H,K-ATPase type 2 contributes to salt-sensitive hypertension induced by K(+) restriction.

Walter, Christine; Tanfous, Mariem Ben; Igoudjil, Katia; Salhi, Amel; Escher, Geneviève; Crambert, Gilles (2016). H,K-ATPase type 2 contributes to salt-sensitive hypertension induced by K(+) restriction. Pflügers Archiv : European journal of physiology, 468(10), pp. 1673-1683. Springer 10.1007/s00424-016-1872-z

Preview

Text s00424-016-1872-z.pdf - Published Version Available under License Publisher holds Copyright. Download (1MB) | Preview

In industrialized countries, a large part of the population is daily exposed to low K(+) intake, a situation correlated with the development of salt-sensitive hypertension. Among many processes, adaptation to K(+)-restriction involves the stimulation of H,K-ATPase type 2 (HKA2) in the kidney and colon and, in this study, we have investigated whether HKA2 also contributes to the determination of blood pressure (BP). By using wild-type (WT) and HKA2-null mice (HKA2 KO), we showed that after 4 days of K(+) restriction, WT remain normokalemic and normotensive (112 ± 3 mmHg) whereas HKA2 KO mice exhibit hypokalemia and hypotension (104 ± 2 mmHg). The decrease of BP in HKA2 KO is due to the absence of NaCl-cotransporter (NCC) stimulation, leading to renal loss of salt and decreased extracellular volume (by 20 %). These effects are likely related to the renal resistance to vasopressin observed in HKA2 KO that may be explained, in part by the increased production of prostaglandin E2 (PGE2). In WT, the stimulation of NCC induced by K(+)-restriction is responsible for the elevation in BP when salt intake increases, an effect blunted in HKA2-null mice. The presence of an activated HKA2 is therefore required to limit the decrease in plasma [K(+)] but also contributes to the development of salt-sensitive hypertension.

Interest & Impact

Downloads

219 since deposited on 04 Jun 2018
41 in the past 12 months

Citations

5 Citations in Web of Science ®
6 Citations in Scopus

Search

in Google Scholar™

Services

Actions (login required)

Edit item

Actions (login required)

Edit item