Activation of nitric oxide modulator effect by isometric contraction in rat resistance arteries.
The participation of nitric oxide (NO) as a modulator of the isometric contraction, as well as the underlying mechanism, was investigated in rat small mesenteric arteries. In the presence of a functional endothelium, L-NAME and L-NA similarly increased the contractions induced by phenylephrine, dependently on the level of contraction. However, no effect was observed in the absence of a functional endothelium. In the presence of selective inhibitors of protein kinase C (PKC) and phosphatidyl-inositol 3-kinase (PI3K), calphostin-C and wortmannin, respectively, the effect of L-NAME was not modified. The same observation was done in the presence of the tyrosine kinase inhibitors, genistein and tyrphostin A-23. However, in the presence of a Ca2+-independent tyrosine kinase inhibitor, erbstatin-A, and on the presence of a non-selective kinase inhibitor, staurosporine, a strong reduction was observed. Our results suggest that protein kinases are involved in the activation of nitric oxide modulator effect on isometric contractions in resistance arteries.
Rezende
Bruno A
BA
Depto. de Fisiologia e Biofísica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte-MG, Brazil.
Lemos
Virgínia S
VS
Cortes
Steyner F
SF
D000818:Animals; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D010656:Phenylephrine / Q000494:pharmacology; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D014655:Vascular Resistance; D014661:Vasoconstriction / Q000187:drug effects*
D010656:Phenylephrine; D009569:Nitric Oxide; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D019331:NG-Nitroarginine Methyl Ester