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At least 397 records · Page 22Linked to original sources
PubMed1990

Effects of E-1020, a new cyclic AMP-specific phosphodiesterase inhibitor, on cyclic AMP and cytosolic free calcium of cultured vascular smooth muscle cells.

The purpose of this study is to clarify the pharmacological effects of E-1020 a new cAMP-specific phosphodiesterase (PDE) inhibitor, on cAMP or cytosolic free calcium (Ca) of cultured vascular smooth muscle cells (VSMC). VSMC were separated from the thoracic aorta of 2- to 3-month-old Wistar Kyoto rats (WKY). cAMP was measured by using the 125I-cAMP radioimmunoassay kit. The cytosolic free Ca of VSMC was measured by using the fluorescence Ca indicator, Fura-2/acetoxymethyl ester (Fura-2/AM). As a result, E-1020 increased the cAMP of VSMC in a dose-dependent manner, and about two fold increase in cAMP was observed by 10(-4) M E-1020. E-1020 decreased the cytosolic free concentration of Ca in a dose-dependent manner, and a significant decrease in cytosolic free Ca was observed by greater than 10(-6) M E-1020. These effects of E-1020 on cAMP and cytosolic free Ca were enhanced in the presence of low concentration (10(-8) M) of DL-noradrenaline. That is, a more prominent decrease in cytosolic free Ca than that of E-1020 alone was observed. Our results show that E-1020 decreases cytosolic free Ca of VSMC in parallel with increase in cAMP, and thereby suggest a potential vasodilating activity in vivo.

Animals↗
PubMed1993

Influence of Mn ion the action of dibutyryl cyclic AMP and forskolin on contraction, membrane response, and cyclic AMP-dependent protein kinase activity in rat myometrium.

Contractile response, membrane activity, and protein kinase A (PKA) activity were measured on the longitudinal muscle taken from the estrogen-treated rat uterus, and the influence of Mn ion on the inhibitory effects caused by db cAMP and forskolin was investigated. Phasic contractions generated in the muscle taken from the middle portion of uterus were depressed to 48 and 83% by 30 microM db cAMP and 0.1 microM forskolin in Mg-free Krebs solution, respectively; phasic contractions were more strongly depressed by the agents in the solution containing 0.2 mM Mn. Action potentials consisted of spike and plateau components, and the duration of the plateau potential was reduced by the application of the agents; membrane activity was more strongly depressed in the presence of 0.2 mM Mn. The contractile depression caused by db cAMP was reduced and by forskolin was enhanced by pretreatment of the tissue with 0.6 mM Mn for 30 min. The PKA activity was increased by 39 and 6% of the control, when 30 microM db cAMP and 0.1 microM forskolin were applied, respectively; the PKA activity in response to db cAMP and forskolin was reduced and enhanced, respectively, when the tissues were pretreated with 0.6 mM Mn. It was proposed that Mn ions permeated into cell interior when the muscle was exposed to 0.6 mM Mn, so that the effects of the agents were differently affected. It was also shown that plateau potential dominated in the muscle taken from the ovarian portion, and the contractile inhibition caused by the agents was far weaker.

Action Potentials↗
PubMed1991

Lack of correlation between activation of cyclic AMP-dependent protein kinase and inhibition of contraction of rat vas deferens by cyclic AMP analogs.

The effects of N6,O2-dibutyrl-adenosine-3',5'-cyclic monophosphate (db-cAMP) and 8-bromo-adenosine-3',5'-cyclic monophosphate (8-Br-cAMP) on tension and cAMP-dependent protein kinase (PKA) activities in rat vas deferens were investigated. A soluble enzyme fraction obtained from the vas deferens was found to contain both type I and type II isozymes of PKA, whereas a particulate fraction contained only the type II isozyme. Exposure of the vas deferens to db-cAMP (1-100 microM) for 30 min caused a concentration-dependent inhibition of phenylephrine-induced contractions, with an EC50 of less than 10 microM. 8-Br-cAMP had no significant effect on contractions over a similar concentration range. Both of the analogs were able to activate PKA significantly at a concentration of 10 microM, and the magnitude of the PKA activation was greater with 8-Br-cAMP than with db-cAMP. Charcoal was added to the homogenization buffer in these experiments to prevent the artifactual activation of PKA by cAMP analogs trapped in the extracellular space. The ability of db-cAMP, but not 8-Br-cAMP, to inhibit the contraction of vas deferens could not be explained on the basis of differential activation of soluble or particulate PKA or of specific isozymes of the enzyme. It is, therefore, concluded that activation of PKA is not responsible for the relaxant effects of cAMP analogs in some smooth muscle.

8-Bromo Cyclic Adenosine Monophosphate↗