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J Neurophysiol (August 6, 2003). doi:10.1152/jn.00222.2003
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Submitted on March 10, 2003
Accepted on July 29, 2003

PI3-KINASE INHIBITORS ABOLISH THE ENHANCED CHRONOTROPIC EFFECTS OF ANGIOTENSIN II IN SPONTANEOUSLY HYPERTENSIVE RAT BRAIN NEURONS

Chengwen Sun1, Jianqing Du2, Colin Sumners1, and Mohan K. Raizada1*

1 Physiology, University of Florida, Gainesville, FL, USA
2 Physiology, Xian Jiaotong University, Xian, China, China

* To whom correspondence should be addressed. E-mail: mraizada{at}phys.med.ufl.edu.

Angiotensin II (Ang II), acting at Ang II type 1 (AT1) receptors, increases the firing rate of neurons from Wistar-Kyoto (WKY) rat brain via protein kinase C (PKC)-and Calcium-calmodulin kinase II (CaMKII)-dependent mechanisms. The objectives of this study were two fold; first, to compare the Ang II-stimulated increase in firing of neurons from WKY and spontaneous hypertensive rats (SHR) and second, to elucidate the signaling mechanisms involved. Action potentials were measured in neurons cultured from SHR and WKY rat brains using the whole cell configuration of the patch clamp technique in the current clamp mode. Ang II (100 nM) caused 3-and 6-fold increases in neuronal firing rate in WKY rat and SHR neurons, respectively, effects that were abolished by the AT1R antagonist losartan (1 µM). Co-administration of calphostin C (10 µM, a PKC inhibitor) and KN-93 (10 µM, a CaMKII inhibitor) completely blocked this Ang II action in WKY rat neurons, while they caused only a ~50% attenuation in SHR neurons. The residual increase in firing rate produced by Ang II in SHR neurons was blocked by the inhibition of phosphatidylinositol 3 Kinase (PI3-kinase), using either LY 294002 (10 µM) or Wortmannin (100 nM). These observations indicate that a PI3-Kinase signaling is exclusively responsible for the enhanced increase in neuronal activity produced by Ang II in SHR neurons.




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