English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Although the contractile performance of the myocardium is under continuous nervous and hormonal regulation, the myocardium possesses a number of intrinsic, load-dependent mechanisms by which it can adjust cardiac output to meet the needs of the circulation over periods ranging from seconds to years. In isolated hearts, an increase in ventricular end-diastolic volume (EDV), produced by increased venous return or decreased aortic outflow, leads immediately to a more powerful contraction via the Frank-Starling mechanism (“heterometric autoregulation”1 ), so that cardiac output increases over a few beats to match venous return. However, over the next few minutes, there is a further increase in myocardial performance, such that EDV returns toward its original value. This second autoregulatory mechanism, the “Anrep effect”2 or “homeometric autoregulation,”1 allows a given change in cardiac output to be achieved with a smaller change in EDV than if the Frank-Starling effect were the only compensatory mechanism. Finally, if the increase in EDV or wall stress is maintained, genes are switched on that eventually lead to myocardial cell hypertrophy.Much is known about the cellular and molecular basis of the Frank-Starling mechanism and of the initial stages of load-induced hypertrophy, but the processes responsible for the Anrep effect are poorly understood. In this issue of Circulation Research , Alvarez et al3 suggest a novel mechanism for the slow increase in myocardial contractility: a stretch-induced activation of the sarcolemmal Na+/H+ exchanger (NHE) by local autocrine/paracrine systems involving angiotensin II (Ang II) and endothelin-1 (ET-1).Our knowledge of the cellular mechanisms involved in the time-dependent increase in contractility after myocardial fiber stretch has come chiefly from studies in which fiber length is controlled (for reviews, see References 44 –6). Parmley and Chuck7 were the first to show that stretch of isolated papillary …

A Role for the Sarcolemmal Na + /H + Exchanger in the Slow Force Response to Myocardial Stretch

A Role for the Sarcolemmal Na ⁺ /H ⁺ Exchanger in the Slow Force Response to Myocardial Stretch