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1 Internal Medicine, University of Iowa, Iowa City, IA, USA
2 Internal Medicine, University of Iowa, Iowa City, IA, USA; Veterans Affairs Medical Center, University of Iowa, Iowa City, IA, USA; Physiology & Biophysics, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA, USA
3 Anatomy and Cell Biology, University of Iowa, Iowa City, IA, USA
4 Internal Medicine, University of Iowa, Iowa City, IA, USA; Physiology & Biophysics, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: curt-sigmund{at}uiowa.edu.
We developed transgenic mice with targeted expression of human renin (hREN) and human angiotensinogen (hAGT) to either neurons (N-AII mice) or glia (G-AII mice) to test the hypothesis that neuronal and glial Ang-II may have differential function. Since baseline blood pressure did not differ between the models (109±3 vs 114±4 mmHg), we stressed the blood pressure regulatory pathway by measuring the heart rate (baroreflex) response to phenylephrine- and nitroprusside-induced changes in arterial blood pressure (BP). The midpoint of the baroreflex curve (BP50) was reset to a significantly higher BP in N-AII mice (131±5 mmHg) compared with littermate controls (115±3 mmHg). Baroreflex gain (slope of BP-HR relation) was similar in N-AII and control mice (12±1 vs 14±2 beats/min/mmHg). In contrast, G-AII mice exhibited less of an increase in BP50 (125±5 mmHg), but a larger decrease in baroreflex gain (8±1 beats/min/mmHg) compared with both control and N-AII mice. Differences in BP50 and gain between N-AII, G-AII, and control mice persisted after parasympathetic blockade with atropine, but were eliminated after sympathetic blockade with propranolol, indicating the effects of Ang-II were selective for cardiosympathetic arm of the reflex. Ang-II-like immunoreactivity was observed more prominently around the PVN and NTS in G-AII mice, but more prominently in the VLM in N-AII mice. We conclude that Ang-II differentially modulates baroreflex control of HR in mice producing Ang-II in neurons vs glia, and its differential function may reflect regional differences in the production of Ang-II in cardiovascular control nuclei of the brain.
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