@article {Chiu934, author = {A T Chiu and J M Bozarth and M S Forsythe and P B Timmermans}, title = {Ca++ utilization in the constriction of rat aorta to stimulation of protein kinase C by phorbol dibutyrate.}, volume = {242}, number = {3}, pages = {934--939}, year = {1987}, publisher = {American Society for Pharmacology and Experimental Therapeutics}, abstract = {To determine the role of activated protein kinase C in vascular smooth muscle contraction, phorbol dibutyrate was used to stimulate this enzyme in order to evaluate the source(s) of Ca++ (10(-8) to 3 X 10(-6) M) elicited a concentration-dependent sustained contraction which was slow in onset but progressive in developed tension. The maximal contractile response induced by phorbol dibutyrate was only partly dependent on influx of extracellular Ca++ as shown by similar reductions (40\%) produced by Ca++-free buffer, LaCl3 (1 mM) or nifedipine (10(-6) M). These data suggest that phorbol dibutyrate is able to open Ca++ channels which are sensitive to nifedipine blockade. However, unlike norepinephrine or K+-depolarization, phorbol dibutyrate evoked a slow 45Ca++ influx which occurred only after extended contact time. Pretreatment with nifedipine again abolished this response. In contrast to norepinephrine, phorbol dibutyrate did not cause 45Ca++ efflux indicating that intracellular Ca++ was not mobilized. It is concluded that the residual 60\% contraction to phorbol dibutyrate most likely occurs via a mechanism independent of the Ca-calmodulin pathway.}, issn = {0022-3565}, URL = {https://jpet.aspetjournals.org/content/242/3/934}, eprint = {https://jpet.aspetjournals.org/content/242/3/934.full.pdf}, journal = {Journal of Pharmacology and Experimental Therapeutics} }