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Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
Rab Cascades01:25

Rab Cascades

Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...

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Related Experiment Video

Updated: Jun 26, 2026

Targeted Neuronal Injury for the Non-Invasive Disconnection of Brain Circuitry
10:58

Targeted Neuronal Injury for the Non-Invasive Disconnection of Brain Circuitry

Published on: September 27, 2020

On target to dual block RAS?

Dimitris P Papadopoulos1, Vasilios Papademetriou, Thomas K Makris

  • 1Hypertension Clinic, Department of Cardiology, Laiko Hospital, Athens, Greece. jimpapdoc@yahoo.com

Angiology
|January 16, 2009
PubMed
Summary
This summary is machine-generated.

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers offer organ protection and may reduce cardiovascular events. Combined therapy might be most effective for managing cardiovascular and metabolic conditions.

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Area of Science:

  • Cardiovascular Pharmacology
  • Renal Medicine
  • Endocrinology

Background:

  • Angiotensin-converting enzyme inhibitors (ACE inhibitors) and angiotensin receptor blockers (ARBs) are recognized for their protective effects on the heart, brain, and kidneys.
  • These drug classes can mitigate endothelial dysfunction and atherosclerosis, potentially lowering cardiovascular event risk.
  • While ACE inhibitors have demonstrated cardiovascular event reduction in coronary artery disease, data for ARBs are less extensive.

Purpose of the Study:

  • To review the cardioprotective, cerebroprotective, and nephroprotective properties of ACE inhibitors and ARBs.
  • To evaluate their role in preventing endothelial dysfunction, atherosclerosis, and cardiovascular events.
  • To explore their impact on target organ damage, cardiovascular mortality/morbidity in heart failure, atrial fibrillation, and metabolic syndrome.

Main Methods:

  • Systematic review of existing clinical data and studies on ACE inhibitors and ARBs.
  • Analysis of evidence regarding their effects on endothelial function and atherosclerosis.
  • Examination of outcomes in cardiovascular events, heart failure, atrial fibrillation, and metabolic syndrome.

Main Results:

  • ACE inhibitors and ARBs demonstrate significant cardioprotective, cerebroprotective, and nephroprotective effects.
  • Both drug classes can reverse endothelial dysfunction and atherosclerosis, contributing to reduced cardiovascular risk.
  • Evidence supports their efficacy in reducing target organ damage and improving outcomes in heart failure, with potential benefits in atrial fibrillation and metabolic syndrome.

Conclusions:

  • ACE inhibitors and ARBs are valuable agents for organ protection and cardiovascular risk reduction.
  • Combined blockade of the renin-angiotensin-aldosterone system with both agents may offer superior therapeutic benefits in certain clinical scenarios.
  • Further research is warranted to fully elucidate the long-term benefits and optimal use of ARBs in cardiovascular disease prevention.