BLOOD-PRESSURE INFLUENCES ON TACTILE STARTLE REACTIVITY

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 系统通过确定是否急性或慢性血液变化 压力改变对非厌恶性触觉刺激的反应， 通过对喷气刺激的惊吓反应来测量。 数据链接 心血管与疼痛抑制系统的关系表明， 血压降低会改变疼痛敏感性。 工作的开展 实验表明，其他躯体感觉神经的反应性 方式也可以由参与的机制决定， 在血压的自我平衡控制中。 我们最近发现 血压正常的大鼠血压升高， 比压力低的大鼠更容易获得触觉刺激， 触觉反应在实验中会减弱 高血压 心血管调节系统 系统调节躯体感觉模态导联之间的敏感性 对非厌恶性反应的假设。触觉刺激 将减弱触觉反应， 刺激将通过血液中的急性或慢性增加而减弱 压力 ?目前的建议将检查触觉反应 在达尔的血压的急性和慢性操作之后， 盐敏感（S）大鼠，当维持 低盐饮食（0.3%NaCl），但当 暴露于高盐（8%NaCl），并在达尔耐盐（R） 大鼠，无论高血压如何， 确定（1）触觉是否有遗传成分 惊吓反应和（2）触觉惊吓是否减弱 当血压通过加压剂的输注而急性升高时 盐酸苯肾上腺素，一种α-肾上腺素能受体 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 氯化物影响反应性和（4）是否降低反应性 将通过急性降低血压产生， 降压药硝普钠，一种直接作用的血管扩张剂。 这些研究将描述血压对 对非厌恶性刺激的体感反应，从而解决 高血压可能会导致广泛的感觉， 赤字

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.