Abstract
Increased blood pressure variability (BPV), which can be experimentally induced by sinoaortic denervation (SAD), has emerged as a new marker of the prognosis of cardiovascular and renal outcomes. Considering that increased BPV can lead to organ-damage, the goal of the present study was to evaluate the effects of SAD on renal function in an experimental model of chronic kidney disease (CKD). SAD was performed in male Wistar rats 2 weeks before 5/6 nephrectomy and the animals were evaluated 4 weeks after the induction of CKD. Our data demonstrated that BPV was increased in SAD and CKD animals and that the combination of both conditions (SAD+CKD) exacerbated BPV. The baroreflex sensitivity index was diminished in the SAD and CKD groups; this reduction was more pronounced when SAD and CKD were performed together. 5/6 nephrectomy led to hypertension, which was higher in SAD+CKD animals. Regarding renal function, the combination of SAD and CKD resulted in reduced renal plasma and blood flow, increased renal vascular resistance and augmented uraemia when compared to CKD animals. Glomerular filtration rate and BPV were negatively correlated in SAD, CKD, and SAD+CKD animals. Moreover, SAD+CKD animals presented a higher level of glomerulosclerosis when compared to all other groups. Cardiac and renal hypertrophy, as well as oxidative stress, was also further increased when SAD and CKD were combined. These results show that SAD prior to 5/6 nephrectomy exacerbates renal dysfunction, suggesting that previous augmented BPV should be considered as an important factor to the progression of renal diseases.
Highlights
It is well-established that the maintenance of blood pressure (BP) at stable levels is a sine qua non condition for adequate tissue perfusion (Vasquez et al, 2012)
chronic kidney disease (CKD) animals presented a greater SAP, diastolic blood pressure (DAP), and mean arterial pressure (MAP) when compared to the sham and sinoaortic denervation (SAD)
These changes were exacerbated in the SAD+CKD animals, which displayed an increased heart rate (HR)
Summary
It is well-established that the maintenance of blood pressure (BP) at stable levels is a sine qua non condition for adequate tissue perfusion (Vasquez et al, 2012). Increased blood pressure variability (BPV) is closely associated with the development, progression and severity of cardiac, vascular, and renal organ damage (Sander et al, 2000; Sega et al, 2002; Mancia and Parati, 2003; Tatasciore et al, 2007) as well as with an augmented risk of cardiovascular and renal outcomes (Kikuya et al, 2000; Pringle et al, 2003; Hansen et al, 2010; Stolarz-Skrzypek et al, 2010). Increased BPV can be induced by the bilateral disruption of the afferent pathway of the arterial baroreflex system (Kudo et al, 2009), known as sinoaortic denervation (SAD). Considering that, we hypothesized that increased BPV prior to the onset of kidney disease could accelerate the disease progression To test this hypothesis, we evaluated the effects of SAD previously to 5/6 nephrectomyinduced CKD on renal function, glomerulosclerosis, oxidative stress, and cardiovascular parameters. Our data demonstrate that augmented BPV prior to CKD exacerbates kidney dysfunction and should be considered as an important risk factor to the progression of renal diseases
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