AJP - Heart and Circulatory Physiology, Vol 257, Issue 2 649-H657, Copyright © 1989 by American Physiological Society
[Ca2+]i and contraction of ear artery in response to rapid stimulation by NE: measurements with quin2 and fura-2
M. Vonderlage and V. Schreiner
Department of Physiology, University of Hamburg, Federal Republic of Germany.
The relationship between the quin2 and fura-2 fluorescence and
isovolumetric contraction of smooth muscle cells of everted segments of the
rabbit ear artery in response to rapid stimulation by norepinephrine (NE)
was investigated. The resting level measured with quin2 (91 +/- 10 nM, n =
4) and with fura-2 (87 +/- 9 nM, n = 5) did not significantly differ. After
addition of NE, an initial slow increase (ISI) in emission could be
measured with quin2; however, Ca2+ buffering by this indicator slowed the
increase of intracellular Ca2+ concentration ([Ca2+]i) and of contraction.
When using fura-2, no ISI could be measured, but this indicator did not
significantly interfere with the normal time course of contraction. Maximal
response in [Ca2+]i to 1 microM NE was 424 +/- 30 nM (with quin2) and 337
+/- 46 nM (with fura-2). Mechanical latency depended not only on the onset
but also on the initial rate of the increase in [Ca2+]i. Contractile
response was quickest around 0.1 s after the onset of the fura-2 signal.
During its rising phase, the rate of pressure development was linearly
correlated with the -log molar Ca2+ concentration (pCa) of the cytoplasm
(pCai), whereas during slow relaxation, pressure was linearly related to
the pCai. These results suggest that contraction may depend not only on
[Ca2+]i but also depend on its rate of change.
