (NEL) and the exercising leg (EL) using the classic one-legged exercise protocol performed by humans. Carotid baroreflex function will be assessed using our well established modeling technique. Comparisons of CBR function curves of BP, MSNA and LVC will be made at rest, in the NEL and the EL (except MSNA) between average fit, high fit endurance trained athletes and NIDDM patients treated with glibenclamide and NIDDM patients treated with Metformin. We anticipate that the findings obtained from this project will provide a comprehensive understanding of the fundamental mechanisms involved in the regulation of arterial blood pressure by the arterial baroreflex and its influence on the regulation of vasomotion in active muscle tissue and inactive muscular tissue in matching blood flow to oxygen demand during exercise in humans. These findings will have implications for the care of patients suffering from non-insulin dependent diabetes mellitus (NIDDM), hypertension and cardiac failure.

描述（由申请人提供）：大量研究表明，动脉压力反射（CBR）控制血压在提供交感神经流出到与动态运动相关的活动和非活动组织床的必要调节方面具有主要作用。此外，我们已经证明，尽管CBR介导的MSNA增加，但训练有素的耐力运动员对低血压的血管收缩反应降低。越来越多的证据表明，交感神经流出到血管的调节作用是由活性组织内释放的代谢副产物调节的，并涉及功能性交感神经溶解的机制。功能性交感神经松解的一种建议机制是收缩诱导的活性肌肉内的代谢物打开ATP敏感性钾（KATP）通道，从而部分抑制交感神经血管收缩。然而，最近已经证明，CBR介导的活动肌肉内的血管收缩在运动期间提供对低血压的最大反射性血管收缩反应。因此，我们假设CBR在静息和运动时对MSNA和骨骼肌血管系统的控制具有重要作用。此外，我们认为，CBR的调节血管功能在运动肌肉改变了局部代谢副产品和它们的相互作用与其他血管活性物质和KATP通道的血管平滑肌内的活性组织。此外，CBR控制血管系统的这些机制通过耐力运动训练来调节。为了解决这些假设：将使用人类进行的经典单腿运动方案在休息、非运动腿（NEL）和运动腿（EL）之间比较血压（BP）、MSNA和腿部血管传导性（LVC）的颈动脉压力反射功能曲线。颈动脉压力感受器反射功能将使用我们完善的建模技术进行评估。将在静息时、NEL和EL（MSNA除外）中，对平均体能、高体能耐力训练运动员和接受格列本脲治疗的NIDDM患者以及接受二甲双胍治疗的NIDDM患者的BP、MSNA和LVC的CBR函数曲线进行比较。我们预计，从这个项目中获得的研究结果将提供一个全面的了解动脉压力感受器反射的动脉血压调节的基本机制，其对调节血管舒缩在活跃的肌肉组织和不活跃的肌肉组织在匹配人体运动过程中的血流量氧气需求的影响。这些发现将对非胰岛素依赖型糖尿病（NIDDM）、高血压和心力衰竭患者的护理产生影响。