AJP - Heart and Circulatory Physiology, Vol 253, Issue 6 1365-H1371, Copyright © 1987 by American Physiological Society
Intracellular calcium levels in phorbol ester-induced contractions of vascular muscle
M. J. Jiang and K. G. Morgan
Cardiovascular Division, Charles A. Dana Research Institute, Boston, Massachusetts.
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 microM) 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(beta-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 alpha
1-adrenergic agonist phenylephrine (10(-5) M) induced less than 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 microM) and DPBA (1
microM) induced contractions without increasing [Ca2+]i; Ca2+-free EGTA-PSS
or the addition of the calcium channel blocker gallopamil (D600, 1 microM),
however, abolished greater than 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
alpha 1-agonists may activate vascular smooth muscle.
