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Addenda

Selective Downregulation of the BKβ1 Subunit in Diabetic Arteriolar Myocytes

Mary K. McGahon, Xiaohong Zhang, C. Norman Scholfield, Timothy M. Curtis and J. Graham McGeown

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Diabetic retinopathy is an important cause of visual loss. Functional abnormalities including vasoconstriction precede structural changes. Using the streptozotocin-model of diabetes in rats, we have identified down-regulation of the β1 subunit of the BK channel in arteriole myocytes as a possible molecular mechanism underlying these early changes. BKβ1 mRNA levels were reduced as early as 1 month after induction of diabetes, and BK Ca2+-sensitivity and caffeine-evoked BK currents were reduced at 3 months. This effect appears to be selective for the regulatory subunit, as BKα subunit expression was not altered at the mRNA level, and voltage-activated BK currents were unaltered. No changes were seen in voltage activated Ca2+-current, Ca2+-activated Cl--current, or A-type voltage activated K+-currents. Reduced Ca2+-activated BK activity may promote depolarization, Ca2+-channel activation and increased contraction under resting conditions or in response to Ca2+-mobilizing agonists.

Authors

Mary K. McGahon

Centre for Vision Sciences; School of Biomedical Sciences; The Queen's University of Belfast, Institute of Clinical Sciences; The Royal Victoria Hospital; Belfast, UK

Xiaohong Zhang

Centre for Vision Sciences; School of Biomedical Sciences; The Queen's University of Belfast, Institute of Clinical Sciences; The Royal Victoria Hospital; Belfast, UK

C. Norman Scholfield

Cell and Metabolic Signaling Group; School of Medicine and Dentistry; The Queen's University of Belfast; Belfast, UK

Timothy M. Curtis

Centre for Vision Sciences; School of Biomedical Sciences; The Queen's University of Belfast, Institute of Clinical Sciences; The Royal Victoria Hospital; Belfast, UK

J. Graham McGeown

Cell and Metabolic Signaling Group; School of Medicine and Dentistry; The Queen's University of Belfast; Belfast, UK

This is an open-access article

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