Intracellular calcium concentration ([Ca2+](i)) was measured with aequorin in ferret and rat aortic strips contracted with phorbol esters. In ferret aorta, 12-deoxyphorbol 13-isobutyrate 20-acetate (DPBA, 1 μM) induced contractions without significantly increasing [Ca2+](i), whereas 21 mM K+ induced smaller contractions with a significant rise in [Ca2+](i). Ca2+-free 2.5 mM ethyleneglycol-bis(β-aminoethylether)-N,N'-tetraacetic acid (EGTA)-physiological saline solution (PSS) had no effect on DPBA-induced tension, whereas it abolished contractions induced by 66 mM K+. The α1-adrenergic agonist phenylephrine (10-5 M) induced <10% of the tension with no initial [Ca2+](i) spike under Ca-free conditions. In rat aorta, both phorbol 12-myristate 13-acetate (PMA, 2 μM) and DPBA (1 μM) induced contractions without increasing [Ca2+](i); Ca2+-free EGTA-PSS or the addition of the calcium channel blocker gallopamil (D600, 1 μM), however, abolished >50% of the tension induced by either phorbol ester with a decrease in [Ca2+](i). These results are consistent with the idea that 1) resting [Ca2+](i) is both sufficient and required to support phorbol ester-induced contractions in two vascular smooth muscles, suggesting an increased sensitivity of the contractile apparatus for Ca2+, and 2) there are differences in the mechanisms by which phorbol esters and α1-agonists may activate vascular smooth muscle.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Publication status||Published - 1987 Dec 1|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)