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Cardiovascular diseases pose an enormous clinical challenge, remaining the most common cause of death in the world. β-adrenoceptors play an important role on cardiac, vascular and/or endothelial function at a cellular level with relevant applications in several cardiovascular diseases, such as heart failure and hypertension. G protein–coupled receptors (GPCRs), including β-adrenergic receptors, constitute the most ubiquitous superfamily of plasma membrane receptors and represent the single most important type of therapeutic drug target. Sympathetic nervous system hyperactivity, which characterizes several cardiovascular diseases, such as heart failure and hypertension, as well as physiological ageing, has been proved to exert in the long-term detrimental effects in a wide range of cardiovascular diseases. Acutely, sympathetic hyperactivity represents the response to an insult to the myocardium, aiming to compensate for decreased cardiac output. This process involves the activation of beta-adrenergic receptors by catecholamine with consequent heart rate and cardiac contractility increase. However, long-term exposure of the heart to elevated norepinephrine and epinephrine levels, originating from sympathetic nerve endings and chromaffin cells of the adrenal gland, results in further progressive deterioration in cardiac structure and function. At the molecular level, sustained sympathetic nervous system hyperactivity is responsible for several alterations including altered beta-adrenergic receptor signaling and function (down-regulation/desensitization). Moreover, the detrimental effects of catecholamine affect also the function of different cell types including, but not limited to, endothelial cells, fibroblasts and smooth muscle cells. Thus, the success of beta-blocker therapy is due, at least in part, to the protection of the heart and the vasculature from the noxious effects of augmented catecholamine levels. The current research topic aims to support the progress towards understanding the role of sympathetic nervous system under physiological conditions, and the contribution of its hyperactivity in the pathogenesis and progression of cardiovascular diseases. The topic is open to original studies, descriptions of new methodologies, reviews and opinions.

Cardiovascular system --- Cardiovascular system --- Cardiovascular system --- GRK2 --- Beta-adrenoceptors --- exercise training --- Heart Failure --- Sympathetic Nervous System --- beta-blockers --- functional recovery --- Diseases. --- Diseases --- Pathogenesis. --- Diseases --- Prevention --- Research. --- GRK2 --- Beta-adrenoceptors --- exercise training --- Heart Failure --- Sympathetic Nervous System --- beta-blockers --- functional recovery

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Cardiovascular diseases pose an enormous clinical challenge, remaining the most common cause of death in the world. β-adrenoceptors play an important role on cardiac, vascular and/or endothelial function at a cellular level with relevant applications in several cardiovascular diseases, such as heart failure and hypertension. G protein–coupled receptors (GPCRs), including β-adrenergic receptors, constitute the most ubiquitous superfamily of plasma membrane receptors and represent the single most important type of therapeutic drug target. Sympathetic nervous system hyperactivity, which characterizes several cardiovascular diseases, such as heart failure and hypertension, as well as physiological ageing, has been proved to exert in the long-term detrimental effects in a wide range of cardiovascular diseases. Acutely, sympathetic hyperactivity represents the response to an insult to the myocardium, aiming to compensate for decreased cardiac output. This process involves the activation of beta-adrenergic receptors by catecholamine with consequent heart rate and cardiac contractility increase. However, long-term exposure of the heart to elevated norepinephrine and epinephrine levels, originating from sympathetic nerve endings and chromaffin cells of the adrenal gland, results in further progressive deterioration in cardiac structure and function. At the molecular level, sustained sympathetic nervous system hyperactivity is responsible for several alterations including altered beta-adrenergic receptor signaling and function (down-regulation/desensitization). Moreover, the detrimental effects of catecholamine affect also the function of different cell types including, but not limited to, endothelial cells, fibroblasts and smooth muscle cells. Thus, the success of beta-blocker therapy is due, at least in part, to the protection of the heart and the vasculature from the noxious effects of augmented catecholamine levels. The current research topic aims to support the progress towards understanding the role of sympathetic nervous system under physiological conditions, and the contribution of its hyperactivity in the pathogenesis and progression of cardiovascular diseases. The topic is open to original studies, descriptions of new methodologies, reviews and opinions.

Cardiovascular system --- Cardiovascular system --- Cardiovascular system --- Diseases. --- Diseases --- Pathogenesis. --- Diseases --- Prevention --- Research. --- GRK2 --- Beta-adrenoceptors --- exercise training --- Heart Failure --- Sympathetic Nervous System --- beta-blockers --- functional recovery

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Cardiovascular diseases pose an enormous clinical challenge, remaining the most common cause of death in the world. β-adrenoceptors play an important role on cardiac, vascular and/or endothelial function at a cellular level with relevant applications in several cardiovascular diseases, such as heart failure and hypertension. G protein–coupled receptors (GPCRs), including β-adrenergic receptors, constitute the most ubiquitous superfamily of plasma membrane receptors and represent the single most important type of therapeutic drug target. Sympathetic nervous system hyperactivity, which characterizes several cardiovascular diseases, such as heart failure and hypertension, as well as physiological ageing, has been proved to exert in the long-term detrimental effects in a wide range of cardiovascular diseases. Acutely, sympathetic hyperactivity represents the response to an insult to the myocardium, aiming to compensate for decreased cardiac output. This process involves the activation of beta-adrenergic receptors by catecholamine with consequent heart rate and cardiac contractility increase. However, long-term exposure of the heart to elevated norepinephrine and epinephrine levels, originating from sympathetic nerve endings and chromaffin cells of the adrenal gland, results in further progressive deterioration in cardiac structure and function. At the molecular level, sustained sympathetic nervous system hyperactivity is responsible for several alterations including altered beta-adrenergic receptor signaling and function (down-regulation/desensitization). Moreover, the detrimental effects of catecholamine affect also the function of different cell types including, but not limited to, endothelial cells, fibroblasts and smooth muscle cells. Thus, the success of beta-blocker therapy is due, at least in part, to the protection of the heart and the vasculature from the noxious effects of augmented catecholamine levels. The current research topic aims to support the progress towards understanding the role of sympathetic nervous system under physiological conditions, and the contribution of its hyperactivity in the pathogenesis and progression of cardiovascular diseases. The topic is open to original studies, descriptions of new methodologies, reviews and opinions.

Cardiovascular system --- Diseases. --- Diseases --- Pathogenesis. --- Prevention --- Research. --- GRK2 --- Beta-adrenoceptors --- exercise training --- Heart Failure --- Sympathetic Nervous System --- beta-blockers --- functional recovery

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The Beta-3 Adrenoreceptor plays an important role in regulating human fat storage and variants of this receptor are thought to be relevant to diabetes.In addition to the major interest in obesity and diabetes expressed by the pharmaceutical industry, increasing numbers of academic groups are attracted by this general research area. This renewed interest is of course in part stimulated by available financing from industry. It also reflects the growing realisation that metabolism remains an open frontier: little is known about adipocyte sub-populations, specific markers, or endocrine functio

Beta adrenoceptors. --- Adrenergic beta agonists. --- Adrenergic beta receptor agonists --- Beta adrenergic agonists --- Beta adrenergic receptor agonists --- Beta adrenoceptor agonists --- Beta agonists --- Beta sympathomimetic agents --- Beta sympathomimetics --- Sympathomimetic agents --- Beta adrenoceptors --- Adrenergic beta receptors --- Adrenergic receptors, Beta --- Adrenoceptors, Beta --- Beta adrenergic receptors --- Receptors, Beta adrenergic --- Adrenaline --- Adrenergic beta agonists --- Adrenergic beta blockers --- Receptors

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Chronic obstructive pulmonary disease (COPD) is a multi-component condition that results in increasingly limited airflow, usually associated with an abnormal inflammatory response of the lung. It constitutes a major public health burden worldwide, while only very few effective therapies are available. This book provides a comprehensive overview of the development of Onbrez Breezhaler, a newly approved once-daily inhaled β2 agonist for the treatment of COPD. It reviews the current pharmacotherapy for COPD and discusses topics such as the chemical design and the pre-clinical pharmacology of the molecule, the early clinical development, the INHANCE study (which provides a successful example of the use of an adaptive design in the confirmatory setting) and the Phase III clinical efficacy study, as well as the history and performance of the Breezhaler device. Finally, a list of emerging targets is included that could well offer future treatment options for COPD.

Lungs --- Adrenergic beta agonists --- Diseases, Obstructive --- Chemotherapy. --- Therapeutic use. --- Adrenergic beta receptor agonists --- Beta adrenergic agonists --- Beta adrenergic receptor agonists --- Beta adrenoceptor agonists --- Beta agonists --- Beta sympathomimetic agents --- Beta sympathomimetics --- Lung --- Medicine. --- Pharmacology. --- Respiratory organs --- Biomedicine. --- Pharmacology/Toxicology. --- Pneumology/Respiratory System. --- Diseases. --- Sympathomimetic agents --- Beta adrenoceptors --- Cardiopulmonary system --- Chest --- Toxicology. --- Pneumology. --- Chemicals --- Medicine --- Pharmacology --- Poisoning --- Poisons --- Toxicology --- Respiratory organs—Diseases. --- Drug effects --- Medical pharmacology --- Medical sciences --- Chemotherapy --- Drugs --- Pharmacy --- Physiological effect