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(Circulation Research. 1996;79:302-309.)
© 1996 American Heart Association, Inc.

Articles

Angiotensin II Type 2 Receptor–Mediated Regulation of Rat Neuronal K⁺ Channels

Jeffrey R. Martens, Desuo Wang, Colin Sumners, Philip Posner, Craig H. Gelband

the Department of Physiology, University of Florida, College of Medicine, Gainesville.

Correspondence to Craig H. Gelband, PhD, Department of Physiology, University of Florida, College of Medicine, PO Box 100274, Gainesville, FL 32610. E-mail gelband@phys.med.ufl.edu.

We have previously shown that angiotensin II (Ang II), via AT₂ receptors, increases whole-cell K⁺ current in cultured rat hypothalamus and brain stem neurons. We have now investigated the AT₂ receptor–mediated effects of Ang II on the activity of single delayed rectifier K⁺ channels in cell-attached membrane patches. In control recordings (bath, 5.4 mmol/L K⁺; pipette, 140 mmol/L K⁺), two voltage-dependent channels were recorded with conductances of 34±4 and 56±6 pS, respectively (n=6). When patches were excised, the channels reversed near a membrane potential expected for a K⁺ channel. In cell-attached patches (-40 mV), Ang II (100 nmol/L) increased open probability of the 56-pS K⁺ channel from 0.03±0.01 to 0.21±0.05 (n=3). The selective AT₂ receptor antagonist PD 123319 (1 µmol/L) but not the AT₁ receptor antagonist losartan (1 µmol/L) blocked the actions of Ang II (n=3). The selective AT₂ receptor agonist CGP 42112 (100 nmol/L) produced similar effects to Ang II. Kinetic analysis of the Ang II effect showed that open-time histograms were best fit by two exponential functions. Ang II increased both open-time constants relative to control (control, ₁=0.9±0.1 milliseconds, ₂=2.3±0.3 milliseconds; Ang II, ₁=3.1±0.4 milliseconds, ₂=12.1±2.4 milliseconds), and PD 123319 blocked this effect (n=3). The closed-time histogram was not affected by Ang II, PD 123319, or losartan. These results suggest that activation of AT₂ receptors modulates rat hypothalamus and brain stem neuronal whole-cell K⁺ current by increasing the open probability of a 56-pS K⁺ channel.

Key Words: angiotensin II • K⁺ channel • neuron • open probability

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