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Related Concept Videos

Regulation of Heart Rates01:31

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The regulation of heart rate is a complex process controlled by the autonomic nervous system (ANS), hormonal influences, and intrinsic cardiac mechanisms. The ANS has two main components: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS).
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The neural regulation of blood pressure involves intricate interactions between the autonomic nervous system (ANS) and cardiovascular system, ensuring adequate perfusion of tissues. This regulation primarily occurs through baroreceptor and chemoreceptor reflexes, involving both short-term and long-term mechanisms.
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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Typical heart performance is influenced by heart rate, rhythm, myocardial contraction, and metabolism or blood flow. The cardiac muscle exhibits distinct electrophysiological features, including pacemaker activity and calcium channel control, which play a vital role in the heart's response to various drugs. The autonomic nervous system, comprising the sympathetic and parasympathetic branches, regulates heart rate. Sympathetic activation increases heart rate, while parasympathetic activation...
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The regulation of the cardiovascular system allows the body to adapt to various demands and maintain homeostasis.
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Dock10 Regulates Cardiac Function under Neurohormonal Stress.

Liad Segal1,2, Sharon Etzion2, Sigal Elyagon1,2

  • 1Department of Physiology and Cell Biology, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel.

International Journal of Molecular Sciences
|September 9, 2022
PubMed
Summary
This summary is machine-generated.

Dedicator of cytokinesis 10 (Dock10) regulates cardiac stress signaling pathways. Ablating Dock10 in mice impaired heart function and worsened pathological responses to Angiotensin II, suggesting its crucial role in cardiac stress adaptation.

Keywords:
Cdc42MAPK signalingRac1Rho GTPasespathological cardiac hypertrophy

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Area of Science:

  • Cardiovascular Biology
  • Molecular Signaling
  • Cell Biology

Background:

  • Dedicator of cytokinesis 10 (Dock10) is a guanine nucleotide exchange factor.
  • Dock10 regulates Cdc42, Rac1, JNK, and p38 MAPK signaling cascades.
  • The role of Dock10 in the myocardium remains largely uncharacterized.

Purpose of the Study:

  • To investigate the function of Dock10 in cardiac myocytes and fibroblasts.
  • To determine Dock10's role in cardiac stress responses and pathological remodeling.
  • To elucidate Dock10's regulation of MAPK signaling in the heart.

Main Methods:

  • Utilized in vitro models with Dock10-ablated neonatal mouse cardiomyocytes and cardiofibroblasts.
  • Employed in vivo models including global Dock10 knockout (KO) and cardiac myocyte-specific KO (CKO) mice.
  • Administered Angiotensin II infusion to assess cardiac response to stress.

Main Results:

  • Dock10 ablation differentially affected p38 and JNK signaling in cardiomyocytes and cardiofibroblasts.
  • Global Dock10 KO mice exhibited reduced systolic function and cardiomyocyte contractility.
  • Dock10 KO, but not CKO, exacerbated Angiotensin II-induced pathological cardiac remodeling.

Conclusions:

  • Dock10 plays a significant role in regulating cardiac stress-related signaling pathways.
  • Dock10 influences MAPK signaling in both cardiac myocytes and fibroblasts.
  • Inhibition of pathological cardiac remodeling is not solely dependent on Dock10 signaling within cardiomyocytes.