
Effect of protein kinase C and protein kinase A inhibitors on contraction of isolated femoral arteries of SHR and Wistar rats
Author(s) -
Manjot Bal,
Ľudovít Paulis,
Josef Zicha,
Jaroslav Kuneš
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931643
Subject(s) - vasoconstriction , protein kinase c , endocrinology , medicine , calcium , chemistry , contraction (grammar) , protein kinase a , vascular smooth muscle , rho kinase inhibitor , extracellular , stimulation , rho associated protein kinase , kinase , biochemistry , smooth muscle
Alterations of calcium handling and other second messengercascades including protein kinase C (PKC) and A (PKA) weresuggested to be responsible for abnormal vascular function inspontaneously hypertensive rats (SHR). However, the relativecontribution of these pathways to vasoconstriction is still notcompletely understood. We investigated the effect of Ro 31-8220(PKC inhibitor) and H89 (PKA inhibitor) on vasoconstrictioninduced 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 andabsence of Ca2+ ions in the incubation medium in order to assessthe role of calcium influx in these contractions. We observed thatwhile the vasoconstriction in the presence of calcium was notdifferent between Wistar and SHR, the difference betweenconstriction elicited by NA addition in the absence and presenceof external calcium was larger in SHR. The inhibition of PKC hadno effect on constrictions in SHR, but diminished constrictions inWistar rats. PKA inhibition slightly enhanced constrictions inWistar rats, but reduced them in the presence of calcium in SHR.We conclude that vasoconstriction elicited by adrenergicstimulation is more dependent on extracellular calcium influx inSHR compared to Wistar rats. Moreover, the activation of PKAcontributes to this calcium-dependent vasoconstriction in SHR butnot in Wistar. On the other hand, PKC activation seems to play aless important role in vasoconstriction in SHR than in Wistar rats.