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1 Hypertension & Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States
2 Charite-Unvierstiy Medicine, Berlin, Germany
3 Hypertension Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States
* To whom correspondence should be addressed. E-mail: ddiz{at}wfubmc.edu.
Endogenous angiotensin (Ang) II and Ang-(1-7) act at the nucleus tractus solitarii (NTS) to differentially modulate neural control of the circulation. The role of these peptides endogenous to NTS on cardiovascular reflex function was investigated in transgenic rats with low brain angiotensinogen (AGT) due to glial over-expression of an antisense to AGT (ASrAOGEN) and in Sprague-Dawley (SD) rats. Arterial baroreceptor reflex sensitivity (BRS) for control of heart rate in response to increases in mean arterial pressure (MAP) was tested before and after bilateral microinjection into the NTS of the AT1 receptor blocker candesartan (CAN) or the Ang-(1-7) receptor blocker (D-Ala7)-Ang-(1-7) in urethane/chloralose anesthetized ASrAOGEN and SD rats. Baseline MAP was higher in ASrAOGEN than SD rats under anesthesia (p< 0.01). Injection of either CAN or (D-Ala7)-Ang-(1-7) into the NTS decreased MAP (p< 0.01) and HR (p< 0.05) in ASrAOGEN but not SD rats. The BRS at baseline was similar in ASrAOGEN and SD rats. CAN increased BRS by 41% in SD rats (p< 0.01), but was without effect in ASrAOGEN rats. In contrast, the reduction in BRS following (D-Ala7)-Ang-(1-7) administration was comparable in SD (31%) and ASrAOGEN rats (34%). These findings indicate that: absence of glial-derived angiotensinogen is associated with 1) an increase in MAP under anesthesia mediated via AT1 and Ang-(1-7) receptors within the NTS; 2) absence of endogenous Ang II contribution to tonic inhibition of BRS; and 3) continued contribution of endogenous Ang-(1-7) to tonic enhancement of BRS.
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