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The diagnosis and management of preterm labor with intact membranes
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Roberto Romero, Tinnakorn Chaiworapongsa, Francesca Gotsch, Lami Yeo, Ichchha Madan, Sonia S. Hassan
The use of beta-adrenergic agents is associated with maternal and fetal side effects. The most common are maternal and fetal tachycardia, tremor, headache, nausea, vomiting, hypokalemia (301), and hyperglycemia (300,301). Hypotension due to peripheral vasodilatation is a common problem (305). Maternal cardiac arrhythmias and myocardial ischemia have been reported during the course of tocolysis with these agents (306). The onset of chest pain should be taken seriously during the course of therapy. Because of metabolic effects (hyperglycemia) of beta-adrenergic agents, it is best to use other agents in patients with glucose intolerance. Neonatal side effects include hypoglycemia (4), hypocalcemia (4), and myocardial damage (case reports) (307).
Targeting the Nervous System
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
There are two different types of adrenergic receptor, known as α- and β-adrenergic receptors, which are G-protein coupled receptors, differing in the type of protein that they are coupled to. Moreover, these two receptors have different sub-types with a different distribution around the body and have subtle structural differences that can allow for selective drug design to target specific organs. The neurotransmitter noradrenaline and hormone adrenaline both activate the adrenergic receptors and belong to a group of compounds called catecholamines. These compounds consist of a catechol ring (1,4-benzenediol) linked to an alkyl amine chain and are synthesised from the amino acid tyrosine. They are metabolised via enzymatic pathways.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The sympathetic nervous system is involuntary and maintains the body in a state of readiness to deal with any problems that arise. It is active during times of stress and generates the body’s ‘fight or flight’ response. Sympathetic fibres arise from the thoracic section of the spinal cord, T1–T12. One of the neurotransmitters released by the sympathetic nervous system is norepinephrine, also known as noradrenaline; consequently, the sympathetic nervous system is described as adrenergic. Noradrenaline binds to adrenergic receptors and creates a physiological effect. Adrenergic receptors are divided into different subtypes: α1, α2, β1, β2.
Nutrition and vasoactive substances in the critically ill patient
Published in South African Journal of Clinical Nutrition, 2022
During the initial phase of shock,1 a decrease in blood pressure activates the sympathetic nervous system (the division of the autonomic nervous system that dominates during emergency states),7 which mediates the compensatory phase of shock.8 In the compensatory phase, to maintain blood flow to the vital organs and to maintain cardiac output, the sympathetic nervous system is activated.1,7,8 The effect of stimulation of the adrenergic system is of specific interest because the vasoactive drugs mimic the result of the sympathetic nervous system.9 The adrenergic receptors consist of alpha (α) and beta (β) receptors. These can be subdivided into α1, α2, β1 and β2 receptors.10 The effect of the catecholamines (adrenaline [epinephrine] and noradrenaline [norepinephrine]) on the different organs or tissue depends on which one of the adrenergic receptors dominates in a specific organ or tissue and the nature of the biochemical response that follows.2
Exercise training ameliorates adrenergic control in spontaneously hypertensive rats
Published in Clinical and Experimental Hypertension, 2021
Munique Tostes Ferreira Miranda, Marina Paiva Lemos, Jeffer Eidi Sasaki, Gustavo R. Mota, Moacir Marocolo, Carla Cristina de Sordi, Thalles Ramos Almeida, Valdo José Dias da Silva, Octávio Barbosa Neto
Adrenergic receptors are also implicated in vascular activity. Stimulation of α and β receptors in response to exposure to their agonists promotes constriction or relaxation of arteries and veins. NO production by endothelial cells is partly mediated by activation of β-adrenergic receptors (35). However, little is known about the role that β-adrenergic receptors play in blood vessels and the influence of physical exercise on these receptors in healthy individuals or patients with different pathological conditions, such as atherosclerosis, hypertension, and diabetes mellitus. NO contributes to the post ET α-adrenergic receptor hyporesponsiveness in animals (36). Factors associated with exercise, such as increases in blood flow, cyclic wall stress associated with pulsatile flow, and catecholamines, stimulate the release of NO (37).
An ɑ2-adrenergic receptor is involved in larval metamorphosis in the mussel, Mytilus coruscus
Published in Biofouling, 2019
Xiao Liang, Ke Chen, Yi-Feng Li, Wei-Yang Bao, Asami Yoshida, Kiyoshi Osatomi, Jin-Long Yang
In many marine invertebrates, GPCRs and related signaling pathways play important roles in the processes of settlement and metamorphosis (Rittschof et al. 1986; Kolberg and Martin 1988; Pawlik 1990; Clare et al. 1995; Amador-Cano et al. 2006). The types of GPCRs and signaling pathways might vary in different invertebrate species. The α2-adrenergic receptors bind to the endogenous catecholamines, such as EPI and norepinephrine, to regulate the actions of the sympathetic nervous system (Cottingham and Wang 2012). In the present study, a full-length cDNA of a member of the α2AR gene family, Mcα2AR, was derived from the adult thick-shelled mussel, M. coruscus. Irrespective of the sex, Mcα2AR was found to express in all the tested tissues of the mussel and was most abundant in hemocytes. The Mcα2AR transcript was present through the entire process of larval development until the post-larval stage, and there was a significant variation in the abundance of the Mcα2AR transcript between pediveliger and post-larvae. The Mcα2AR-knockdown resulted in a substantial reduction in the levels of Mcα2AR transcript, and significantly inhibited the mussel metamorphosis. This finding is consistent with the authors’ hypothesis that knock-down of Mcα2AR by RNA interference would disrupt larval metamorphosis in M. coruscus.