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Am J Physiol Heart Circ Physiol 292: H1412-H1419, 2007. First published November 3, 2006; doi:10.1152/ajpheart.00984.2006
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Baroreceptor reflex regulation in anesthetized transgenic rats with low glia-derived angiotensinogen

¹Hypertension and Vascular Disease Center, Department of General Surgery, and Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina; and ²Charite-University Medicine Berlin, Berlin, Germany

Submitted 8 September 2006 ; accepted in final form 1 November 2006

Endogenous angiotensin (ANG) II and ANG-(1–7) act at the nucleus tractus solitarius (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 (Aogen) due to glial overexpression of an antisense to Aogen (ASrAOGEN) and in Sprague-Dawley (SD) rats. Arterial baroreceptor reflex sensitivity (BRS) for control of heart rate (HR) in response to increases in mean arterial pressure (MAP) was tested before and after bilateral microinjection of the angiotensin type 1 (AT₁) receptor blocker candesartan or the ANG-(1–7) receptor blocker (D-Ala⁷)-ANG-(1–7) into the NTS of urethane-chloralose-anesthetized ASrAOGEN and SD rats. Baseline MAP was higher in ASrAOGEN than in SD rats under anesthesia (P < 0.01). Injection of candesartan or (D-Ala⁷)-ANG-(1–7) 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. Candesartan increased BRS by 41% in SD rats (P < 0.01) but was without effect in ASrAOGEN rats. In contrast, the reduction in BRS after (D-Ala⁷)-ANG-(1–7) administration was comparable in SD (31%) and ASrAOGEN rats (34%). These findings indicate that the absence of glia-derived Aogen is associated with 1) an increase in MAP under anesthesia mediated via AT₁ and ANG-(1–7) receptors within the NTS, 2) the absence of an endogenous ANG II contribution to tonic inhibition of BRS, and 3) a continued contribution of endogenous ANG-(1–7) to tonic enhancement of BRS.

baroreceptors; solitary tract nucleus; brain renin-angiotensin system; transgenic rats

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