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1 Physiology and Functional Genomics, University of Florida, Gainesville, FL, USA; McKnight Brain Institute, University of Florida, Gainesville, FL, USA
* To whom correspondence should be addressed. E-mail: csumners{at}phys.med.ufl.edu.
Prior studies utilizing neurons cultured from the hypothalamus and brainstem of newborn rats have demonstrated that angiotensin II (Ang II)-induced modulation of neuronal firing involves activation of both protein kinase C (PKC) and Ca2+/calmodulin dependent protein kinase II (CaMKII). The present studies were performed to determine whether these signaling molecules are also involved in physiological responses elicited by Ang II in the brain in vivo. Central injection of Ang II (10 ng/2 µL) into the lateral cerebroventricle (icv) of Sprague-Dawley rats increased water intake in a time dependent manner. This Ang II-mediated dipsogenic response was attenuated by central injection of the PKC inhibitors chelerythrine chloride (0.5-50 µM, 2 µL) and Go6976 (2.3 nM, 2 µL) and by the CaMKII inhibitor KN-93 (10 µM, 2 µL). Conversely, icv injection of chelerythrine chloride (50 µM, 2 µL) and KN-93 (10 µM, 2 µL) had no effect on the dipsogenic response elicited by central injection of carbachol (200ng/2 µL). Furthermore, injection of Ang II (10 ng/2 µL) icv increases the activity of both PKC
and CaMKII in rat septum and hypothalamus. These data suggest that signaling molecules involved in Ang II-induced responses in vitro are also relevant in physiological responses elicited by Ang II in the whole animal model.
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