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Am J Physiol Heart Circ Physiol 271: H2469-H2476, 1996;
0363-6135/96 $5.00
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AJP - Heart and Circulatory Physiology, Vol 271, Issue 6 2469-H2476, Copyright © 1996 by American Physiological Society

ARTICLES

Alpha-adrenoceptor activation of a chloride conductance in rat iris arterioles

D. J. Gould and C. E. Hill
Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra, Australia.

Changes in membrane potential associated with alpha-adrenoceptor-mediated contraction of rat iris arterioles after nerve stimulation (10 Hz, 1 s) have been measured with conventional intracellular recording techniques. Two different types of intracellular responses were recorded. Cells that show a depolarization are proposed to represent the arteriolar smooth muscle cells because the characteristics of the depolarization are correlated with those of the contraction. Cells that show no response or a small hyperpolarization in response to nerve stimulation are proposed to represent the endothelial cells of the arteriole. Both the depolarization and the contraction were abolished by tetrodotoxin (1 microM), benextramine (10 microM), and prazosin (0.1 mM), indicating that they result from nerve-mediated activation of alpha-adrenoceptors. A small but significant part of the contraction (30%) and the depolarization (11%) was nifedipine sensitive (10 microM). Caffeine (1 mM) abolished the contraction and reduced the depolarization by one-half. Reducing the external chloride concentration also abolished the contraction and reduced the depolarization by 90%. Flufenamic acid (250 mM) abolished both the contraction and the depolarization. It is suggested that, in iris arterioles, the activation of synaptic alpha-adrenoceptors leads to the release of intracellular calcium that activates both the chloride channels in the cell membrane leading to depolarization and the intracellular contractile apparatus leading to vasoconstriction.


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