Altered expression of Aquaporin-2 in one-kidney, one-clip hypertension

VATTA, MARCELO; BARCHUK, MAGALÍ; ALBERTONI BORGHESE, MARIA FLORENCIA; DAVIO, CARLOS; MAJOWICZ, MÓNICA; ORTIZ, MARIA DEL CARMEN; KESSLER, CAMILA; HOPE, SANDRA

LIFE SCIENCES

PERGAMON-ELSEVIER SCIENCE LTD

Lugar: Amsterdam; Año: 2018 vol. 208 p. 72 - 78

0024-3205

Aims: The aim of the present study was to evaluate the regulation of Aquaporin-2 (AQP2) water channel in thekidney of one-kidney, one-clip rats (Goldblatt-1 model). In addition, some mechanisms that underlie the role ofAQP2 in the Goldblatt-1 model were evaluated.Main methods: Sprague-Dawley rats were divided in three groups: control two-kidney, no clip (C, 2 K-NC); nephrectomizedone-kidney, no clip (N, 1 K-NC) and Goldblatt one-kidney, one-clip (G, 1 K-1C). AQP2 expression(by westernblot, real time PCR, immunohistochemistry and immunofluorescence), vasopressin V2 receptor expression(by real time PCR), cAMP concentration, NFkB and TonEBP (cytosol to nucleus ratio) were evaluated inthe renal medulla.Key findings: AQP2 expression, V2 receptor expression and cAMP concentration were decreased in the renalmedulla of 1 K-1C rats, NFkB translocation was favoured towards the nucleus suggesting its activation whileTonEBP translocation was not altered in this model of hypertension.Significance: In this model of hypertension the decrease of AQP2 expression could be a mechanism that counteractsthe high blood pressure promoting water excretion and this may be consequence of decreased vasopressinsensitivity and/or the increased activity of NFkB at renomedullary collecting duct level. Given that renovascularhypertension is among the most common causes of secondary hypertension, it is important to elucidate all therelevant mechanisms involved in the generation or in the compensation of the hypertensive state in order toimprove the diagnoses and treatment of the patients.