BLOOD PRESSURE CONTROL

这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。内源性一氧化氮和β-肾上腺素能激动剂导致动脉血管扩张受损的高血压患者，在硝酸盐和β-受体激动剂的作用下，将有正常的换气。高血压患者对阿尔法激动剂的升压反应过度，对阿尔法激动剂的血管收缩反应正常。低血压和体位性低血压的患者会对一氧化氮产生过度的动、静脉扩张反应。β-2肾上腺素能受体和α-1肾上腺素能受体的多态可以解释对这些药物的药理反应的部分但不是全部的变化。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Patients with essential hypertension who have impaired arterial vasodilation in response to endogenous nitric oxide and beta adrenergic agonists will have normal ventilation in response to nitrates and beta agonists. Patients with essential hypertension have exaggerated pressor responses to alpha agonists will have normal venoconstrictor responses to alpha agonists. Patients with low blood pressure and postural hypotension will have exaggerated arterial and venous dilation in response to nitric oxide. Polymorphisms of the beta-2-adrenergic receptor and alpha-1 adrenergic receptors will explain some but not all of the variations in pharmacological responses to these agents.