BLOOD-PRESSURE INFLUENCES ON TACTILE STARTLE REACTIVITY

血压对触觉惊吓反应的影响

• 批准号: 3429143
• 负责人: CARROL H WOODWORTH
• 金额: $ 3.48万
• 依托单位: UNIVERSITY OF IOWA
• 依托单位国家: 美国
• 财政年份: 1989
• 资助国家: 美国
• 起止时间: 1989-06-01 至 1990-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3429143
• 关键词: cardiovascular pharmacology; dietary mineral; hypertension; laboratory rat; nutrition related tag; phenylephrine; sensory thresholds; startle reaction; touch; vasoconstrictors; vasodilators

The following proposal will extend our understanding of interactions between cardiovascular and somatosensory regulatory systems by determine whether acute or chronic changes in blood pressure alter reactivity to nonaversive, tactile stimulation as measured by the startle response to airpuff stimuli. Data linking cardiovascular with pain-inhibitory systems suggest that regulation off blood pressure acts to modify pain sensitivity. Work in our laboratory suggests that reactivity in other somatosensory modalities may also be determined by mechanisms that participate in the homeostatic control of blood pressure. We recently found that normotensive rats with higher blood pressure have higher Thresholds for tactile stimulation than rats with lower pressure, and that tactile reactivity is attenuated in experimental hypertension. The possibility that cardiovascular regulatory systems modulate sensitivity across somatosensory modalities leads to the hypothesis that reactivity to nonaversive. tactile stimuli will be attenuated tactile reactivity to nonaversive,, tactile stimuli will be attenuated by acute or chronic increases in blood pressure. ?he current proposal will examine tactile reactivity following acute and chronic manipulations of blood pressure in Dahl salt-sensitive (S) rats, which remain normotensive when maintained on low dietary salt (0.3% NaC1) but develop hypertension when exposed to high salt (8% NaC1), and in Dahl salt-resistant (R) rats, which remain normotensive regardless of hypertension to determine (1) whether there is a genetic component to tactile startle reactivity and (2) whether tactile startle is attenuated when blood pressure is elevated acutely by infusion of the pressor agent phenylephrine hydrochloride, an alpha-adrenergic receptor agonist. In additional experiments, 33 days to ascertain (3) whether either high blood pressure or intake of excess sodium chloride affects reactivity and (4) whether decreased reactivity will be produced by acutely reducing blood pressure with the depressor agent sodium nitroprusside, a direct-acting vasodilator. These studies will delineate the impact of blood pressure on somatosensory reactivity to nonaversive stimuli, thus addressing the possibility that hypertension may cause widespread sensory deficits.

以下建议将扩大我们对 心血管和躯体感觉调节之间的相互作用 系统通过确定血液中的急性或慢性变化 压力将反应性改变为非厌恶的触觉刺激，如 通过对喷气刺激的惊吓反应来衡量。数据链接 心血管的疼痛抑制系统表明，调节 血压过低起到调节疼痛敏感性的作用。在我们的 实验室表明，其他躯体感觉的反应性 模式也可以由参与的机制来确定 在血压的动态平衡控制方面。我们最近发现 血压正常的大鼠血压越高 触觉刺激阈值高于压力较低的大鼠， 而这种触觉反应性在实验中被减弱 高血压。心血管调节的可能性 系统调节体感通道导联的灵敏度 对非厌恶的反应性的假设。触觉刺激 将使触觉的反应性减弱到非厌恶的，触觉 刺激将通过急性或慢性的血液增加而减弱 压力。？目前的提案将检查触觉反应性 Dahl患者的急性和慢性血压控制 盐敏感(S)大鼠，维持正常血压 低食盐(0.3%NaCl2)，但在以下情况下会患高血压 暴露在高盐(8%NaCl2)中，在Dahl耐盐(R)中 大鼠，保持正常血压，无论高血压到 确定(1)是否存在触觉的遗传成分 惊吓反应性和(2)触觉惊吓是否减弱 当通过输注加压剂而使血压急剧升高时 α-肾上腺素能受体盐酸苯肾上腺素 激动剂。在额外的实验中，33天来确定(3) 无论是高血压还是摄入过量的钠 氯化物影响反应性以及(4)反应性是否降低 会通过急剧降低血压而产生 降压剂硝普钠，一种直接作用的血管扩张剂。 这些研究将描绘出血压对 对非厌恶刺激的躯体感觉反应性，从而解决 高血压可能导致广泛的感官 赤字。