期刊
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
卷 314, 期 5, 页码 R693-R699出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00380.2017
关键词
arterial pressure; autonomic function; circulatory control; GIRK channels; heart rate; sympathetic nervous system
类别
资金
- National Institutes of Health [R01-AR-059397, P01-HL-134609]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL134609] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR059397] Funding Source: NIH RePORTER
mu-Opioid G protein-coupled receptors (MOR) interact with ion channels to decrease neuronal excitability. In humans. intrathecal administration of the MOR agonist fentanyl inhibits the exercise pressor reflex, an effect that can be attributed to either the opening of inward rectifying potassium channels (GIRK) or the closing of N-type calcium channels. The purpose of this study was to determine if the highly selective MOR agonist [D-Ala(2),N-MePhe(4),Gly-ol]-enkephalin (DAMGO) attenuates the exercise pressor reflex and which of these two channels are responsible for this effect. In decerebrate rats, we determined the effect of intrathecal injection of either tertiapin-LQ. which blocks the GIRK channel or omega-conotoxin-GVIA, which blocks the N-type calcium channel on the exercise pressor reflex, which was evoked by contracting the triceps surae muscles. Initially, we established that intrathecal injection of DAMGO inhibited the exercise pressor reflex relative to no intrathecal injection or intrathecal saline injection (P < 0.001, n = 5). We then found that intrathecal injection of two doses of tertiapin-LQ (1 and 10 mu g) had no effect on the exercise pressor reflex (n = 6 and n = 7, respectively; P > 0.05). Importantly, neither dose of tertiapin-LQ prevented the DAMGO-induced inhibition of the exercise pressor reflex. Last, we found that intrathecal injection of w-conotoxin-GVIA markedly attenuated the exercise pressor reflex (P < 0.001, n = 7). The cardio-accelerator response to contraction did not appear to be effected in any of the experiments. We conclude that N-type voltage-gated calcium channel inhibition appears to be the mechanism by which MOR activation inhibits the exercise pressor reflex in decerebrate rats.
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