Prestimulation of tissues with forskolin significantly affected activation kinetics and binding characteristics.
2
Concentration-response curves for isoprenaline and forskolin were generated in the cerebral cortex.
3
THC was also able to antagonize the forskolin-induced elevation of intracellular cAMP concentration.
4
The effect of forskolin on cGMP regulation was investigated using dispersed rat pinealocytes.
5
Similar structure-dependent inhibitory effects were observed in forskolin-stimulated rat colonic epithelium.
6
A similar rank order of potency is seen for inhibition of forskolin-stimulated cyclic AMP.
7
Secretion furthermore was increased by overnight but not acute treatment with forskolin or 8-CPT-cAMP.
8
Removal of forskolin in cultured cotransfected cells yielded a rapid decrease in cAMP levels.
9
This was associated with decreased basal and forskolin-stimulated HGP.
10
When the cells were treated with forskolin, translocation of AQP2 to the apical membrane was observed.
11
It was significantly prolonged in forskolin-prestimulated atria, and was significantly larger in atria from failing hearts.
12
In contrast, forskolin inhibited mediator release and the inhibition increased gradually in proportion to the preincubation period.
13
When forskolin and PKC phosphorylation are combined, type V AC catalytic activity is increased 100-fold over basal levels.
14
Using forskolin as a direct stimulant of AC, alterations in the enzymatic activity of AC could be excluded.
15
CASK knockdown attenuated forskolin-enhanced insulin release, but Cask overexpression did not change the insulin-secretion suppression induced by nifedipine.
16
L-CCG-I evoked an inhibition of the forskolin-stimulated cyclic AMP production characteristic of mGluR4 with a potency comparable to L-glutamate.