Abnormal central control underlies impaired baroreflex control of heart rate and sympathetic nerve activity in female Lewis polycystic kidney rats.

OBJECTIVE: Why baroreflex dysfunction occurs in females with chronic kidney disease is unknown. We therefore aimed to examine whether temporal changes in baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) occur in female Lewis polycystic kidney (LPK) rats and whether this is associated with any changes in afferent, central or efferent processing of the reflex pathway. METHOD: Using urethane-anaesthetized juvenile and adult LPK and Lewis control rats (n = 40), baroreflex-mediated changes in HR, RSNA and aortic depressor nerve activity (ADNA) were examined. Reflex changes to aortic depressor and vagal efferent nerve stimulation were also determined. RESULTS: In the juvenile LPK rats, except for a slight reduction in the gain of the normalized HR and RSNA baroreflex function curves, no difference in baroreflex control of HR, RSNA or ADNA was observed. Responses to aortic depressor and vagal efferent nerve stimulation were also comparable. In the adult hypertensive LPK rats, the range of both HR (35 ±â€Š8 vs. 78 ±â€Š9  bpm, P ≤ 0.05 LPK vs. Lewis) and RSNA (60 ±â€Š7 vs. 80 ±â€Š3%, P ≤ 0.05 LPK vs. Lewis) was also reduced. This was not associated with any change in the ADNA baroreflex function curves or reflex HR responses to vagal efferent nerve stimulation, but was associated with a reduction in the reflex bradycardic (-21 ±â€Š4 vs. -34 ±â€Š8 bpm, P < 0.01 LPK vs. Lewis) and sympathoinhibitory (-30 ±â€Š8 vs. -54 ±â€Š12%, P < 0.001 LPK vs. Lewis) responses to aortic depressor nerve stimulation. CONCLUSION: In female LPK rats, baroreflex dysfunction results from impaired central processing of the reflex.