Author:
Bal MS,Paulis L,Zicha J,Kuneš J
Abstract
Alterations of calcium handling and other second messenger
cascades including protein kinase C (PKC) and A (PKA) were
suggested to be responsible for abnormal vascular function in
spontaneously hypertensive rats (SHR). However, the relative
contribution of these pathways to vasoconstriction is still not
completely understood. We investigated the effect of Ro 31-8220
(PKC inhibitor) and H89 (PKA inhibitor) on vasoconstriction
induced by 120 mM KCl or by addition of 10 µM noradrenaline
(NA) in isolated femoral arteries of control Wistar rats and SHR.
Moreover, we investigated these responses in the presence and
absence of Ca2+ ions in the incubation medium in order to assess
the role of calcium influx in these contractions. We observed that
while the vasoconstriction in the presence of calcium was not
different between Wistar and SHR, the difference between
constriction elicited by NA addition in the absence and presence
of external calcium was larger in SHR. The inhibition of PKC had
no effect on constrictions in SHR, but diminished constrictions in
Wistar rats. PKA inhibition slightly enhanced constrictions in
Wistar rats, but reduced them in the presence of calcium in SHR.
We conclude that vasoconstriction elicited by adrenergic
stimulation is more dependent on extracellular calcium influx in
SHR compared to Wistar rats. Moreover, the activation of PKA
contributes to this calcium-dependent vasoconstriction in SHR but
not in Wistar. On the other hand, PKC activation seems to play a
less important role in vasoconstriction in SHR than in Wistar rats.
Publisher
Institute of Physiology of the Czech Academy of Sciences
Subject
General Medicine,Physiology
Cited by
3 articles.
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