Key result
Carotid body denervation maintains ~36% higher resting renal blood flow in rats with CHF.
Why the study?
The study sought to determine the role of carotid body chemoreceptor activity on GFR, RBF, and renal PO2 in chronic heart failure, assess additive effects of intermittent asphyxia, and identify renal gene expression changes.
Does carotid body denervation improve renal hemodynamics and tissue PO2 in a rat model of chronic heart failure?
Does carotid body denervation improve renal hemodynamics and tissue PO2 in a rat model of chronic heart failure?
Carotid body denervation improves renal blood flow and oxygenation in a rat model of heart failure, suggesting aberrant chemoreceptor function contributes to renal hemodynamic compromise in heart failure.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in rat heart failure; leaves open translation to human renal outcomes or practice.
Aberrant carotid body chemoreceptor (CBC) function contributes to increased sympathetic nerve activity (SNA) and reduced renal blood flow (RBF) in chronic heart failure (CHF). Intermittent asphyxia (IA) mimicking sleep apnea is associated with additional increases in SNA and may worsen reductions in RBF and renal PO2 (RPO2) in CHF. The combined effects of decreased RBF and RPO2 may contribute to biochemical changes precipitating renal injury. This study sought to determine the role of CBC activity on glomerular filtration rate (GFR), RBF and RPO2 in CHF, and to assess the additive effects of IA. Furthermore, we sought to identify changes in gene expression that might contribute to renal injury. We hypothesized that GFR, RBF, and RPO2 would be reduced in CHF, that decreases in RBF and RPO2 would be worsened by IA, and that these changes would be ameliorated by CBC ablation (CBD). Finally, we hypothesized that CHF would be associated with pro-oxidative pro-fibrotic changes in renal gene expression that would be ameliorated by CBD. CHF was induced in adult male Sprague Dawley rats using coronary artery ligation (CAL). Carotid body denervation was performed by cryogenic ablation. GFR was assessed in conscious animals at the beginning and end of the experimental period. At 8-weeks post-CAL, cardiac function was assessed via echocardiography, and GFR, baseline and IA RBF and RPO2 were measured. Renal gene expression was measured using qRT-PCR. GFR was lower in CHF compared to sham ( p < 0.05) but CBD had no salutary effect. RBF and RPO2 were decreased in CHF compared to sham ( p < 0.05), and this effect was attenuated by CBD ( p < 0.05). RBF and RPO2 were reduced to a greater extent in CHF vs. sham during exposure to IA ( p < 0.05), and this effect was attenuated by CBD for RBF ( p < 0.05). Downregulation of antioxidant defense and fibrosis-suppressing genes was observed in CHF vs. sham however CBD had no salutary effect. These results suggest that aberrant CBC function in CHF has a clear modulatory effect on RBF during normoxia and during IA simulating central sleep apnea.
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Kious et al. (2022) studied Chronic heart failure with reduced ejection fraction (n=53). Carotid body denervation (CBD) vs. Sham denervation (CHF control) was evaluated on Baseline renal blood flow (ml/min/gBW) (p=<0.05). Carotid body denervation in rats with chronic heart failure significantly attenuated the reductions in resting renal blood flow (0.019 vs 0.014 ml/min/gBW) and renal tissue PO2 (37 vs 28 mmHg).
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