The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform

Jian-pu Zheng - One of the best experts on this subject based on the ideXlab platform.

  • REM Sleep Deprivation induces endothelial dysfunction and hypertension in middle-aged rats: Roles of the eNOS/NO/cGMP pathway and supplementation with L-arginine.
    PloS one, 2017
    Co-Authors: Jiaye Jiang, Zhongyuan Gan, Wenqi Zhao, Jian-pu Zheng
    Abstract:

    Sleep loss can induce or aggravate the development of cardiovascular and cerebrovascular diseases. However, the molecular mechanism underlying this phenomenon is poorly understood. The present study was designed to investigate the effects of REM Sleep Deprivation on blood pressure in rats and the underlying mechanisms of these effects. After Sprague-Dawley rats were subjected to REM Sleep Deprivation for 5 days, their blood pressures and endothelial function were measured. In addition, one group of rats was given continuous access to L-arginine supplementation (2% in distilled water) for the 5 days before and the 5 days of REM Sleep Deprivation to reverse Sleep Deprivation-induced pathological changes. The results showed that REM Sleep Deprivation decreased body weight, increased blood pressure, and impaired endothelial function of the aortas in middle-aged rats but not young rats. Moreover, nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) concentrations as well as endothelial NO synthase (eNOS) phosphorylation in the aorta were decreased by REM Sleep Deprivation. Supplementation with L-arginine could protect against REM Sleep Deprivation-induced hypertension, endothelial dysfunction, and damage to the eNOS/NO/cGMP signaling pathway. The results of the present study suggested that REM Sleep Deprivation caused endothelial dysfunction and hypertension in middle-aged rats via the eNOS/NO/cGMP pathway and that these pathological changes could be inhibited via L-arginine supplementation. The present study provides a new strategy to inhibit the signaling pathways involved in insomnia-induced or insomnia-enhanced cardiovascular diseases.

  • REM Sleep Deprivation induces endothelial dysfunction and hypertension in middle aged rats roles of the enos no cgmp pathway and supplementation with l arginine
    PLOS ONE, 2017
    Co-Authors: Jiaye Jiang, Zhongyuan Gan, Wenqi Zhao, Jian-pu Zheng
    Abstract:

    Sleep loss can induce or aggravate the development of cardiovascular and cerebrovascular diseases. However, the molecular mechanism underlying this phenomenon is poorly understood. The present study was designed to investigate the effects of REM Sleep Deprivation on blood pressure in rats and the underlying mechanisms of these effects. After Sprague-Dawley rats were subjected to REM Sleep Deprivation for 5 days, their blood pressures and endothelial function were measured. In addition, one group of rats was given continuous access to L-arginine supplementation (2% in distilled water) for the 5 days before and the 5 days of REM Sleep Deprivation to reverse Sleep Deprivation-induced pathological changes. The results showed that REM Sleep Deprivation decreased body weight, increased blood pressure, and impaired endothelial function of the aortas in middle-aged rats but not young rats. Moreover, nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) concentrations as well as endothelial NO synthase (eNOS) phosphorylation in the aorta were decreased by REM Sleep Deprivation. Supplementation with L-arginine could protect against REM Sleep Deprivation-induced hypertension, endothelial dysfunction, and damage to the eNOS/NO/cGMP signaling pathway. The results of the present study suggested that REM Sleep Deprivation caused endothelial dysfunction and hypertension in middle-aged rats via the eNOS/NO/cGMP pathway and that these pathological changes could be inhibited via L-arginine supplementation. The present study provides a new strategy to inhibit the signaling pathways involved in insomnia-induced or insomnia-enhanced cardiovascular diseases.

David W. Carley - One of the best experts on this subject based on the ideXlab platform.

  • Cardiopulmonary interactions following REM Sleep Deprivation in Sprague-Dawley rats.
    Experimental Neurology, 1997
    Co-Authors: Miodrag Radulovacki, Sinisa M. Trbovic, David W. Carley
    Abstract:

    We characterized the effects of 48 h of rapid-eye-movement (REM) Sleep Deprivation on cardiovascular and respiratory variables and on Sleep-related cardiopulmonary interactions in adult male Sprague-Dawley rats. Rats were instrumented for monitoring EEG, EMG, and aortic blood pressure. Respiratory rate and minute ventilation were measured by unrestrained single-chamber plethysmography. By using radiotelemetry to monitor blood pressure we clearly demonstrated progressive decreases in mean blood pressure with transitions from wakefulness to non-rapid-eye-movement and REM Sleep which were unaffected by REM Sleep Deprivation. Mirror-image state-dependent increases in heart period suggest that baroreflexes were augmented during Sleep with respect to wakefulness. REM Sleep Deprivation was also associated with lower blood pressure and longer heart period over all Sleep/wake states, although this achieved statistical significance only during REM Sleep and only during the first hour of recovery Sleep. These cardiovascular changes coupled with the observed decreases in respiratory rate and minute ventilation suggest a further augmentation of baroreflexes following REM Sleep Deprivation.

  • Effect of REM Sleep Deprivation on Sleep Apneas in Rats
    Experimental neurology, 1996
    Co-Authors: David W. Carley, Sinisa M. Trbovic, Miodrag Radulovacki
    Abstract:

    Abstract We studied the effects of 48 h of REM Sleep Deprivation on spontaneous and post-sigh central apneas in Sprague–Dawley rats by simultaneously monitoring Sleep by the EEG and respiration for 6 h. During the recovery Sleep following REM Deprivation a decrease in post-sigh apneas occurred in total Sleep. There was no change in spontaneous apneas. The results suggest the existence of partially distinct mechanisms for the two types of apneas.

Jiaye Jiang - One of the best experts on this subject based on the ideXlab platform.

  • REM Sleep Deprivation induces endothelial dysfunction and hypertension in middle-aged rats: Roles of the eNOS/NO/cGMP pathway and supplementation with L-arginine.
    PloS one, 2017
    Co-Authors: Jiaye Jiang, Zhongyuan Gan, Wenqi Zhao, Jian-pu Zheng
    Abstract:

    Sleep loss can induce or aggravate the development of cardiovascular and cerebrovascular diseases. However, the molecular mechanism underlying this phenomenon is poorly understood. The present study was designed to investigate the effects of REM Sleep Deprivation on blood pressure in rats and the underlying mechanisms of these effects. After Sprague-Dawley rats were subjected to REM Sleep Deprivation for 5 days, their blood pressures and endothelial function were measured. In addition, one group of rats was given continuous access to L-arginine supplementation (2% in distilled water) for the 5 days before and the 5 days of REM Sleep Deprivation to reverse Sleep Deprivation-induced pathological changes. The results showed that REM Sleep Deprivation decreased body weight, increased blood pressure, and impaired endothelial function of the aortas in middle-aged rats but not young rats. Moreover, nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) concentrations as well as endothelial NO synthase (eNOS) phosphorylation in the aorta were decreased by REM Sleep Deprivation. Supplementation with L-arginine could protect against REM Sleep Deprivation-induced hypertension, endothelial dysfunction, and damage to the eNOS/NO/cGMP signaling pathway. The results of the present study suggested that REM Sleep Deprivation caused endothelial dysfunction and hypertension in middle-aged rats via the eNOS/NO/cGMP pathway and that these pathological changes could be inhibited via L-arginine supplementation. The present study provides a new strategy to inhibit the signaling pathways involved in insomnia-induced or insomnia-enhanced cardiovascular diseases.

  • REM Sleep Deprivation induces endothelial dysfunction and hypertension in middle aged rats roles of the enos no cgmp pathway and supplementation with l arginine
    PLOS ONE, 2017
    Co-Authors: Jiaye Jiang, Zhongyuan Gan, Wenqi Zhao, Jian-pu Zheng
    Abstract:

    Sleep loss can induce or aggravate the development of cardiovascular and cerebrovascular diseases. However, the molecular mechanism underlying this phenomenon is poorly understood. The present study was designed to investigate the effects of REM Sleep Deprivation on blood pressure in rats and the underlying mechanisms of these effects. After Sprague-Dawley rats were subjected to REM Sleep Deprivation for 5 days, their blood pressures and endothelial function were measured. In addition, one group of rats was given continuous access to L-arginine supplementation (2% in distilled water) for the 5 days before and the 5 days of REM Sleep Deprivation to reverse Sleep Deprivation-induced pathological changes. The results showed that REM Sleep Deprivation decreased body weight, increased blood pressure, and impaired endothelial function of the aortas in middle-aged rats but not young rats. Moreover, nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) concentrations as well as endothelial NO synthase (eNOS) phosphorylation in the aorta were decreased by REM Sleep Deprivation. Supplementation with L-arginine could protect against REM Sleep Deprivation-induced hypertension, endothelial dysfunction, and damage to the eNOS/NO/cGMP signaling pathway. The results of the present study suggested that REM Sleep Deprivation caused endothelial dysfunction and hypertension in middle-aged rats via the eNOS/NO/cGMP pathway and that these pathological changes could be inhibited via L-arginine supplementation. The present study provides a new strategy to inhibit the signaling pathways involved in insomnia-induced or insomnia-enhanced cardiovascular diseases.

Miodrag Radulovacki - One of the best experts on this subject based on the ideXlab platform.

  • Cardiopulmonary interactions following REM Sleep Deprivation in Sprague-Dawley rats.
    Experimental Neurology, 1997
    Co-Authors: Miodrag Radulovacki, Sinisa M. Trbovic, David W. Carley
    Abstract:

    We characterized the effects of 48 h of rapid-eye-movement (REM) Sleep Deprivation on cardiovascular and respiratory variables and on Sleep-related cardiopulmonary interactions in adult male Sprague-Dawley rats. Rats were instrumented for monitoring EEG, EMG, and aortic blood pressure. Respiratory rate and minute ventilation were measured by unrestrained single-chamber plethysmography. By using radiotelemetry to monitor blood pressure we clearly demonstrated progressive decreases in mean blood pressure with transitions from wakefulness to non-rapid-eye-movement and REM Sleep which were unaffected by REM Sleep Deprivation. Mirror-image state-dependent increases in heart period suggest that baroreflexes were augmented during Sleep with respect to wakefulness. REM Sleep Deprivation was also associated with lower blood pressure and longer heart period over all Sleep/wake states, although this achieved statistical significance only during REM Sleep and only during the first hour of recovery Sleep. These cardiovascular changes coupled with the observed decreases in respiratory rate and minute ventilation suggest a further augmentation of baroreflexes following REM Sleep Deprivation.

  • Effect of REM Sleep Deprivation on Sleep Apneas in Rats
    Experimental neurology, 1996
    Co-Authors: David W. Carley, Sinisa M. Trbovic, Miodrag Radulovacki
    Abstract:

    Abstract We studied the effects of 48 h of REM Sleep Deprivation on spontaneous and post-sigh central apneas in Sprague–Dawley rats by simultaneously monitoring Sleep by the EEG and respiration for 6 h. During the recovery Sleep following REM Deprivation a decrease in post-sigh apneas occurred in total Sleep. There was no change in spontaneous apneas. The results suggest the existence of partially distinct mechanisms for the two types of apneas.

Socorro Retana-marguez - One of the best experts on this subject based on the ideXlab platform.

  • Effects of short- and long-term REM Sleep Deprivation on sexual behavior in male rats
    Physiology & behavior, 1996
    Co-Authors: Javier Velasquez-moctezuma, Emilio Domiguez Alazar, Socorro Retana-marguez
    Abstract:

    Abstract The influence of selective REM Sleep Deprivation on masculine sexual behavior has been a matter of controversy. In the present study, the sexual behavior of male rats was analyzed in subjects deprived of REM Sleep by the island technique for 24 or 16 h daily during 20 days. When compared to control rats, both groups displayed changes in sexual performance since the first day. The effects were: an increase in mount, intromission and ejaculation latencies and in mount frequency as well; a decrease of ejaculation frequency and of the Hit rate. The effects became stronger as REM Sleep Deprivation progressed. Rats deprived of REM Sleep for 24 h were extREMely debilitated after 12 days and some of them died, whereas the rats REM deprived for 16 h REMained healthy during the 20 days. These data indicate that REM Sleep Deprivation interferes with the mechanisms that regulate male sexual behavior.