Alpha 2-adrenoceptor mediated inhibition of forskolin-stimulated cyclic AMP accumulation in isolated porcine palmar lateral veins.

The aim of this study was to use a 3H-adenine pre-labelling technique to characterise the effect of alpha 2-adrenoceptor activation on forskolin-stimulated cyclic AMP accumulation in the isolated porcine palmar lateral vein. Forskolin (10(-7)-10(-4) M) stimulated 3H-cyclic AMP accumulation in the isolated porcine palmar lateral vein in a biphasic and concentration-dependent manner. In the absence of the cyclic AMP-selective phosphodiesterase inhibitor rolipram, forskolin stimulated 3H-cyclic AMP accumulation approximately 7-8 fold. The response reached a peak after 5 min. In the presence of rolipram (10(-5) M), basal 3H-cyclic AMP levels were approximately 70% higher than in its absence (basal: 1823 +/- 57 dpm; rolipram: 3088 +/- 229, n = 3) and forskolin (3 x 10(-5) M) stimulated 3H-cyclic AMP accumulation approximately 8 fold. The latter response reached a plateau 10 min after the addition of forskolin. In all subsequent studies, the tissues were incubated with forskolin (3 x 10(-5) M) for 5 min in the absence of rolipram. Noradrenaline (NA; 10(-9)-10(-4) M) and UK14304 (10(-9)-10(-4) M) inhibited forskolin-stimulated 3H-cyclic AMP accumulation in a concentration-dependent manner with mean pIC50 values of 7.61 +/- 0.37 (n = 4) and 7.76 +/- 0.23 (n = 5), respectively. With either NA or UK14304, the maximal inhibition of the forskolin response obtained was approximately 75%. Neither NA (10(-4) M) nor UK14304 (10(-4) M) altered basal 3H-cyclic AMP levels.(ABSTRACT TRUNCATED AT 250 WORDS)