Studies were performed to determine the significance of temporal variation
in vascular smooth muscle Ca2+ signaling during acute arteriolar myogenic c
onstriction and, in particular, the importance of the stretch-induced intra
cellular Ca2+ concentration ([Ca2+](i)) transient in attaining a steady-sta
te mechanical response. Rat cremaster arterioles (diameter similar to 100 m
u m) were dissected from surrounding tissues, and vessel segments were pres
surized in the absence of intraluminal flow. For [Ca2+](i) measurements, ve
ssels were loaded with fura 2 and fluorescence emitted by excitation at 340
and 380 am was measured using video-based image analysis. Ca2+ and diamete
r responses were examined after increases in intravascular pressure were ap
plied as an acute step increase or a ramp function. Additional studies exam
ined the effect of longitudinal vessel stretch on [Ca2+](i) and arteriolar
diameter. Step increase in intraluminal pressure (from 50 to 120 mmHg) caus
ed biphasic change in [Ca2+](i) and diameter. [Ca2+](i) transiently increas
ed to 114.0 +/- 2.0% of basal levels and subsequently declined to 106.7 +/-
4.4% at steady state. Diameter initially distended to 125.4 +/- 2.1% of ba
sal levels before constricting to 71.1 +/- 1.2%. In contrast, when the same
pressure increase was applied as a ramp function (over 5 min) transient ve
ssel distension and transient increase in [Ca2+](i) were prevented, yet at
steady state vessels constricted to 71.3 +/- 2.5%. Longitudinal stretch res
ulted in a large [Ca2+](i) transient (158 +/- 19% of basal) that returned t
o baseline despite maintenance of the stretch stimulus. The data demonstrat
e that the initial vessel distension (reflecting myocyte stretch) and assoc
iated global [Ca2+](i) transient are not obligatory for myogenic contractio
n. Thus, although arteriolar smooth muscle cells are responsive to acute st
retch, the resulting changes in myogenic tone may be more closely related t
o other mechanical variables such as wall tension.