Key result
Fructose-1,6-bisphosphate reverses L-kynurenine-induced blood pressure reductions and HRV increases in rats.
Why the study?
L-kynurenine causes vasodilation and hypotensive shock via KCNQ channels during systemic inflammation, while fructose-1,6-bisphosphate acts as an ion channel modulator and anti-inflammatory agent.
Does Fructose-1,6-bisphosphate reverse the hypotensive effect caused by L-kynurenine in Wistar male rats?
Does Fructose-1,6-bisphosphate reverse the hypotensive effect caused by L-kynurenine in Wistar male rats?
Fructose-1,6-bisphosphate reverses L-kynurenine-induced hypotension in rats, highlighting a potential novel target for treating inflammation-related hypotensive shock.
Answers are grounded in this paper and cite their sources.
May support novel target exploration in hypotensive shock models; leaves open translation to human inflammation-related states.
Hypotension is one of the main characteristics of the systemic inflammation, basically caused by endothelial dysfunction. Studies have shown that the amino acid L-kynurenine (KYN) causes vasodilation in mammals, leading to hypotensive shock. In hypotensive shock, when activated by the KYN, the voltage-gated potassium channel encoded by the family KCNQ (Kv7) gene can cause vasodilation. Fructose-1,6-bisphosphate (FBP) it is being considered in studies an anti-inflammatory, antioxidant, immunomodulator, and a modulator of some ion channels (Ca2+, Na+, and K+). We analyzed the effects of KYN and FBP on mean blood pressure (MBP), systolic and diastolic (DBP) blood pressure, and heart rate variability (HRV) in Wistar rats. Results demonstrated that the administration of KYN significant decreased MBP, DBP, and increased HRV. Importantly, the FBP treatment reversed the KYN effects on MBP, DBP, and HRV. Molecular Docking Simulations suggested that KYN and FBP present a very close estimated free energy of binding and the same position into structure of KCNQ4. Our results did demonstrate that FBP blunted the decrease in BP, provoked by KYN. Results raise new hypotheses for future and studies in the treatment of hypotension resulting from inflammation.
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Catarina et al. (2024) studied Hypotension. Fructose-1,6-bisphosphate (FBP) vs. L-kynurenine (KYN) was evaluated on Mean blood pressure (MBP), systolic and diastolic (DBP) blood pressure, and heart rate variability (HRV). Fructose-1,6-bisphosphate treatment reversed the decreases in mean and diastolic blood pressure and the increase in heart rate variability caused by L-kynurenine in Wistar male rats.
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