LEADER 04303nam 2200565 450 001 9910688341403321 005 20230621140025.0 035 $a(CKB)3710000000526088 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/40169 035 $a(EXLCZ)993710000000526088 100 $a20151214h20152015 fy| 0 101 0 $aeng 135 $aurmu#---uuuuu 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 04$aThe adrenergic system in cardiovascular physiology and pathophysiology$b[electronic resource] /$fedited by: Giuseppe Rengo 205 $aSecond edition. 210 $cFrontiers Media SA$d2015 210 1$a[Lausanne, Switzerland] :$cFrontiers Media SA,$d2015 210 4$aŠ2015 215 $a1 online resource (78 pages) $cillustrations; digital, PDF file(s) 225 1 $aFrontiers Research Topics 225 1 $aFrontiers in Physiology 311 $a2-88919-398-5 320 $aIncludes bibliographical references. 330 3 $aCardiovascular diseases pose an enormous clinical challenge, remaining the most common cause of death in the world. ?-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 ?-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. 410 0$aFrontiers research topics. 410 0$aFrontiers in physiology. 606 $aCardiovascular system$xDiseases 606 $aCardiovascular system$xDiseases$xPathogenesis 606 $aCardiovascular system$xDiseases$xPrevention$xResearch 610 $aGRK2 610 $aBeta-adrenoceptors 610 $aexercise training 610 $aHeart Failure 610 $aSympathetic Nervous System 610 $abeta-blockers 610 $afunctional recovery 615 0$aCardiovascular system$xDiseases. 615 0$aCardiovascular system$xDiseases$xPathogenesis. 615 0$aCardiovascular system$xDiseases$xPrevention$xResearch. 700 $aGiuseppe Rengo$4auth$01351517 702 $aRengo$b Giuseppe 712 02$aFrontiers Research Foundation, 801 2$bUkMaJRU 906 $aBOOK 912 $a9910688341403321 996 $aThe adrenergic system in cardiovascular physiology and pathophysiology$93114716 997 $aUNINA