Control of catecholamine synthesis and secretion by angiotensin II.

在应激反应中，包括肾上腺素在内的儿茶酚胺由肾上腺和大脑分泌。这导致新的儿茶酚胺的合成，以取代那些丢失的。儿茶酚胺的合成受酪氨酸羟化酶的活性和数量的控制。因此儿茶酚胺的合成和分泌是一个基本的生理过程。这可以通过许多机制来控制，包括激素，如血管紧张素II。血管紧张素II具有多种功能，包括控制血压和体液平衡。血管紧张素II作用于肾上腺，交感神经和大脑产生这些效果。它是通过增加儿茶酚胺的分泌来实现的，而儿茶酚胺又反过来调节血压和体液平衡。血管紧张素II诱导儿茶酚胺分泌的机制尚不清楚，也不知道这如何导致酪氨酸羟化酶活性和合成的增加。因此，这项资助的目的是确定血管紧张素II如何诱导酪氨酸羟化酶的激活、儿茶酚胺的分泌和新的酪氨酸羟化酶的合成。这项工作的意义在于，它将使我们更好地了解血管紧张素II是如何工作的，它将为高血压的产生和控制以及应激反应的机制提供见解。众所周知，血管紧张素II刺激儿茶酚胺分泌的途径可被蛋白激酶抑制剂阻断，从而导致血压降低。因此，这项工作很可能具有治疗意义。

In the stress response the catecholamines, including adrenaline, are secreted by the adrenal gland and the brain. This leads to the synthesis of new catecholamines in order to replace those that were lost. Synthesis of catecholamines is controlled by the activity and the amount of the enzyme tyrosine hydroxylase. Catecholamine synthesis and secretion is therefore a fundamental physiological process. This can be controlled by a number of mechanisms, including hormones such as angiotensin II. Angiotensin II has a number of functions including the control of blood pressure and body fluid homeostasis. Angiotensin II acts on the adrenal glands, the sympathetic nerves and the brain to produce these effects. It does so by increasing the secretion of catecholamines and these in turn modulate blood pressure and fluid homeostasis. The mechanism(s) whereby angiotensin II induces catecholamine secretion is not known, nor is it known how this leads to increased tyrosine hydroxylase activity and synthesis. The aim of this grant is therefore to determine how angiotensin II induces the activation of tyrosine hydroxylase, the secretion of catecholamines and the synthesis of new tyrosine hydroxylase. The significance of this work is that it will allow us to better understand how angiotensin II works and it will provide insights into the generation and control of hypertension and the mechanisms of the stress response. It is known that the pathways involved in angiotensin II stimulation of catecholamine secretion can be blocked by inhibitors of protein kinases and this leads to a reduction in blood pressure. It is therefore likely that this work will have therapeutic implications.