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-adrenergic activation of rabbit vena
cava
The iCAPTUR4E Center, University of British Columbia, St. Paul's Hospital, Vancouver, British Columbia V6Z 1Y6, Canada
1-Aderenoceptor-mediated
constriction of rabbit inferior vena cava (IVC) is signaled by
asynchronous wavelike Ca2+ oscillations in the in situ
smooth muscle. We have shown previously that a putative nonselective
cationic channel (NSCC) is required for these oscillations. In this
report, we show that the application of 2-aminoethoxyphenyl borate
(2-APB) to antagonize inositol 1,4,5-trisphosphate (InsP3)-sensitive Ca2+ release channels
(IP3R channels) can prevent the initiation and abolish
ongoing 1-aderenoceptor-mediated tonic constriction of the venous smooth muscle by inhibiting the generation of these intracellular Ca2+ concentration
([Ca2+]i) oscillations. The observed effects
of 2-APB can only be attributed to its selective inhibition on the
IP3R channels, not to its slight inhibition of the L-type
voltage-gated Ca2+ channel and the sarco(endo)plasmic
reticulum Ca2+ ATPase. Furthermore, 2-APB had no effect on
the ryanodine-sensitive Ca2+ release channel and the
store-operated channel (SOC) in the IVC. These results indicate that
the putative NSCC involved in refilling the sarcoplasmic reticulum (SR)
and maintaining the tonic contraction is most likely an SOC-type
channel because it appears to be activated by
IP3R-channel-mediated SR Ca2+ release or store
depletion. This is in accordance with its sensitivity to
Ni2+ and La3+ (SOC blockers). More
interestingly, RT-PCR analysis indicates that transient receptor
potential (Trp1) mRNA is strongly expressed in the rabbit IVC. The Trp1
gene is known to encode a component of the store-operated NSCC. These
new data suggest that the activation of both the IP3R
channels and the SOC are required for PE-mediated [Ca2+]i oscillations and constriction of the
rabbit IVC.
inosital 1,4,5-trisphosphate; store-operated channels; transient receptor potential gene; vascular smooth muscle
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