背景:肾素-血管紧张素-醛固酮系统在慢性肾病(CKD)猫中的作用尚未完全了解。
目的:表征CKD猫肾内肾素-血管紧张素系统(RAS)的成分。
方法:11只自然发生CKD的猫(CKD组)和8只健康对照猫。
方法:通过逆转录聚合酶链反应评估肾组织样本中的肾素,血管紧张素原,血管紧张素转换酶(ACE),和血管紧张素II1型受体转录水平,并通过液相色谱-质谱法对血管紧张素I进行定量,II,III,和IV浓度。线性混合模型用于比较各组之间的基因转录水平和血管紧张肽的浓度。
结果:与健康对照猫相比,CKD组的猫明显年龄较大(P<.001),并且更可能被绝育(P=.007)。与对照猫相比,患有CKD的猫的肾脏具有明显更高的血管紧张素原转录水平(P<.001)和更低的ACE转录水平(P<.001)。与对照肾脏相比,CKD中的肾脏血管紧张素I浓度增加(P=0.001)。两组之间肾脏转录水平或血管紧张肽浓度没有其他显着差异。
结论:CKD猫肾内RAS可能被激活。小样本量和年龄差异,中性状态,两组之间的饮食钠摄入量可能限制了确定肾脏血管紧张素II浓度显着差异的能力。
BACKGROUND: The role of the renin-angiotensin-aldosterone system in cats with chronic kidney disease (CKD) is incompletely understood.
OBJECTIVE: To characterize components of the intrarenal renin-angiotensin system (RAS) in cats with CKD.
METHODS: Eleven cats with naturally occurring CKD (CKD group) and 8 healthy control cats.
METHODS: Renal tissue samples were evaluated by reverse-transcription polymerase chain reaction for renin, angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin II type 1 receptor transcript levels, and by liquid chromatography-mass spectrometry for quantification of angiotensin I, II, III, and IV concentrations. Linear mixed models were used to compare gene transcript levels and concentrations of angiotensin peptides between groups.
RESULTS: Cats of the CKD group were significantly older (P < .001) and more likely to be neutered (P = .007) than healthy control cats. Kidneys from cats with CKD had significantly higher transcript levels of angiotensinogen (P < .001) and lower transcript levels of ACE (P < .001) than those from control cats. Renal angiotensin I concentrations were increased in CKD compared with control kidneys (P = .001). No other significant differences in renal transcript levels or angiotensin peptide concentrations were noted between groups.
CONCLUSIONS: The intrarenal RAS might be activated in cats with CKD. Small sample size and differences in age, neuter status, and dietary sodium intake between groups might have limited the ability to identify a significant difference in concentration of renal angiotensin II.