Schrör K
Institut für Pharmakologie, Heinrich-Heine-Universität, Düsseldorf, Fed. Rep. of Germany.
Arzneimittelforschung. 1993 Feb;43(2A):236-41.
The adequate biological function of the renin-angiotensin system in blood pressure regulation and volume control involves additional factors for a fully balanced response. This includes arachidonic acid-derived lipid mediators, the eicosanoids. Angiotensin II (Ang II) causes (AT1)-receptor mediated stimulation of phospholipase C, resulting in generation of IP3 (inositol triphosphate) and activation of protein kinase C, elevated cytosolic Ca+ and stimulation phospholipase A2. These processes culminate in the generation of cell-specific eicosanoids and their autocrine action on the generating cell or paracrine effects on cells in the vicinity. In vascular tissue, liberated arachidonic acid is mainly converted into vasodilator prostaglandins, i.e. prostacyclin (PGI2) and PGE2. These prostaglandins may attenuate any direct Ang II-induced vasoconstriction, lower systemic vascular resistance and stimulate renal sodium excretion. In some vessels, arachidonic acid released by Ang II may also be converted to vasoconstrictor eicosanoids, i.e. thromboxane A2, PGF2 alpha and 12-HETE. The biological significance of endogenous eicosanoid generation becomes evident if vasoactive eicosanoids become limiting factors for maintaining homoiostasis, i.e. in the fetal circulation, Bartter's syndrome and congestive heart failure where vasodilating eicosanoids (PGE2, PGI2) are involved in maintenance of low vascular resistance and reduced or absent vasoconstriction by Ang II. Vasoconstrictor eicosanoids (thromboxane A2, PGF2 alpha, 12-HETE) contribute to high blood pressure in (renovascular) hypertension and pregnancy-induced hypertension. Alternatively, generation of vasodilator prostaglandins may be reduced in these situations. The vascular renin-angiotensin system is subject to the action of a number of drugs and chemicals, most notably specific inhibitors of the angiotensin-converging enzyme and drugs affecting kidney function (furosemide) and/or vessel tone (propranolol).(ABSTRACT TRUNCATED AT 250 WORDS)
肾素 - 血管紧张素系统在血压调节和容量控制中的充分生物学功能涉及其他因素，以实现完全平衡的反应。这包括花生四烯酸衍生的脂质介质，即类二十烷酸。血管紧张素II（Ang II）通过（AT1）受体介导刺激磷脂酶C，导致三磷酸肌醇（IP3）生成和蛋白激酶C激活，细胞溶质Ca +升高并刺激磷脂酶A2。这些过程最终导致细胞特异性类二十烷酸的生成及其对生成细胞的自分泌作用或对附近细胞的旁分泌作用。在血管组织中，释放的花生四烯酸主要转化为血管舒张性前列腺素，即前列环素（PGI2）和PGE2。这些前列腺素可减弱任何直接由Ang II诱导的血管收缩，降低全身血管阻力并刺激肾钠排泄。在某些血管中，Ang II释放的花生四烯酸也可能转化为血管收缩性类二十烷酸，即血栓素A2、PGF2α和12 - HETE。当血管活性类二十烷酸成为维持体内平衡的限制因素时，内源性类二十烷酸生成的生物学意义就变得明显，例如在胎儿循环、巴特综合征和充血性心力衰竭中，血管舒张性类二十烷酸（PGE2、PGI2）参与维持低血管阻力以及减少或消除Ang II引起的血管收缩。血管收缩性类二十烷酸（血栓素A2、PGF2α、12 - HETE）在（肾血管性）高血压和妊娠高血压中导致高血压。或者，在这些情况下，血管舒张性前列腺素的生成可能会减少。血管肾素 - 血管紧张素系统受到多种药物和化学物质的作用，最显著的是血管紧张素转换酶特异性抑制剂以及影响肾功能（速尿）和/或血管张力（普萘洛尔）的药物。（摘要截断于250字）
