Journal of hypertension · 2026
Kidney-brain neural interaction in cardiorenal syndrome: insights from volume-overloaded spontaneously hypertensive rats with aorto-caval fistula.
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Honetschlägerová Zuzana, Miklovič Matúš, Kikerlová Soňa, Sadowski Janusz, Vaňourková Zdenka, Škaroupková Petra, Vacková Šárka, Táborský Miloš, Tichánek Filip, Červenka Luděk
Аннотация
OBJECTIVE: We hypothesized, first, that impairment of autoregulation of renal blood flow (RBF), glomerular filtration rate (GFR), and of the pressure-natriuresis in spontaneously hypertensive rats (SHR) is present in early phase of heart failure and precedes its decompensation. Second, that both the total renal denervation (T-RDN) and/or selective renal afferent denervation (A-RDN) would improve renal autoregulation and pressure-natriuresis in SHR with heart failure.
METHODS: Heart failure was elicited by volume overload achieved using aorto-caval fistula (ACF). T-RDN and A-RDN were performed 1 week after ACF creation. Two weeks later, animals were prepared for studies examining RBF, GFR, urine flow, and sodium excretion (UNaV) responses to stepwise changes in renal arterial pressure (RAP) induced by aortic clamping.
RESULTS: Basal values of RBF, urine flow, and UNaV were lower in ACF SHR than in sham-ACF SHR. In sham-ACF SHR, stepwise reductions in RAP decreased RBF and GFR, whereas in ACF SHR both parameters remained unchanged. Stepwise reductions in RAP decreased urine flow and UNaV in sham-ACF SHR and ACF SHR, with greater decrease in the former. T-RDN as well as A-RDN increased basal urine flow and UNaV and improved the pressure natriuresis compared with innervated ACF SHR.
CONCLUSION: In this model of heart failure, renal hemodynamics autoregulation is preserved, suggesting that heart failure decompensation cannot be simply ascribed to impaired autoregulatory capacity. Both T-RDN and A-RDN enhanced the pressure-natriuresis in ACF SHR, suggesting an important role of kidney-brain neural interactions in the pathophysiology of HF.
METHODS: Heart failure was elicited by volume overload achieved using aorto-caval fistula (ACF). T-RDN and A-RDN were performed 1 week after ACF creation. Two weeks later, animals were prepared for studies examining RBF, GFR, urine flow, and sodium excretion (UNaV) responses to stepwise changes in renal arterial pressure (RAP) induced by aortic clamping.
RESULTS: Basal values of RBF, urine flow, and UNaV were lower in ACF SHR than in sham-ACF SHR. In sham-ACF SHR, stepwise reductions in RAP decreased RBF and GFR, whereas in ACF SHR both parameters remained unchanged. Stepwise reductions in RAP decreased urine flow and UNaV in sham-ACF SHR and ACF SHR, with greater decrease in the former. T-RDN as well as A-RDN increased basal urine flow and UNaV and improved the pressure natriuresis compared with innervated ACF SHR.
CONCLUSION: In this model of heart failure, renal hemodynamics autoregulation is preserved, suggesting that heart failure decompensation cannot be simply ascribed to impaired autoregulatory capacity. Both T-RDN and A-RDN enhanced the pressure-natriuresis in ACF SHR, suggesting an important role of kidney-brain neural interactions in the pathophysiology of HF.