Abstract
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 (), 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.
Highlights
Breathing is a vital behavior that is generated by a medullary region, called the preBötzinger Complex, and is regulated by a complex system that depends on chemical feedback of the carotid body and central chemoreceptors [1,2,3]
TRPC1/3/4/5 and 6 channels are expressed in the carotid chemosensory pathway [9], and contribute to acid sensing in a respiratory chemosensitive nucleus [4], suggesting that these channels can be involved in the ventilatory response to hypoxia and hypercapnia
Several studies have reported the role of TRPV1 on thermoregulation and nociception; none has addressed the influence of this channel on ventilatory and cardiovascular responses to hypoxia and hypercapnia in unanesthetized rats
Summary
Breathing is a vital behavior that is generated by a medullary region, called the preBötzinger Complex (preBötC), and is regulated by a complex system that depends on chemical feedback of the carotid body (peripheral chemoreceptors) and central chemoreceptors [1,2,3]. TRPV1 receptors are widely expressed in peripheral and central locations, including the dorsal horn of the spinal cord [13], the brainstem and forebrain [14,15,16,17,18]. The expression of these receptors in regions such as the preBötC, parafacial respiratory region, locus coeruleus, nucleus of solitary tract [19,20,21], and in petrosal neurons innervating carotid body glomus cells [22], suggests a role in the control of breathing and chemoreception
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