Pyridine nucleotide redox potential in coronary smooth muscle couples myocardial blood flow to cardiac metabolism.

ABSTRACT: Adequate oxygen delivery to the heart during stress is essential for sustaining cardiac function. Acute increases in myocardial oxygen demand evoke coronary vasodilation and enhance perfusion via functional upregulation of smooth muscle voltage-gated K⁺ (Kv) channels. Because this response is controlled by Kv1 accessory subunits (i.e., Kvβ), which are NAD(P)(H)-dependent aldo-keto reductases, we tested the hypothesis that oxygen demand modifies arterial [NAD(H)]_i, and that resultant cytosolic pyridine nucleotide redox state influences Kv1 activity. High-resolution imaging mass spectrometry and live-cell imaging reveal cardiac workload-dependent increases in NADH:NAD⁺ in intramyocardial arterial myocytes. Intracellular NAD(P)(H) redox ratios reflecting eleva

SUBMITTER: Dwenger MM 

PROVIDER: S-EPMC9018695 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature