Systemic furosemide abolished TGF-mediated hemodynamic responses, while inhibiting sodium-glucose co-transporters decreased local microcirculatory blood flow and weakened oscillations in rats.
Does inhibition of Na-K-2Cl and sodium-glucose co-transporters alter TGF-induced cortical hemodynamics in rats?
The study demonstrates that furosemide abolishes TGF-mediated hemodynamic responses, while SGLT inhibition weakens them, providing insights into renal microcirculatory regulation.
The tubuloglomerular feedback (TGF) mechanism modulates renal hemodynamics and glomerular filtration rate in individual nephrons. Our study aimed to evaluate the TGF-induced vascular responses by inhibiting Na-K-2Cl co-transporters and sodium-glucose co-transporters in rats. We assessed cortical hemodynamics with high-resolution laser speckle contrast imaging, which enabled the evaluation of blood flow in individual microvessels and analysis of their dynamical patterns in the time-frequency domain. We demonstrated that a systemic administration of furosemide abolishes TGF-mediated hemodynamic responses. Furthermore, we showed that the local microcirculatory blood flow decreased, and the TGF-induced hemodynamic oscillations were sustained but weakened after inhibiting sodium-glucose co-transporters in Sprague-Dawley rats.
Lee et al. (Wed,) reported a other. Inhibition of Na-K-2Cl and sodium-glucose co-transporters (furosemide) was evaluated on Cortical hemodynamics and TGF-induced vascular responses. Systemic furosemide abolished TGF-mediated hemodynamic responses, while inhibiting sodium-glucose co-transporters decreased local microcirculatory blood flow and weakened oscillations in rats.