China
Africa
Explore chapters and articles related to this topic
Diabetes Mellitus and Ischemic Heart Disease
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
Of major significance in the pathogenesis of IHD is the violation of the regulatory function of the catecholamines [14, 54, 85, 262, 368, 388, 539]. The primary stage in the action of catecholamines on organs and tissues is their reaction with adrenergic receptors. Their predominating form in the heart is beta-1, and to a smaller extent, alpha-1-adrenoreceptors. The high concentrations of catecholamines in stress exhibit a cardiotoxic effect that is realized chiefly via excess beta-adrenergic stimulation. In hypercatecholemia in the myocardium, a number of unfavorable metabolic changes appear in DM and IHD patients. Special significance here is attached to activation of FPOL and overloading of the cardiac myocytes with calcium.
An Overview of Experimental Methods
Published in Richard Beasley, Neil E. Pearce, The Role of Beta Receptor Agonist Therapy in Asthma Mortality, 2020
The Lands et al.1 classification that beta1 and beta2 receptors were response-specific and likely to be distributed to specific organs or tissues has been proven incorrect. Initially, stimulation of beta1 receptors alone was thought to be responsible for both positive chronotropic (heart rate increase) and inotropic (increase in contractility) effects. There is now ample evidence that both beta1 and beta2 receptors are present and functional,7 in atrial and ventricular myocardium in all species including humans, but with different numbers of the two types of receptors across the species.7-10 In general, in myocardium beta, receptors are present in greater numbers than beta2 receptors.
Antihypertensive Drug Classes
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Engi Abdel-Hady Algharably, Reinhold Kreutz
Currently used beta-blockers can be divided into three groups (2) (Table 40.5) based on their pharmacodynamics properties: Nonselective beta-blockers. They block both beta 1 and beta 2 receptors without selectivity.Cardioselective beta-blockers. They block beta 1 receptors, for example in the heart, with higher selectivity than beta 2 receptors, for example in the lung, when used in approved doses. Overall, cardioselectivity of these drugs is still weak, dose-dependent and decreases with higher doses.Beta-blockers with additional vasodilatory effects. Carvedilol and labetalol exhibit additional vasodilatory effects by blocking adrenergic alpha 1 receptors in arteries, while both compounds are non-selective blockers of both beta 1 and beta 2 receptors. Nebivolol is the beta-blocker with the highest beta 1 selectivity and induces its vasodilatory effect by activating nitric oxide (NO). The vasodilation enhances the BP-lowering effect of these compounds and may improve their tolerability and metabolic profile.
The current and future status of inotropes in heart failure management
Published in Expert Review of Cardiovascular Therapy, 2023
Angelos Arfaras-Melainis, Ioannis Ventoulis, Effie Polyzogopoulou, Antonios Boultadakis, John Parissis
Beta agonists exert their effects by binding to the beta-1 adrenergic receptor located on the sarcolemma of cardiomyocytes. This binding event initiates a signaling cascade that involves the activation of intracellular adenylate cyclase, leading to increased production of cAMP and increased subsequent release of Ca2+ from the sarcoplasmic reticulum. The resulting increase in Ca2+ concentration within the cardiomyocyte leads to enhanced actin-myosin cross-bridging, ultimately culminating in increased contractility on the one hand and increased demand for myocardial oxygen on the other hand. The pharmacological and mechanistic properties of beta agonists differ among various agents due to their distinct affinity for beta-1 receptors and their effects on other receptors [7,8,14].
Association of beta blocker use and hearing ability in adults: a cross-sectional study
Published in International Journal of Audiology, 2022
Deanna Wung, Thadé Goderie, Marieke F. van Wier, Mariska Stam, Sophia E. Kramer
Beta blockers were designed for cardiovascular use and the majority are specific to the beta1 adrenergic receptors (ARs), predominantly located in the heart. However, beta receptors in other parts of the body can cause off-target effects, which brings us to wonder about downstream effects if beta receptors are present in the ear. For example, respiratory exacerbations can be provoked by beta blockers’ unintended activity on beta2 receptors in the lungs (Malerba et al. 2015; Sirak, Jelic, and Le Jemtel 2004). Although most beta blockers target beta1, non-specific beta blockers can bind to beta2 as well. For instance, carvedilol blocks both beta1 and beta2 in addition to alpha ARs (Messerli and Grossman 2004), thus opening the potential to more off-target effects. Most pertinent to the current study, Fauser, Schimanski, and Wangemann (2004) demonstrated that beta1 ARs are present in inner ear epithelial cells, neuronal cells involved in auditory transmission, as well as in hair cells in both the inner and outer ear. In a histochemical study, Khan et al. (2007) showed that alpha, beta1 and beta2 ARs are present in the Organ of Corti and the spiral ganglion of rats. This raises the question about whether beta blockers, even when selective for beta1, may have unintended effects in the ear. Schimanski, Scofield, and Wangemann (2001) found the presence of beta2 receptors in nonstrial tissues in the cochlear lateral wall in gerbils. If beta ARs are present in the auditory system, there is reason to believe that specific and/or non-specific beta blockers may contribute to hearing impairment.
Scoping review of complications associated with epinephrine use in arthroscopy fluid
Published in The Physician and Sportsmedicine, 2021
Taher Abdelrahman, Scott Tulloch, Kate Lebedeva, Ryan M. Degen
The incidence of epinephrine-related complications when used in irrigation during arthroscopic procedures is unknown. Cho et al however noted their experience which is 2 in 2000 cases or an incidence of 1:1000 [3]. To our knowledge, there are no guidelines in the literature with regards to this use of epinephrine. Epinephrine is an adrenergic alpha-agonist, and adrenergic beta-agonist. Stimulating vascular alpha-adrenergic receptors, it causes vasoconstriction, increasing the blood pressure. Beta-1 receptor-stimulating effect, increases the force and rate of myocardial contraction. Epinephrine-induced pulmonary edema has been reported in the literature and is thought to be dose-related [24]. Both endogenous and exogenous catecholamines can induce pulmonary edema. The proposed mechanism of action is through alpha-adrenergic stimulation with increased pulmonary arterial and capillary pressure, which can be maintained and aggravated by inflammation and disruption of the alveolar-capillary barrier. Beta-adrenergic stimulation increases cardiac output and leads to generalized vasodilation, with ensuing pulmonary overperfusion [25].