Publications by authors named "Xuping Bao"

Cardiovascular diseases (CVD) and frailty are common health problems among the elderly. This research aims to investigate the hotspots and frontiers of the field of CVD with frailty. Data of publications between 2000 and 2021 were collected from the Web of Science Core Collection (WoSCC) and CiteSpace was used for analyzing the hotspots and frontiers of cardiovascular diseases with frailty research from high-impact countries/regions, institutions, authors, cited references, cited journals, high-frequency keywords, and burst keywords.

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Epinephrine (E) is a hormone released from the adrenal medulla in response to low blood sugar and other stresses. E and related β2-adrenergic agonists are used to treat asthma, but a side effect is high blood sugar. C57BL/6 mice prone to overfeeding induced type II diabetes had the PNMT gene knocked out to prevent E synthesis.

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Phenylethanolamine N-methyltransferase (PNMT) catalyzes synthesis of epinephrine (E) and is present in the brain, heart, and adrenal. E is a neurotransmitter and important hormone; however, its role in regulating cardiovascular dynamics is still unclear. We generated an E-deficient mouse model by knocking out the PNMT gene.

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To define the in vivo role of adrenergic catecholamines (CAs), we generated a mouse model whereby tyrosine hydroxylase (TH) was knocked out (KO) in phenylethanolamine N-methyltransferase-expressing cells. These adrenergic specific TH-KO mice were viable and grossly normal. Their resting heart rate and blood pressure, as monitored by telemetry, were unchanged.

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The pithed rat model has been used extensively to study peripheral cardiovascular responses to electrical stimulation of the sympathetic nervous system, as pithing eliminates central and reflex effects. However, since the transgenic mouse has become a standard and economical model organism, an electrically stimulated pithed mouse would facilitate a variety of studies. We have developed surgical techniques, drug doses and stimulation parameters for an electrically stimulated pithed mouse to study peripheral sympathetic nerve effects on blood pressure.

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GTP cyclohydrolase 1 (GCH1) is rate limiting in the provision of the cofactor tetrahydrobiopterin for biosynthesis of catecholamines and NO. We asked whether common genetic variation at GCH1 alters transmitter synthesis and predisposes to disease. Here we undertook a systematic search for polymorphisms in GCH1, then tested variants' contributions to NO and catecholamine release as well as autonomic function in twin pairs.

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Background: Epinephrine (EPI) is an important neurotransmitter and hormone. Its role in regulating cardiovascular function at rest and with stress is unclear, however.

Methods And Results: An epinephrine-deficient mouse model was generated in which the epinephrine-synthesizing enzyme phenylethanolamine N-methyltransferase was knocked out (KO).

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Background: Drugs that stimulate the beta2-adrenergic receptor have been reported to prolong the QT interval corrected for heart rate (QTc interval), a potential mechanism for cardiac toxicity.

Objective: This study evaluated whether beta2-adrenergic agonist drugs prolong the QTc interval when different correction formulas for the effect of heart rate are used.

Methods: Healthy subjects of both sexes aged 19 to 33 years were recruited with advertisements.

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Few studies have examined to what extent genetic variants of the beta2-adrenoceptor (ADRB2) are involved in the development of hypertension with age, although beta2-adrenergic receptor responsiveness declines in older subjects. To investigate this, 10 common single-nucleotide polymorphisms (SNPs) in the promoter and coding regions of the ADRB2 gene were genotyped in an unrelated population consisting of 2 ethnic groups: European American (EA; n=610) and African American (AA; n=420). ADRB2 haplotypes were estimated by expectation maximization (EM) algorithm-based methods.

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It is well established that after acclimatization at high altitude, many sympathetic pathways are hyperactive yet heart rate (HR) remains unchanged. In this study, we attempted to determine if this unchanged heart rate is due to compensatory mechanisms such as changes in parasympathetic activity or levels of receptors for autonomic neurotransmitters. We also examined the role played by hypoxia in these autonomic adaptations to high altitude.

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Background: Many studies support a link between obstructive sleep apnea (OSA), increased blood pressure (BP) and/or BP variability, and sympathetic nervous system (SNS) activity. We assessed the relationship between SNS activity and 24-h BP variability in patients with OSA, and the effect of continuous positive airway pressure (CPAP) on BP variability.

Design: Forty-one patients with a respiratory disturbance index (RDI) > 15 were randomized into CPAP or CPAP placebo groups for a 1-week trial.

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Phenylethanolamine N-methyltransferase (PNMT) methylates norepinephrine (NE) to form epinephrine (E). It is present in a high concentration in the adrenal medula but occurs in many other tissues throughout the body. In the brain stem and retina PNMT is present in specific neurons.

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