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Hypertension. 2007;49:1163-1169
Published online before print March 19, 2007, doi: 10.1161/HYPERTENSIONAHA.106.084004
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(Hypertension. 2007;49:1163.)
© 2007 American Heart Association, Inc.


Original Articles

Voltage-Dependent Calcium Currents Are Enhanced in Nucleus of the Solitary Tract Neurons Isolated From Renal Wrap Hypertensive Rats

Gleb Tolstykh; Patricia M. de Paula; Steve Mifflin

From the University of Texas Health Science Center at San Antonio.

Correspondence to Steve Mifflin, Department of Pharmacology, Mail Code 7764, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr, San Antonio, TX 78229-3900. E-mail mifflin{at}uthscsa.edu

The nucleus of the solitary tract (NTS) is the central site of termination of baroreceptor afferents. We hypothesize that changes occur in voltage-gated calcium channels (VGCCs) within NTS neurons as a consequence of hypertension. Whole-cell patch-clamp recordings were obtained from adult normotensive (109±2 mm Hg; n=6 from 6 sham-operated and 31 nonsurgically treated) and hypertensive (158±6 mm Hg; n=24) rats. In some experiments, 4-(4-[dihexadecylamino]styryl)-N-methylpyridinium iodide was applied to the aortic nerve to visualize NTS neurons receiving baroreceptor synaptic contacts. Ba2+ currents (500 ms; –80 mV prepotential; 500 ms voltage steps in 5-mV increments to +15mV) peaked between –20 and –10 mV and were blocked by 100 µm of Cd2+. Peak VGCCs were not different comparing non-4-(4-[dihexadecylamino]styryl)-N-methylpyridinium iodide-labeled and 4-(4- [dihexadecylamino]styryl)-N-methylpyridinium iodide-labeled NTS neurons in hypertensive and normotensive rats. The peak VGCC was significantly greater in cells from hypertensive compared with normotensive rats for both non–DiA-labeled (P=0.02) and DiA-labeled (P=0.04) neurons. To separate high-voltage activated (HVA) and low-voltage activated (LVA) components of VGCCs, voltage ramps (–110 mV to +30 mV over 50 ms) were applied from a holding potential of –60 mV (LVA channels inactivated) and a holding potential of –100 mV (both LVA and HVA currents activated). HVA currents were subtracted from HVA+LVA currents to yield the LVA current. Peak LVA currents were not different between hypertensive (8.9±0.8 pA/pF) and normotensive (7.8±0.6 pA/pF) groups of NTS neurons (P=0.27). These results demonstrate that 4 weeks of renal wrap hypertension induce an increase in Ca2+ influx through HVA VGCCs in NTS neurons receiving arterial baroreceptor inputs.


Key Words: baroreflex • nucleus of the solitary tract • calcium channels • ion channels • central nervous system • arterial hypertension