Reasons For Performing Study: Adrenergic activity accompanies intense exercise and mediates physiological and metabolic responses to exercise. Guanabenz, an antihypertensive drug marketed for human usage, depresses brain vasomotor and cardioaccelerator centres, blocks peripherally adrenergic neurons and is reportedly used as a calming agent in horses but little is known of its effects in the species.
Objectives: To determine if guanabenz induces measurable signs of adrenergic suppression on fit Thoroughbred horses undergoing intense exercise.
Methods: In a random crossover design, 12 exercise conditioned Thoroughbred horses each received guanabenz (0.08 mg/kg bwt i.v.) and placebo at 3-week intervals. An incremental exercise test to exhaustion on a treadmill followed treatment by 1 h. Heart rate, oxygen consumption, carbon dioxide production, plasma lactate, catecholamines, adrenocorticotropic hormone (ACTH) and cortisol, and time to fatigue were monitored. Statistical analysis was performed using mixed-effects linear modelling.
Results: Mean heart rate during the exercise period was lower in guanabenz-treated horses (P = 0.04). Mean concentrations of plasma cortisol (P = 0.02) and adrenaline (P = 0.03) were lower for guanabenz-treated horses during the exercise period. Mean run time was slightly but not significantly longer for guanabenz-treated horses, (P = 0.053). No significant effects of guanabenz administration were found for oxygen consumption, carbon dioxide production nor for plasma lactate, noradrenaline and ACTH concentrations.
Conclusion: Guanabenz administration induced signs of adrenergic suppression including plasma cortisol and adrenaline concentrations and heart rate and may enhance endurance, but did not eliminate increases in hormone concentrations induced by exercise. Clear determination of a positive performance effect of adrenaline, but not noradrenaline, suppression is needed before clinical significance can be determined.
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http://dx.doi.org/10.1111/j.2042-3306.2006.tb05550.x | DOI Listing |
J Ovarian Res
January 2025
Key Laboratory of Molecular Target & Clinical Pharmacology and the State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and The Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Background: Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder among women of reproductive age. It is characterized by hyperandrogenism, ovulatory dysfunction, and the presence of polycystic ovarian morphology (PCOM) on ultrasound, often accompanied by metabolic disturbances such as insulin resistance and obesity. Current treatments, including oral contraceptives and anti-androgen medications, often yield limited efficacy and undesirable side effects.
View Article and Find Full Text PDFJ Physiol Sci
January 2025
Laboratory of Regulation in Metabolism and Behavior, Faculty of Agriculture, Kyushu University, 744 Motooka, Nishi-Ku, 819-0395, Fukuoka, Japan. Electronic address:
Intraocular pressure (IOP) plays a crucial role in glaucoma development, involving the dynamics of aqueous humor (AH). AH flows in from the ciliary body and exits through the trabecular meshwork (TM). IOP follows a circadian rhythm synchronized with the suprachiasmatic nucleus (SCN), the circadian pacemaker.
View Article and Find Full Text PDFSci Adv
January 2025
Department of Neuroscience, Helen Wills Neuroscience Institute, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA.
Homeostatic sleep regulation is essential for optimizing the amount and timing of sleep for its revitalizing function, but the mechanism underlying sleep homeostasis remains poorly understood. Here, we show that optogenetic activation of locus coeruleus (LC) noradrenergic neurons immediately increased sleep propensity following a transient wakefulness, contrasting with many other arousal-promoting neurons whose activation induces sustained wakefulness. Fiber photometry showed that repeated optogenetic or sensory stimulation caused a rapid reduction of calcium activity in LC neurons and steep declines in noradrenaline/norepinephrine (NE) release in both the LC and medial prefrontal cortex (mPFC).
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
January 2025
Department of Cardiology, Sanya Central Hospital, Sanya 572000, China.
Objectives: To explore the mechanism that mediate the therapeutic effect of quercetin on heart failure.
Methods: We searched the TCMSP and Swiss ADME databases for the therapeutic targets of quercetin and retrieved heart failure targets from the Genecards and OMIM databases. The intersecting targets were analyzed with GO and KEGG pathway analysis using DAVID database, and the key genes were identified PPI analysis.
Bioact Mater
April 2025
Musculoskeletal Research Laboratory of Department of Orthopaedics & Traumatology, Innovative Orthopaedic Biomaterial and Drug Translational Research Laboratory, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Biodegradable magnesium (Mg) implant generally provides temporary fracture fixation and facilitates bone regeneration. However, the exact effects of generated Mg ions (Mg), hydrogen gas (H), and hydroxide ions (OH) by Mg degradation on enhancing fracture healing are not fully understood. Here we investigate the degradation of Mg intramedullary nail (Mg-IMN), revealing the generation of these degradation products around the fracture site during early stages.
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