Yamaguchi K, Hama H, Watanabe K
Department of Physiology, Niigata University School of Medicine, Japan.
Eur J Endocrinol. 1996 Feb;134(2):243-50. doi: 10.1530/eje.0.1340243.
We have reported previously that regions encompassing the cerebral ventricle may contain dopamine receptors responsible for facilitatory roles in the osmotic release of vasopressin in conscious rats. In order to explore the location of these receptors, we injected (0.5 mul) the dopamine antagonist haloperidol (13.3 nmol) or dopamine (26.4 nmol) topically into the anteroventral third ventricular region or the paraventricular nucleus of rats, and their effects on the levels of plasma vasopressin and its controlling factors were examined in the presence or absence of an osmotic stimulus. The effects of haloperidol injections into the ventral tegmental area were also tested to study whether information associated with drinking behavior may affect the osmotic vasopressin secretion. Intravenous infusion (0.1 ml kg-1 body wt min-1) of hypertonic saline (2.5 mol/l) enhanced plasma vasopressin 15 and 30 min later, and this was accompanied by an augmentation of plasma osmolality, sodium and chloride, and by elevated or unaltered arterial pressure. The vasopressin response was abolished by haloperidol injection into the anteroventral third ventricular region 10 min before the beginning of the hypertonic saline infusion. The injection sites were confirmed histologically to have been in or near the organum vasculosum of the laminae terminalis and a ventral part of the median preoptic nucleus. Similarly, a partial but significant reduction of the vasopressin response was noted after bilateral injections of haloperidol into the ventral tegmental area, whereas bilateral haloperidol injections into the paraventricular nucleus had no appreciable effect. The responses of plasma osmolality, electrolytes and arterial pressure to the osmotic load were not affected significantly by haloperidol injections into the anteroventral third ventricular region, ventral tegmental area or the paraventricular nucleus. The iv infusion of isotonic saline (0.15 mol/l) did not change plasma vasopressin and the other variables significantly, and this was also the case when preceded by application of haloperidol into the anteroventral third ventricular region, ventral tegmental area or the paraventricular nucleus. Dopamine injection into the anteroventral third ventricular region increased plasma vasopressin 5 min later, without affecting plasma osmolality, electrolytes or arterial pressure. On the basis of these results, we concluded that dopamine receptors responsible for facilitatory roles in osmotically stimulated vasopressin secretion may exist in the anteroventral third ventricular region and ventral tegmental area.
我们之前曾报道，包含脑室的区域可能含有多巴胺受体，这些受体在清醒大鼠中对血管加压素的渗透性释放起促进作用。为了探究这些受体的位置，我们将多巴胺拮抗剂氟哌啶醇（13.3 nmol，0.5 μl）或多巴胺（26.4 nmol）局部注射到大鼠的前腹侧第三脑室区域或室旁核中，并在有无渗透刺激的情况下，检测它们对血浆血管加压素水平及其控制因素的影响。还测试了向腹侧被盖区注射氟哌啶醇的效果，以研究与饮水行为相关的信息是否会影响渗透性血管加压素分泌。静脉输注（0.1 ml·kg-1体重·min-1）高渗盐水（2.5 mol/l）在15和30分钟后可提高血浆血管加压素水平，同时伴有血浆渗透压、钠和氯的升高，以及动脉压升高或未改变。在开始输注高渗盐水前10分钟，向大鼠前腹侧第三脑室区域注射氟哌啶醇可消除血管加压素反应。经组织学证实，注射部位位于终板血管器或视前正中核腹侧部分内或其附近。同样，向腹侧被盖区双侧注射氟哌啶醇后，血管加压素反应有部分但显著的降低，而向室旁核双侧注射氟哌啶醇则没有明显影响。向大鼠前腹侧第三脑室区域、腹侧被盖区或室旁核注射氟哌啶醇，对血浆渗透压、电解质和动脉压对渗透负荷的反应没有显著影响。静脉输注等渗盐水（0.15 mol/l）对血浆血管加压素和其他变量没有显著影响，在向大鼠前腹侧第三脑室区域、腹侧被盖区或室旁核注射氟哌啶醇后再输注等渗盐水时也是如此。向大鼠前腹侧第三脑室区域注射多巴胺5分钟后可提高血浆血管加压素水平，而不影响血浆渗透压、电解质或动脉压。基于这些结果，我们得出结论，在大鼠前腹侧第三脑室区域和腹侧被盖区可能存在对渗透性刺激血管加压素分泌起促进作用的多巴胺受体。
