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1 Institute of Membrane & Systems Biology, University of Leeds, Leeds, United Kingdom
* To whom correspondence should be addressed. E-mail: d.j.beech{at}leeds.ac.uk.
Smooth muscle cells in arterioles have pivotal roles in the determination of blood pressure and distribution of local blood flow. The cells exhibit calcium-entry in response to passive store-depletion but the mechanisms and relevance of this phenomenon are poorly understood. Previously, a role for canonical transient receptor potential 1 (TRPC1) was indicated but heterologous expression studies showed TRPC1 to have poor function in isolation, suggesting requirement for additional proteins. Here we test the hypothesis that TRPC5 is such an additional protein because TRPC5 forms heteromultimeric channels with TRPC1 and RNA encoding TRPC5 is present in arterioles. Recordings were from arteriolar fragments freshly isolated from rabbit pial membrane. Ionic current in response to store-depletion has properties like that of the TRPC1/TRPC5 heteromultimer and so the effect of the E3-targeted externally-acting anti-TRPC5 blocking antibody (T5E3) was explored. T5E3 suppressed calcium entry in store-depleted arterioles but had no effect in the absence of store-depletion. T5E3 pre-adsorbed to its antigenic peptide did not inhibit calcium-entry. TRPC6 is commonly detected in smooth muscle and is present in the arterioles, but T5E3 had no effect on TRPC6. The data suggest that calcium entry occurring in response to passive store-depletion in smooth muscle cells of arterioles involves TRPC5 as well as TRPC1.
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