Autonomic nervous system activity changes in patients with hypertension and overweight: role and therapeutic implications

The incidence and prevalence of hypertension is increasing worldwide, with approximately 1.13 billion of people currently affected by the disease, often in association with other diseases such as diabetes mellitus, chronic kidney disease, dyslipidemia/hypercholesterolemia, and obesity. The autonomic nervous system has been implicated in the pathophysiology of hypertension, and treatments targeting the sympathetic nervous system (SNS), a key component of the autonomic nervous system, have been developed; however, current recommendations provide little guidance on their use. This review discusses the etiology of hypertension, and more specifically the role of the SNS in the pathophysiology of hypertension and its associated disorders. In addition, the effects of current antihypertensive management strategies, including pharmacotherapies, on the SNS are examined, with a focus on imidazoline receptor agonists.

Very Low-Calorie Ketogenic Diet Modulates the Autonomic Nervous System Activity through Salivary Amylase in Obese Population Subjects

In obesity, to reduce visceral adipose tissue (VAT), caloric restriction is a valid strategy. Salivary amylase is an enzyme that cleaves large starch carbohydrates molecules and its production is modulated by the central nervous system. In addition, heart rate variability (HRV) is simply a measure of the variation in time between each heartbeat. This variation is controlled by the autonomic nervous system. In the light of this evidence, the aim of this study is to characterize the effect of a very low-calorie ketogenic diet (VLCKD) on the autonomic nervous system in obese patients. Twenty subjects affected by obesity were recruited before and after 8 weeks of VLCKD intervention to evaluate salivary amylase by the ELISA test and HRV analysis. These parameters significantly increased after dietary treatment, and positively correlate to each other. VLCKD exerts a positive effect on salivary amylase and HRV, ameliorating body composition and biochemical features. In brief, this dietary intervention improves the autonomic nervous system activity. This is the first study about the effects of VLCKD upon the autonomic nervous system, but further studies are needed to elucidate the mechanism undergone VLCKD effects.

Leptin Decreases Energy Expenditure Despite Increased Thyroid Hormone in Patients with Lipodystrophy

Context Leptin is an adipokine that signals energy sufficiency. In rodents, leptin deficiency decreases energy expenditure (EE), which is corrected following leptin replacement. In humans, data are mixed regarding leptin-mediated effects on EE. Objective To determine the effects of metreleptin on EE in patients with lipodystrophy. Design, setting, and patients Non-randomized crossover study of 25 patients with lipodystrophy (NIH, 2013-2018). Intervention The initiation cohort consisted of 17 patients without prior exposure to metreleptin, studied before and after 14 days of metreleptin. The withdrawal cohort consisted of 8 previously metreleptin-treated patients, studied before and after 14 days of metreleptin withdrawal. Main outcomes 24-hour energy expenditure (TEE), resting energy expenditure (REE), autonomic nervous system activity (heart rate variability, HrV), plasma free T3, free T4, epinephrine, norepinephrine, and dopamine. Results In the initiation cohort, TEE and REE decreased by 5.0% (121±152 kcal/day; p=0.006) and 5.9% (120±175 kcal/day; p=0.02). Free T3 increased by 19.4% (40±49 pg/dL; p=0.01). No changes in catecholamines or HrV were observed. In the withdrawal cohort, free T3 decreased by 8.0% (p=0.04), free T4 decreased by 11.9% (p=0.002), and norepinephrine decreased by 34.2% (p=0.03), but no changes in EE, epinephrine, dopamine, or HrV were observed. Conclusions Metreleptin initiation decreased EE in patients with lipodystrophy, but no changes were observed after metreleptin withdrawal. Thyroid hormone was higher on metreleptin in both initiation and withdrawal cohorts. Decreased EE after metreleptin in lipodystrophy may result from reductions in energy-requiring metabolic processes that counteract increases in EE via adipose tissue-specific neuroendocrine and adrenergic signaling.

Indirect autonomic nervous system activity assessment in patients with myocardial infarction

Funding Acknowledgements Type of funding sources: None. Introduction. Abnormalities in the cardiac sympathetic nervous system have been documented in myocardial infarction (MI) and have been directly implicated in pathogenesis and progression of MI. Assessment of the autonomic nervous system activity in acute stage of MI allowed us to identify groups of high-risk patients. Purpose. To investigate the sympathetic nervous system activity in patients with MI by assessing the condition of beta-adrenergic reactivity of erythrocytes. To analyze ADRB1 Arg389Gly associations with the state of beta-adrenergic reactivity of erythrocytes in patients with MI. Methods. During the study period, 62 patients were enrolled. The patients were divided into 2 groups. The first group consisted of 11 patients (nine women and two men, median age of 54.0 [49.0;61.0] years) with normal beta-adrenergic reactivity of erythrocytes, the second group consisted of 51 patients (40 women and 11 man, median age of 61.0 [48.0;72.0] years) with abnormal beta-adrenergic reactivity of erythrocytes. The research of beta-adrenergic reactivity of erythrocytes was conducted by analysis of changing erythrocyte osmoresistance under the influence of beta blocker in the first 6 hours from the onset of the heart attack. The genetic research was conducted by PСR method in real time. Results. Groups of patients were comparable in main clinical indicators (anamnesis of ischemic heart disease and chronic heart failure, frequency of beta blockers administration before and during of MI, electrocardiography features: elevation of ST-segment, Q-wave and etc.). The second group presented with a higher occurrence of acute left ventricular failure (33.3% vs 0%, p = 0.026) and arterial hypertension (90.2% vs 63.6%, p = 0.044). Parameters of myocardial damage were significantly higher in the second group than the first group. Primarily, this manifested in the presence of a greater number of hypokinesis zones on echocardiography (p = 0.015). In addition, patients of the second group had a lower ejection fraction according to echocardiography (51.0 [46.5;59.0]% vs 58.0 [52.0;63.0]%, p = 0.042). Levels of blood necrosis biomarkers were significantly higher in the second group, e.g. Troponin I (24.1 [9.9;68.0] ng/ml vs 1.3 [0.2;1.8] ng/ml, p = 0.001). At the same time statistically significant distinctions of the severity of coronary atherosclerosis in groups were not revealed. The analysis of ADRB1 Arg389Gly demonstrated association of CC-genotype with abnormal beta-adrenergic reactivity of erythrocytes [OR 5.9, 95% СI 1.16-30.25, p = 0.043]. Conclusion. Patients with an abnormal beta-adrenergic reactivity were characterized by a greater volume of damage to the heart muscle. Moreover, association of CC-genotype of gene ADRB1 Arg389Gly with abnormal beta-adrenergic reactivity of erythrocytes was identified.