A Cross-sectional Study of the Relationship Between Habitual Tea Consumption and Arterial Stiffness.

BACKGROUND AND AIMS: To explore the relationship between habitual tea consumption and arterial stiffness. METHODS: This is a cross-sectional, epidemiological survey of 6589 male and female residents aged 40-75 in Wuyishan, Fujian Province, China. Tea consumption and other lifestyle characteristics were obtained by structured questionnaires. Pulse wave velocity (PWV) and ankle-brachial pressure index (ABI) were measured using an automated analyzer. RESULTS: Among the 5006 analyzed subjects, 1564 adults (31.2%) consumed tea once or more per week for at least one year. The levels of brachial-ankle pulse wave velocity (ba-PWV) were lowest among subjects who consumed tea habitually for more than 10 years compared with the other 3 subgroups (nonhabitual, 1 to 5 years, and 6 to 10 years habitual tea drinkers), and the levels of ba-PWV were lower with subjects who consumed 10-20 and >20 g/d tea habitually compared to nonhabitual tea drinkers. As the duration and the daily amount of habitual tea consumption increased the average ba-PWV decreased. Multiple logistic regression models revealed that habitual tea consumption was a positive predictor for ba-PWV (odds ratio [OR] = 0.63, 95% confidence interval [CI], 0.57-0.70). CONCLUSIONS: Habitual tea consumption may have a protective effect against arterial stiffness, especially for subjects who have habitually consumed tea for more than 6 years and >10 g daily.

Metabotropic glutamate receptor 5 modulates nociceptive plasticity via extracellular signal-regulated kinase-Kv4.2 signaling in spinal cord dorsal horn neurons.

Metabotropic glutamate receptors (mGluRs) play important roles in the modulation of nociception. The group I mGluRs (mGlu1 and mGlu5) modulate nociceptive plasticity via activation of extracellular signal-regulated kinase (ERK) signaling. We reported recently that the K+ channel Kv4.2 subunit underlies A-type K+ currents in the spinal cord dorsal horn and is modulated by the ERK signaling pathway. Kv4.2-mediated A-type currents are important determinants of dorsal horn neuronal excitability and central sensitization that underlies hypersensitivity after tissue injury. In the present study, we demonstrate that ERK-mediated phosphorylation of Kv4.2 is downstream of mGlu5 activation in spinal cord dorsal horn neurons. Activation of group I mGluRs inhibited Kv4.2-mediated A-type K+ currents and increased neuronal excitability in dorsal horn neurons. These effects were mediated by activation of mGlu5, but not mGlu1, and were dependent on ERK activation. Analysis of Kv4.2 phosphorylation site mutants clearly identified S616 as the residue responsible for mGlu5-ERK-dependent modulation of A-type currents and excitability. Furthermore, nociceptive behavior induced by activation of spinal group I mGluRs was impaired in Kv4.2 knock-out mice, demonstrating that, in vivo, modulation of Kv4.2 is downstream of mGlu5 activation. Altogether, our results indicate that activation of mGlu5 leads to ERK-mediated phosphorylation and modulation of Kv4.2-containing potassium channels in dorsal horn neurons. This modulation may contribute to nociceptive plasticity and central sensitization associated with chronic inflammatory pain conditions.