Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.21 (CPT)
 4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous work has suggested that end-stage renal disease (ESRD) patients may have an exaggerated sympathetic nervous system (SNS) response during exercise. We hypothesized that ESRD patients have an exaggerated blood pressure (BP) response during moderate static handgrip exercise (SHG 30%) and that the exaggerated BP response is mediated by SNS overactivation, characterized by augmented mechanoreceptor activation and blunted metaboreceptor control, as has been described in other chronic diseases. We measured hemodynamics and muscle sympathetic nerve activity (MSNA) in 13 ESRD and 16 controls during: 1) passive hand movement (PHM; mechanoreceptor isolation); 2) low-level rhythmic handgrip exercise (RHG 20%; central command and mechanoreceptor activation); 3) SHG 30%, followed by posthandgrip circulatory arrest (PHGCA; metaboreceptor activation); and 4) cold pressor test (CPT; nonexercise stimulus). ESRD patients had exaggerated increases in systolic BP during SHG 30%; however, the absolute and relative increase in MSNA was not augmented, excluding SNS overactivation as the cause of the exaggerated BP response. Increase in MSNA was not exaggerated during RHG 20% and PHM, demonstrating that mechanoreceptor activation is not heightened in ESRD. During PHGCA, MSNA remained elevated in controls but decreased rapidly to baseline levels in ESRD, indicative of markedly blunted metaboreceptor control of MSNA. MSNA response to CPT was virtually identical in ESRD and controls, excluding a generalized sympathetic hyporeactivity in ESRD. In conclusion, ESRD patients have an exaggerated increase in SBP during SHG 30% that is not mediated by overactivation of the SNS directed to muscle. SBP responses were also exaggerated during mechanoreceptor activation and metaboreceptor activation, but without concomitant augmentation in MSNA responses. Metaboreceptor control of MSNA was blunted in ESRD, but the overall ability to mount a SNS response was not impaired. Other mechanisms besides SNS overactivation, such as impaired vasodilatation, should be explored to explain the exaggerated exercise pressor reflex in ESRD.
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PMID:Exercise pressor reflex in humans with end-stage renal disease. 1868 67

Aerobic exercise is a proven measure to enhance the cardio-respiratory efficiency. This improvement isprimarily due to improvement in autonomic function where in there is increase in the parasympathetic function and decrease in sympathetic function. Exercise also affects many metabolic activities in our body and may be one of the factors which reduce the oxidative stress. The aim of the present study was to see the effect of moderate aerobic exercise training on autonomic function and its correlation with antioxidant status. 30 healthy volunteers in the age group of 18-22 years were screened. Autonomic function tests included activity (tone) and reactivity parameters. Antioxidant status was assessed by the level of malondialdehyde in plasma. We observed a significant change in SBP, DBP, LF nu, HF nu, delta value of DBP in CPT and MDA. Our findings are consistent with earlier findings that short duration physical training is known to reduce blood pressure and that there is a relationship between HF (in HRV) and training response Physical exercise also provides a favorable change in the biochemical parameters such as MDA.
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PMID:Effect of Moderate Aerobic Exercise Training on Autonomic Functions and its Correlation with the Antioxidant Status. 2668 3