Submitted on March 1, 2008
Accepted on June 23, 2008
SUBFORNICAL ORGAN DIFFERENTIALLY MODULATES BAROREFLEX FUNCTION
IN NORMOTENSIVE AND TWO KIDNEY-ONE CLIP HYPERTENSIVE RATS
Maria Maliszewska-Scislo1, Haiping Chen1, Robert A Augustyniak2, Dale M Seth3, and Noreen F. Rossi1*
1 Internal Medicine/Physiology, Wayne State University, Detroit, Michigan, United States
2 Internal Medicine/Physiology, Wayne State Univeristy School of Medicine, Detroit, Michigan, United States
3 Physiology and Renal and Hypertension Center, Tulane University, New Orleans, Louisiana, United States
* To whom correspondence should be addressed. E-mail: nrossi{at}med.wayne.edu.
During activation of the renin-angiotensin system, hindbrain circumventricular organs such as area postrema have been implicated in modulating the arterial baroreflex. This study was undertaken to test the hypothesis that the subfornical organ (SFO), a forebrain circumventricular structure, may also modulate the baroreflex. Studies were performed in rats with two-kidney one-clip (2K-1C) hypertension as a model of endogenously activated renin-angiotensin system. Baroreflex function was ascertained during ramp infusions of phenylephrine and nitroprusside in conscious sham-clipped and five-week 2K-1C rats with either a sham-lesioned or electrolytically-lesioned SFO. Lesioning significantly decreased mean arterial pressure in 2K-1C rats from 158 ± 7 to 131 ± 4 mmHg, but not in sham-clipped rats. SFO-lesioned, sham-clipped rats had a significantly higher upper plateau and range of the renal sympathetic nerve activity-mean arterial pressure relationship compared with sham-clipped rats with SFO ablation. In contrast, lesioning the SFO in 2K-1C rats significantly decreased both the upper plateau and range of the baroreflex control of renal sympathetic nerve activity, but only the range of the baroreflex response of heart rate decreased. Thus, during unloading of the baroreceptors the SFO differentially modulates the baroreflex responses in sham-clipped versus 2K-1C rats. Since lesioning the SFO did not influence plasma Ang II, the effects of the SFO lesion are not caused by changes in circulating levels of angiotensin II (Ang II). These findings support a pivotal role for the SFO in the sympathoexcitation observed in renovascular hypertension and in baroreflex regulation of sympathetic activity in both normal and hypertensive states.
