Edo Ayaka, Hirooka Kazuyuki, Onoe Hiromitsu, Kiuchi Yoshiaki
Department of Ophthalmology and Visual Sciences, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8551, Japan.
Jpn J Ophthalmol. 2025 May 16. doi: 10.1007/s10384-025-01201-7.
To elucidate whether systemic blood pressure affects retinal ganglion cell (RGC) survival in rats administered systemic aldosterone STUDY DESIGN: Experimental study design METHODS: Rats were continuously administered aldosterone or vehicle via a subcutaneous osmotic mini-pump. Hypertension was induced by the provision of saline as their drinking water. Systolic and diastolic blood pressures and intraocular pressure (IOP) were measured at the baseline and at 1-6 weeks after administration of aldosterone-water, aldosterone-saline, vehicle-water, or vehicle-saline. The number of retrogradely labelled RGCs in retinal flat mounts were counted after 6 weeks of treatment. Aldosterone-treated rats also received eplerenone (a mineralocorticoid receptor antagonist) or hydralazine (a vasodilator), and changes in systolic and diastolic blood pressures, IOP, and the number of RGCs were examined.
The number of RGCs was significantly reduced in rats treated with aldosterone, regardless of whether they drank water or saline (aldosterone/saline group vs vehicle/saline group: 1464.8 ± 29.7 vs 1763.3 ± 106.5, respectively, P = 0.01; aldosterone/water group vs vehicle/water group: 1433.3 ± 30.2 vs 1815.0 ± 193.9, respectively, P <0.01). No change in IOP with aldosterone or saline administration was observed (P >0.05). Although eplerenone or hydralazine treatment in animals receiving aldosterone and saline reduced the systolic and diastolic blood pressures as compared with in the controls, the number of RGCs was only preserved in the eplerenone-treated group (eplerenone group vs control group: 1868.5 ± 177.7 vs 1464.8 ± 29.7, respectively, P <0.01; hydralazine group vs control group 1554.5 ± 34.9 vs 1464.8 ± 29.7, respectively, P = 0.48). No change in IOP after eplerenone or hydralazine treatment was observed (P >0.05).
Aldosterone-induced RGC loss is not affected by systemic blood pressure or IOP.
阐明全身血压是否会影响接受全身性醛固酮治疗的大鼠视网膜神经节细胞（RGC）的存活。
实验性研究设计
通过皮下渗透微型泵持续给大鼠输注醛固酮或赋形剂。通过提供盐水作为饮用水诱导高血压。在给予醛固酮-水、醛固酮-盐水、赋形剂-水或赋形剂-盐水后的基线以及1至6周时测量收缩压、舒张压和眼压（IOP）。治疗6周后，对视网膜平铺片中逆行标记的RGC数量进行计数。接受醛固酮治疗的大鼠还接受了依普利酮（一种盐皮质激素受体拮抗剂）或肼屈嗪（一种血管扩张剂），并检测收缩压、舒张压、眼压和RGC数量的变化。
无论饮用的是水还是盐水，接受醛固酮治疗的大鼠RGC数量均显著减少（醛固酮/盐水组与赋形剂/盐水组分别为1464.8±29.7和1763.3±106.5，P = 0.01；醛固酮/水组与赋形剂/水组分别为1433.3±30.2和1815.0±193.9，P<0.01）。未观察到给予醛固酮或盐水后眼压有变化（P>0.05）。尽管接受醛固酮和盐水治疗的动物中，依普利酮或肼屈嗪治疗降低了收缩压和舒张压，但仅在依普利酮治疗组中RGC数量得以保留（依普利酮组与对照组分别为1868.5±177.7和1464.8±29.7，P<0.01；肼屈嗪组与对照组分别为1554.5±34.9和1464.8±29.7，P = 0.48）。未观察到依普利酮或肼屈嗪治疗后眼压有变化（P>0.05）。
醛固酮诱导的RGC丢失不受全身血压或眼压的影响。
