Effect of Chronic Kidney Disease on Changes in Vasopressin System Expression in the Kidney Cortex in Rats with Nephrectomy

Abstract

It is believed that the vasopressinergic system plays an important role in the pathogenesis of chronic kidney disease (CKD). The aim of this study was to evaluate the effect of CKD on changes in vasopressin system expression in the kidney cortex in rats with nephrectomy. The study was performed on 4 groups of Sprague Dawley (SPRD) rats: a control group (CN), 1/2 nephrectomy (N1/2), 2/3 nephrectomy (N2/3), and 5/6 nephrectomy (N5/6). Blood and the kidney cortex were collected to evaluate plasma copeptin concentrations and mRNA expressions of V1a vasopressin receptors (V1aR) and V2 vasopressin receptors (V2R) and V1aR, V2R, and aquaporin 2 (AQP2) protein levels. V1aR and V2R mRNA expression in the kidney cortex was significantly lower in the CN group compared with the other groups. In contrast, the V1aR, V2R, and AQP2 protein levels were significantly higher in the CN group compared with all of the nephrectomized groups. Plasma copeptin concentration was significantly lower in the CN group than in the nephrectomized groups. CKD caused significant changes in the expression of the vasopressinergic system. Further research is needed to explain the mechanisms of the impact of the vasopressinergic system on the kidney in CKD.

Comparative quantitation of aquaporin-2 and arginine vasopressin receptor-2 localizations among chronic kidney disease and healthy kidney in dogs

“…As a result, CKD caused a significant change in the AVPR2 protein in the nephrectomy group compared to the control group in rat kidney with experimental nephrectomy models, and the findings revealed that CKD caused by nephrectomy was strongly associated with polyuria and a vasopressin-resistant decreased expression of AQP2 [48], which was similar to our findings. The rat with hypercalcemia and hypokalemia had vasopressin-resistant polyuria in urinary concentrating ability [45,49] and increased prostaglandin production [50], there were decreased adenylate cyclase and cAMP (the second messenger for vasopressin action), resulting in decrease in AQP2 expression [13].…”

Soluble ACE2-mediated cell entry of SARS-CoV-2 via interaction with proteins related to the renin-angiotensin system

“…It can also control tonicity of body fluids by converting to arginine vasopressin (AVP) that can further regulate the arterial blood pressure (Demiselle et al, 2020). Consistently, due to their regulatory roles in maintaining homeostasis of kidney and heart, dysregulated expressions of vasopressin and AVP were also directly linked to the development of renal failure and cardiovascular system diseases (Czarzasta et al, 2018). Therefore, further investigation of the identified VDFs involved in cardiac and renal disease development may provide mechanistic insights into SARS-CoV-2-induced extrapulmonary diseases.…”

Local cyclic adenosine monophosphate signalling cascades—Roles and targets in chronic kidney disease

“…Hyperactivation of the AVP system is associated with kidney damage, such as glomerular hyperfiltration and kidney hypertrophy and CKD progression, as initially recognized in rats 90 . Rats respond to 5/6 nephrectomy with an increase in vasopressin V1a and V1b receptors (V1aR and V1bR), as well as with elevated V2R and AVP mRNA levels in the kidney cortex 91 . An increase in serum AVP and excessive stimulation of V2R leads to the progression of CKD 90,92 .…”

“…90 Rats respond to 5/6 nephrectomy with an increase in vasopressin V1a and V1b receptors (V1aR and V1bR), as well as with elevated V2R and AVP mRNA levels in the kidney cortex. 91 An increase in serum AVP and excessive stimulation of V2R leads to the progression of CKD. 90,92 Brattleboro rats cannot produce AVP, and Brattleboro rats with 5/6 nephrectomy display a milder course of CKD compared to control animals that express AVP; kidney hypertrophy, hyperfiltration, proteinuria and progression of CKD are less pronounced if AVP is absent.…”