Key result
TRPV1 antagonists exaggerated the hypoxic ventilatory response and blunted the hypoxia-induced drop in body temperature, indicating TRPV1 exerts an inhibitory modulation on the hypoxic drive to breathe.
Why the study?
Few studies have investigated the role of transient receptor potential channels in mammalian cardiorespiratory control.
TRPV1 channels exert an inhibitory modulation on the hypoxic drive to breathe and stimulate body temperature reduction during hypoxia in rats.
Potential respiratory effects warrant caution with TRPV1 antagonists; leaves open translation to human hypoxic responses.
Receptors of the transient receptor potential (TRP) channels superfamily are expressed in many tissues and have different physiological functions. However, there are few studies investigating the role of these channels in cardiorespiratory control in mammals. We assessed the role of central and peripheral TRPV1 receptors in the cardiorespiratory responses to hypoxia (10% O₂) and hypercapnia (7% CO₂) by measuring pulmonary ventilation ( V ˙ E ), heart rate (HR), mean arterial pressure (MAP) and body temperature (Tb) of male Wistar rats before and after intraperitoneal (AMG9810 [2.85 µg/kg, 1 mL/kg]) or intracebroventricular (AMG9810 [2.85 µg/kg, 1 µL] or AMG7905 [28.5 μg/kg, 1 µL]) injections of TRPV1 antagonists. Central or peripheral injection of TRPV1 antagonists did not change cardiorespiratory parameters or Tb during room air and hypercapnic conditions. However, the hypoxic ventilatory response was exaggerated by both central and peripheral injection of AMG9810. In addition, the peripheral antagonist blunted the drop in Tb induced by hypoxia. Therefore, the current data provide evidence that TRPV1 channels exert an inhibitory modulation on the hypoxic drive to breathe and stimulate the Tb reduction during hypoxia.
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Patrone et al. (2019) studied Hypoxia and hypercapnia. TRPV1 antagonists (AMG9810 or AMG7905) vs. Before injection was evaluated on Cardiorespiratory responses to hypoxia (10% O2) and hypercapnia (7% CO2). TRPV1 antagonists exaggerated the hypoxic ventilatory response and blunted the hypoxia-induced drop in body temperature, indicating TRPV1 exerts an inhibitory modulation on the hypoxic drive to breathe.
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