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This Article Full Text Full Text (PDF) All Versions of this Article: 586/6/1605    most recent jphysiol.2007.147413v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Sonner, P. M. Articles by Stern, J. E. PubMed PubMed Citation Articles by Sonner, P. M. Articles by Stern, J. E. Related Collections Neuroscience

¹ Department of Psychiatry, University of Cincinnati, Cincinnati, OH, USA

Accumulating evidence supports a contribution of the hypothalamic paraventricular nucleus (PVN) to sympathoexcitation and elevated blood pressure in renovascular hypertension. However, the underlying mechanisms resulting in altered neuronal function in hypertensive rats remain largely unknown. Here, we aimed to address whether the transient outward potassium current (I_A) in identified rostral ventrolateral medulla (RVLM)-projecting PVN neurones is altered in hypertensive rats, and whether such changes affected single and repetitive action potential properties and associated changes in intracellular Ca²⁺ levels. Patch-clamp recordings obtained from PVN-RVLM neurons showed a reduction in I_A current magnitude and single channel conductance, and an enhanced steady-state current inactivation in hypertensive rats. Morphometric reconstructions of intracellularly labelled PVN-RVLM neurons showed a diminished dendritic surface area in hypertensive rats. Consistent with a diminished I_A availability, action potentials in PVN-RVLM neurons in hypertensive rats were broader, decayed more slowly, and were less sensitive to the K⁺ channel blocker 4-aminopyridine. Simultaneous patch clamp recordings and confocal Ca²⁺ imaging demonstrated enhanced action potential-evoked intracellular Ca²⁺ transients in hypertensive rats. Finally, spike broadening during repetitive firing discharge was enhanced in PVN-RVLM neurons from hypertensive rats. Altogether, our results indicate that diminished I_A availability constitutes a contributing mechanism underlying aberrant central neuronal function in renovascular hypertension.

(Received 29 October 2007; accepted after revision 24 January 2008; first published online 31 January 2008)
Corresponding author J. Stern: Department of Psychiatry, University of Cincinnati, Genome Research Institute, 2170 E. Galbraith Rd, Cincinnati, OH 45237, USA. Email: javier.stern{at}psychiatry.uc.edu