Bell F R, Doris P A, Wood T J
Brain Res. 1985 Jan 28;325(1-2):143-50. doi: 10.1016/0006-8993(85)90310-5.
Changes in plasma (pAII) and cerebrospinal fluid (csf AII) immunoreactive angiotensin II have been measured in 6 unrestrained steers during dehydration and rehydration. Prior to dehydration, plasma osmolarity (pOsm) was 301.3 +/- 0.62 mOsm/l (mean +/- S.E.M.) and on dehydration progressive elevation of pOsm developed so that after 4 days it was 338.5 +/- 3.00 mOsm/l (P less than 0.001). Packed cell volume was elevated during dehydration from 39.9 +/- 0.64% to 44.7 +/- 1.24% (P less than 0.001). Radioimmunoassay (RIA) of pAII indicated a similar pattern of progressive elevation during dehydration when after 4 days pAII had risen from 54.7 +/- 11.6 fM/ml to 177.6 +/- 18.4 fM/ml (P less than 0.001). RIA of csf AII, however, indicated no complementary pattern of change during dehydration, the only significant alteration from basal levels of 166.0 +/- 13.2 fM/ml occurred after 2 days when csf AII was reduced to 83.1 +/- 14.5 fM/ml (P less than 0.01). Antiserum specificity tests indicated that some of the csf AII could have been due to metabolites of AII, and high performance liquid chromatographic separation of angiotensin peptides in csf suggested that the major contributants were AII and AIII. These analogues which may have central neural effects were not consistently elevated during dehydration of cattle. It is concluded therefore, that the role of angiotensin in central neural mechanisms of fluid balance in dehydrated animals depends primarily on the systemic renin-angiotensin system and not an endogenous brain renin-angiotensin system.
在6头未受限制的公牛脱水和补液过程中,测量了血浆(pAII)和脑脊液(csf AII)中免疫反应性血管紧张素II的变化。脱水前,血浆渗透压(pOsm)为301.3±0.62mOsm/l(平均值±标准误),脱水过程中pOsm逐渐升高,4天后达到338.5±3.00mOsm/l(P<0.001)。脱水期间,红细胞压积从39.9±0.64%升高至44.7±1.24%(P<0.001)。pAII的放射免疫分析(RIA)表明,脱水过程中呈现类似的逐渐升高模式,4天后pAII从54.7±11.6fM/ml升至177.6±18.4fM/ml(P<0.001)。然而,csf AII的RIA表明,脱水期间没有互补的变化模式,与基础水平166.0±13.2fM/ml相比,唯一显著的变化发生在2天后,此时csf AII降至83.1±14.5fM/ml(P<0.01)。抗血清特异性测试表明,部分csf AII可能是由AII的代谢产物引起的,脑脊液中血管紧张素肽的高效液相色谱分离表明,主要成分是AII和AIII。这些可能具有中枢神经作用的类似物在牛脱水期间并未持续升高。因此得出结论,血管紧张素在脱水动物体液平衡中枢神经机制中的作用主要取决于全身肾素-血管紧张素系统,而非内源性脑肾素-血管紧张素系统。