No apparent role for T-type Ca2+ channels in renal autoregulation

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Rasmus Hassing Frandsen, Max Salomonsson, Pernille B. Lærkegaard Hansen, Lars Jørn Jensen, Thomas Hartig Braunstein, Niels-Henrik von Holstein-Rathlou, Charlotte Mehlin Sørensen

Renal autoregulation protects glomerular capillaries
against increases in renal perfusion pressure (RPP). In
the mesentery, both L- and T-type calcium channels are involved
in autoregulation. L-type calcium channels participate
in renal autoregulation, but the role of T-type channels is not
fully elucidated due to lack of selective pharmacological inhibitors.
The role of T- and L-type calcium channels in the
response to acute increases in RPP in T-type channel knockout
mice (CaV3.1) and normo- and hypertensive rats was examined.
Changes in afferent arteriolar diameter in the kidneys
from wild-type and CaV3.1 knockout mice were assessed.
Autoregulation of renal blood flow was examined during
acute increases in RPP in normo- and hypertensive rats under
pharmacological blockade of T- and L-type calcium channels
using mibefradil (0.1 μM) and nifedipine (1 μM). In contrast
to the results from previous pharmacological studies, genetic
deletion of T-type channels CaV3.1 did not affect renal autoregulation.
Pharmacological blockade of T-type channels
using concentrations of mibefradil which specifically blocks
T-type channels also had no effect in wild-type or knockout
mice. Blockade of L-type channels significantly attenuated
renal autoregulation in both strains. These findings are supported by in vivo studies where blockade of T-type channels
had no effect on changes in the renal vascular resistance
after acute increases in RPP in normo- and hypertensive rats.
These findings show that genetic deletion of T-type channels
CaV3.1 or treatment with low concentrations of mibefradil
does not affect renal autoregulation. Thus, T-type calcium
channels are not involved in renal autoregulation in response
to acute increases in RPP.
OriginalsprogEngelsk
TidsskriftPflügers Archiv - European Journal of Physiology
Vol/bind468
Udgave nummer4
Sider (fra-til)541-550
Antal sider10
ISSN0031-6768
DOI
StatusUdgivet - 2016

ID: 153732711