Related Experiment Video

Updated: Aug 7, 2026

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography
07:51

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Published on: September 22, 2011

Receptor-activated increases in intracellular calcium and protein tyrosine phosphorylation in vascular smooth muscle

L A Semenchuk1, J Di Salvo

  • 1Department of Medical and Molecular Physiology, School of Medicine, University of Minnesota-Duluth 55812, USA.

FEBS Letters
|August 14, 1995
PubMed

Insights

Protein tyrosine kinase inhibitors block receptor-activated calcium increases in smooth muscle cells. These inhibitors also prevent protein tyrosine phosphorylation, suggesting a link between calcium signaling and tyrosine phosphorylation.

Area of Science:

  • Cellular Biology
  • Biochemistry
  • Physiology

Background:

  • Vascular smooth muscle cells (VSMCs) regulate blood pressure.
  • Receptor activation triggers intracellular calcium ([Ca2+]i) increases and protein tyrosine phosphorylation.
  • The relationship between these signaling pathways in VSMCs is not fully understood.

Purpose of the Study:

  • To investigate the role of protein tyrosine kinases in receptor-mediated calcium signaling in canine femoral arterial smooth muscle cells.
  • To determine if protein tyrosine kinase inhibitors affect receptor-activated calcium influx and protein tyrosine phosphorylation.

Main Methods:

  • Cultured canine femoral arterial smooth muscle cells were used.
  • Fura-2 imaging was employed to measure intracellular calcium ([Ca2+]i).
  • Immunoblot analysis with antiphosphotyrosine antibodies assessed protein tyrosine phosphorylation.

Main Results:

  • Receptor agonists (serotonin, phenylephrine) induced transient and sustained increases in [Ca2+]i, primarily via extracellular calcium influx.
  • Genistein and tyrphostin (protein tyrosine kinase inhibitors) significantly inhibited the agonist-evoked [Ca2+]i rise.
  • Agonists increased tyrosine phosphorylation of several proteins, including rasGAP, which was blocked by kinase inhibitors.

Conclusions:

  • Receptor-activated calcium increases in VSMCs are closely linked to receptor-activated protein tyrosine phosphorylation.
  • Protein tyrosine kinases play a crucial role in mediating calcium signaling pathways in vascular smooth muscle.

More Related Videos

Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries09:23

Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries

Published on: November 26, 2013

Measurement of Calcium Fluctuations Within the Sarcoplasmic Reticulum of Cultured Smooth Muscle Cells Using FRET-based Confocal Imaging10:05

Measurement of Calcium Fluctuations Within the Sarcoplasmic Reticulum of Cultured Smooth Muscle Cells Using FRET-based Confocal Imaging

Published on: June 20, 2016

Related Concept Videos

Amplifying Signals via Second Messengers01:15

Amplifying Signals via Second Messengers

Many receptor binding ligands are hydrophilic; they do not cross the cell membrane but bind to cell-surface receptors. Thus, their message must be relayed by second messengers present in the cell cytoplasm. There are several second messenger pathways, each with its own way of relaying information. For example, the G protein-coupled receptors can activate both phosphoinositol and cyclic AMP (cAMP) second messenger pathways. The phosphoinositol pathway is active when the receptor induces...
Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Nitric Oxide Signaling Pathway01:28

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...
Smooth Muscle Contraction01:25

Smooth Muscle Contraction

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.
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
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,...