Hajdu I, Obál F, Gardi J, Laczi F, Krueger J M
Department of Physiology, University of Szeged, A. Szent-Györgyi Medical Center, Szeged, Hungary.
Am J Physiol Regul Integr Comp Physiol. 2000 Jul;279(1):R271-7. doi: 10.1152/ajpregu.2000.279.1.R271.
The involvement of central angiotensinergic and cholinergic mechanisms in the effects of the intracerebroventricularly injected somatostatin analog octreotide (Oct) on drinking, blood pressure, and vasopressin secretion in the rat was investigated. Intracerebroventricular Oct elicited prompt drinking lasting for 10 min. Water consumption depended on the dose of Oct (0.01, 0.1, and 0. 4 microgram). The drinking response to Oct was inhibited by pretreatments with the intracerebroventricularly injected angiotensin-converting enzyme inhibitor captopril, the AT(1)/AT(2) angiotensin receptor antagonist saralasin, the selective AT(1) receptor antagonist losartan, or the muscarinic cholinergic receptor antagonist atropine. The dipsogenic effect of Oct was not altered by prior subcutaneous injection of naloxone. Oct stimulated vasopressin secretion and enhanced blood pressure. These responses were also blocked by pretreatments with captopril or atropine. Previous reports indicate that the central angiotensinergic and cholinergic mechanisms stimulate drinking and vasopressin secretion independently. We suggest that somatostatin acting on sst2 or sst5 receptors modulates central angiotensinergic and cholinergic mechanisms involved in the regulation of fluid balance.
研究了中枢血管紧张素能和胆碱能机制在脑室内注射生长抑素类似物奥曲肽（Oct）对大鼠饮水、血压和血管加压素分泌影响中的作用。脑室内注射Oct引发持续10分钟的快速饮水。饮水量取决于Oct的剂量（0.01、0.1和0.4微克）。预先脑室内注射血管紧张素转换酶抑制剂卡托普利、AT(1)/AT(2)血管紧张素受体拮抗剂沙拉新、选择性AT(1)受体拮抗剂氯沙坦或毒蕈碱胆碱能受体拮抗剂阿托品可抑制对Oct的饮水反应。预先皮下注射纳洛酮不会改变Oct的致渴作用。Oct刺激血管加压素分泌并升高血压。这些反应也可被卡托普利或阿托品预处理所阻断。先前的报道表明，中枢血管紧张素能和胆碱能机制独立刺激饮水和血管加压素分泌。我们认为，作用于sst2或sst5受体的生长抑素可调节参与液体平衡调节的中枢血管紧张素能和胆碱能机制。
