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Related Concept Videos

Lipid-Lowering Drugs: Statins and Miscellaneous Agents01:20

Lipid-Lowering Drugs: Statins and Miscellaneous Agents

Hyperlipidemia, a medical condition often referred to as high cholesterol, is characterized by abnormally elevated levels of lipids in the bloodstream. When present in excess, these lipids, specifically cholesterol and triglycerides, can lead to serious health complications, often involving cardiovascular diseases. Illnesses like atherosclerosis, heart attacks, and pancreatitis have all been linked to untreated hyperlipidemia. This means controlling and regulating cholesterol and triglyceride...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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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Antianginal Drugs: Calcium Channel Blockers and Ranolazine

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The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
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Antihypertensive Drugs: Angiotensin II Receptor Blockers

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Related Experiment Video

Updated: Jun 25, 2026

Detection of Small GTPase Prenylation and GTP Binding Using Membrane Fractionation and GTPase-linked Immunosorbent Assay
13:51

Detection of Small GTPase Prenylation and GTP Binding Using Membrane Fractionation and GTPase-linked Immunosorbent Assay

Published on: November 11, 2018

Statins decrease dendritic arborization in rat sympathetic neurons by blocking RhoA activation.

Woo-Yang Kim1, Eugene A Gonsiorek, Chris Barnhart

  • 1Department of Pharmacology and Toxicology, SUNY, Buffalo, New York, USA.

Journal of Neurochemistry
|February 12, 2009
PubMed
Summary
This summary is machine-generated.

Statins reduce sympathetic nerve activity by decreasing the size of sympathetic neuron dendrites. This novel mechanism, involving RhoA pathway inhibition, may explain statins

Related Experiment Videos

Last Updated: Jun 25, 2026

Detection of Small GTPase Prenylation and GTP Binding Using Membrane Fractionation and GTPase-linked Immunosorbent Assay
13:51

Detection of Small GTPase Prenylation and GTP Binding Using Membrane Fractionation and GTPase-linked Immunosorbent Assay

Published on: November 11, 2018

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cardiovascular Science

Background:

  • Clinical evidence suggests statins reduce sympathetic activity.
  • The peripheral mechanisms, particularly direct effects on sympathetic neurons, remain unclear.
  • Sympathetic neuron activity correlates with dendritic arbor size.

Purpose of the Study:

  • To investigate if statins decrease dendritic arborization in sympathetic neurons.
  • To elucidate the molecular mechanisms underlying statin-induced changes in sympathetic neurons.

Main Methods:

  • In vivo studies using atorvastatin in adult male rats.
  • In vitro studies on cultured sympathetic neurons.
  • Investigated the role of mevalonate, isoprenoids, cholesterol, and RhoA signaling.

Main Results:

  • Atorvastatin significantly reduced dendritic arborization in vivo.
  • Statins caused dendrite retraction and blocked growth in cultured neurons without affecting survival or axonal growth.
  • Mevalonate/isoprenoids attenuated statin effects; isoprenoid synthesis inhibition mimicked statin effects.
  • Statins inhibited RhoA membrane translocation; constitutively active RhoA reversed statin effects.

Conclusions:

  • Statins decrease dendritic arborization in sympathetic neurons.
  • This effect is mediated by blocking RhoA activation, likely via inhibition of isoprenoid synthesis.
  • This provides a novel mechanism for statin-induced reduction in sympathetic activity and cardiovascular protection.