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1 Neuroscience Program, Michigan State University, East Lansing, Michigan, USA
2 Neuroscience Program, Michigan State University, East Lansing, Michigan, USA; Pharmacology & Toxicology, Michigan State University, East Lansing, Michigan, USA
3 Neuroscience Program, Michigan State University, East Lansing, Michigan, USA; Department of Physiology, Michigan State University, East Lansing, Michigan, USA
* To whom correspondence should be addressed. E-mail: finkg{at}msu.edu.
Dai et al (2004) found that (ET) stimulated O2- production in sympathetic ganglion neurons in vitro by activating ETB receptors. The objective of the present study was to determine if activation of ETB receptors in vivo elevates O2- levels in sympathetic ganglia. Since ETB receptor activation increases blood pressure, we also sought to determine if alteration in O2- levels was a direct effect of ETB receptor activation on sympathetic ganglia or an indirect consequence of hypertension. Male Sprague-Dawley rats received iv infusions of either the specific ETB receptor agonist sarafotoxin 6c (S6c, 5 pmol/kg/min) or isotonic saline at 0.01 ml/min (control) for 120 minutes. To measure O2- levels, we removed the inferior mesenteric ganglion immediately following infusion and stained it with dihydroethidine (DHE). Mean arterial pressure increased 26.6±1.7 mmHg in the S6c treated rats and 3.65±6 mmHg in control rats. Measurements of average pixel intensity revealed that the DHE fluorescence in ganglionic neurons and surrounding glial cells were 96.7% and 160% greater in S6c than in control rats, respectively. To evaluate the effect of elevated blood pressure on O2- production, a separate group of rats received phenylephrine (PE; 10 µg/kg/min, iv) for 2 h. MAP increased 31±1.2 mmHg in PE infused rats. The DHE fluorescent intensity in ganglia of PE rats was significantly greater than that of control rats, 137.7% in neurons and 104.6% in glia, but significantly lower than in ganglia from S6c rats. We conclude that ETB receptor activation in vivo significantly enhances O2- levels in sympathetic ganglia, due to both pressor effects and direct stimulation of ETB receptors in ganglion cells.
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