Activation by alpha 1-adrenergic agonists of the progression phase in the proliferation of primary cultures of smooth muscle cells in mouse and rat aorta.

The effects of catecholamines on the competence and progression phases in the proliferation of vascular smooth muscle cells (SMCs) in mouse and rat were investigated in primary cultures: alpha,beta-Adrenergic agonists such as epinephrine and norepinephrine, and the alpha-adrenergic agonist, phenylephrine, stimulated proliferation of primary cultured SMCs, whereas the alpha 2-adrenergic agonist, clonidine, and beta-adrenergic agonist, isoproterenol, did not. The stimulating effect of epinephrine was maximal at 0.54 microM and was then decreased at higher concentrations. The alpha-adrenergic antagonist, phentolamine, and alpha 1-adrenergic antagonist, prazosin, inhibited epinephrine-induced SMC proliferation, while the alpha 2-adrenergic antagonist, yohimbine, and beta-adrenergic antagonist, propranolol, did not. In primary cultured and synchronized SMCs at the G0 phase, norepinephrine accelerated the rate of SMC proliferation, but did not change the starting time of DNA synthesis and proliferation. These results show that catecholamines activate the progression phase in primary cultured aortic SMCs alpha 1-adrenergic receptors.