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Related Concept Videos

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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G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
Smooth Muscle Contraction01:25

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Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
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Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
Autoregulation of Blood Flow01:17

Autoregulation of Blood Flow

Autoregulation mechanisms are characterized by their inherent capacity for self-regulation without necessitating specific nervous stimulation or endocrine control. These mechanisms facilitate the adjustment of blood flow and, therefore, perfusion specific to each tissue region. This self-regulation encompasses chemical signals and myogenic controls.
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Related Experiment Video

Updated: Jun 16, 2026

Exploring Arterial Smooth Muscle Kv7 Potassium Channel Function using Patch Clamp Electrophysiology and Pressure Myography
11:02

Exploring Arterial Smooth Muscle Kv7 Potassium Channel Function using Patch Clamp Electrophysiology and Pressure Myography

Published on: September 14, 2012

Galectin-3 Regulates Smooth Muscle Contraction and Blood Pressure by Modulating CaV1.2 Channel Function.

Kelvin Wei Zhern Loh1,2, Yanruo Zhou1,3, Cong Liu1,2

  • 1Department of Physiology, National University of Singapore (K.W.Z.L., Y.Z., C.L., J.Z., D.Y., M.C.L., Z.H., T.W.S.).

Circulation
|June 15, 2026
PubMed
Summary
This summary is machine-generated.

Galectin-3 (Gal-3) enhances CaV1.2 calcium channel activity, contributing to hypertension. Blocking this interaction with iGal3BP peptide offers a novel therapeutic strategy for lowering blood pressure (BP).

Keywords:
galectin 3hypertensionmuscle contractionpeptides

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Last Updated: Jun 16, 2026

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07:25

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Published on: June 7, 2013

Area of Science:

  • Cardiovascular Physiology
  • Molecular Biology
  • Pharmacology

Background:

  • CaV1.2 calcium channels regulate smooth muscle contraction and blood pressure (BP).
  • Binding proteins fine-tune CaV1.2 activity, representing a novel mechanism for BP regulation.
  • Galectin-3 (Gal-3) is a newly identified CaV1.2-binding protein with an unknown role in hypertension.

Purpose of the Study:

  • To elucidate the role of galectin-3 (Gal-3) in the pathogenesis of hypertension.
  • To investigate the molecular mechanisms by which Gal-3 binds to and modulates CaV1.2 channels.
  • To evaluate the therapeutic potential of blocking the Gal-3 and CaV1.2 interaction for hypertension.

Main Methods:

  • Utilized in vitro, ex vivo, and in vivo experiments, including molecular assays, electrophysiology, and pressure myography.
  • Employed transfected cells, smooth muscle cells, and arteries from Gal-3 knockout mice, hypertensive rats, and human patients.
  • Administered inhibitory galectin-3-binding peptide (iGal3BP) in vivo to assess its effect on blood pressure.

Main Results:

  • Identified Gal-3 as a novel positive modulator of CaV1.2 channels, increasing their expression and activity.
  • Observed upregulation of both CaV1.2 and Gal-3 in hypertensive models and human pulmonary arteries.
  • Demonstrated that blocking the Gal-3/CaV1.2 interaction with iGal3BP significantly reduced blood pressure in hypertensive rats, showing sustained efficacy.

Conclusions:

  • Gal-3 binding to CaV1.2 channels is a key mechanism contributing to hypertension.
  • Gal-based CaV1.2 channel modulators represent novel therapeutic pathways for normalizing blood pressure.
  • The iGal3BP peptide exhibits potent and sustained antihypertensive effects, surpassing current treatments in efficacy.