In vitro activity: Isoprenaline (300 nM, 3 min) increases particulate cGMP- and cilostamide-inhibited, low-Km cAMP phosphodiesterase (cAMP-PDE) activity by about 100% in intact rat fat cells. Isoprenaline inhibits insulin-stimulated glucose transport activity in rat adipocytes. Isoprenaline, in the absence of adenosine, promotes a time-dependent (t1/2 approximately 2 min) decrease in the accessibility of insulin-stimulated cell surface GLUT4 of> 50%, which directly correlated with the observed inhibition of transport activity. Isoprenaline (5 nM and 10 mM) increases cyclic AMP levels and this effect is potentiated by cilostamide (10 mM), by rolipram, a cyclic AMP-specific PDE (PDE 4) inhibitor (10 mM) and by cyclic GMP-elevating agents (50 nM ANF or 30 nM SNP plus 100 nM DMPPO). Isoprenaline increases the transcriptional activity of Gi alpha-2 gene to 140% of the control value, whereas gene specific hybridization for Gs alpha remains unchanged. Isoprenaline (20 nM) increases the amplitude of total iK and causes a negative shift of approximately 10 mV in the activation curve for iK, both in the absence and in the presence of 300 nM nisoldipine to block the L-type Ca2+ current. Isoprenaline (20 nM) increases the spontaneous pacemaker rate of sino-atrial node pacemaker cells by 16% in rabbit isolated pacemaker cells.

Cell Assay: In human umbilical vein endothelial cells (HUVECs), isoprenaline (100 nM) significantly increased the expression of connexins Cx43 and also increased Cx40 and Cx37. Also, isoprenaline increased the number of coupling cells. Isoprenaline enhanced the formation of branches and complex tube networks.

Proc Natl Acad Sci U S A. 1990 Jan;87(2):533-7; Biochem J. 1992 Nov 15;288 ( Pt 1):325-30.