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Articles in PresS, published online ahead of print December 6, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00637.2001
Submitted on July 23, 2001
Accepted on December 3, 2001
1-adrenoceptor mediated venoconstriction
1 The iCAPTUR4E Center, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia, Canada
* To whom correspondence should be addressed. E-mail: chenghan{at}interchange.ubc.ca.
1-aderenoceptor mediated constriction of rabbit inferior vena cava (IVC) is signaled by asynchronous Ca2+ oscillations in the in situ smooth muscle. We have shown previously that a putative non-selective cationic channel (NSCC) is required for these oscillations. In this report, we showed that the application of 2-APB to antagonize IP3-sensitive Ca2+ release channel (IP3R-channels) can prevent the initiation and abolish ongoing 1-adrenoceptor mediated tonic constriction of the venous smooth muscle by inhibiting the generation of these [Ca2+]i oscillations. Moreover, the observed effects of 2-APB can only be attributed to its selective inhibition on the IP3R-channels, not to its slight inhibition on the L-type voltage-gated Ca2+ channels or sarcoplasmic/endoplasmic 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 findings indicate that the putative NSCC involved in refilling of the sarcoplasmic reticulum (SR) is most likely a SOC-type channel as 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 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.
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