Background:

Isoprenaline HCl is an agonist of β-adrenergic receptor [1].

The adrenergic receptors are a class of G protein-coupled receptors that are targets of norepinephrine and epinephrine. When reacting with epinephrine, β-adrenergic receptor causes vasodilation.

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 [2].

In the isolated field stimulated rat vas deferens, isoprenaline inhibited contractions with EC50 value of 45.6 nM. In tissues in which β 2-adrenoreceptors were maximally blocked by timolol, isoprenaline inhibited contractility with EC50 value of 1.5 μM [1]. In CFW mice, IPR caused the maximal proliferative response of bone marrow cells and increased erythropoietic activity. These results suggested that isoprenaline activated beta-adrenergic receptor, which then increased the proliferative and differentiation activities of hemopoietic stem cells [3].

参考文献:
[1].  Lotti VJ, Cerino D, Kling P. Characterization of the adrenoreceptor activities of isoprenaline in the field stimulated rat vas deferens: selective supersensitivity to beta 2-mediated responses following reserpine treatment. J Auton Pharmacol, 1982, 2(3): 169-174.
[2].  Dhein S, Gaertner C, Georgieff C, et al. Effects of isoprenaline on endothelial connexins and angiogenesis in a human endothelial cell culture system. Naunyn Schmiedebergs Arch Pharmacol, 2015, 388(1): 101-108.
[3].  Lipski S. Effect of beta-adrenergic stimulation by isoprenaline on proliferation and differentation of mouse bone marrow cells in vivo. Pol J Pharmacol Pharm, 1980, 32(3): 281-287.