This synopsis focuses on the role that tyrosine kinase pathways may play in the acute regulation of smooth muscle contractility by receptor-kinase-activating growth factors, such as epidermal growth factor-urogastrone (EGF-URO) and by G-protein-coupled agonists, such as angiotensin-II. Growth factor-activated response paradigms that modulate smooth muscle contractility are summarized and the parallels between the actions of G-protein-coupled agonists and growth factors in these response systems are pointed out. A possible dynamic interplay between tyrosine kinase and tyrosine phosphatase activities to modulate tissue tension is also hypothesized. Finally, a model is proposed, wherein an intermediary tyrosine kinase pathway is suggested as a point of convergence for the regulation of smooth muscle contractility by agonists as diverse as EGF-URO and angiotensin-II.