Pulmonary Artery Smooth Muscle Cells
Pulmonary Artery Smooth Muscle Cells - Related Videos
08:02
Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
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Cited by 16 •
2013
We have developed a novel and reproducible technique to isolate primary cultures of pulmonary artery smooth muscle cells (PASMC) from mice as young as P7, thereby allowing better study of the signaling pathways involved in neonatal smooth muscle cell contraction and relaxation.
08:06
Isolation of Human Umbilical Arterial Smooth Muscle Cells (HUASMC)
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Cited by 8 •
2010
The umbilical cords are used to isolate smooth muscle cells by different ways. In this work we used the enzymatic treatment to isolated smooth muscle cells.
08:24
Isolation of Murine Coronary Vascular Smooth Muscle Cells
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Cited by 11 •
2016
The purpose of this protocol is to demonstrate the isolation and culture techniques of murine primary vascular smooth muscle cells (VSMCs) from the coronary circulation. Once VSMCs have been isolated, they can be used for many standard culture techniques.
11:02
Exploring Arterial Smooth Muscle Kv7 Potassium Channel Function using Patch Clamp Electrophysiology and Pressure Myography
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Cited by 8 •
2012
Measurements of Kv7 (KCNQ) potassium channel activity in isolated arterial myocytes (using patch clamp electrophysiological techniques) in parallel with measurements of constrictor/dilator responses (using pressure myography) can reveal important information about the roles of Kv7 channels in vascular smooth muscle physiology and pharmacology.
07:56
Isolation of Intrapulmonary Artery and Smooth Muscle Cells to Investigate Vascular Responses
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2022
Vascular responses of arterial pulmonary circulation can be explored using intrapulmonary artery (IPA) and vascular smooth muscle cells (VSMCs). The present study describes the isolation of IPA in detail and the protocols used for investigating vasorelaxation in response to physiological stimuli.
FAQs
Contraction begins when vasoconstrictor signals raise intracellular calcium through increased calcium entry or release. The elevated calcium activates myosin, the contractile machinery responsible for generating force, so the vessel narrows. This calcium-dependent sequence provides a mechanistic basis for examining how pharmacological agents influence pulmonary vascular tone and alter the resistance encountered by blood flow.
Calcium entry and intracellular calcium release represent two routes by which vasoconstrictor signals can increase the calcium available to the contractile apparatus. Either route can promote myosin activation and greater force, whereas relaxing signals reduce calcium-dependent force. Distinguishing these mechanisms helps investigators identify whether a drug response is linked to calcium movement, force generation, or both.
These pathways provide distinct pharmacological points of control. Endothelin signaling is associated with regulation of pulmonary vascular contraction, while cyclic nucleotide pathways and nitric oxide-mediated signaling are examined in relation to relaxation. Studying them separately helps clarify how different drug mechanisms influence calcium-dependent force, vascular tone, and the balance between narrowing and relaxation.
The cells serve as a model for examining drug responses in the pulmonary vasculature. Investigators can focus on changes in calcium signaling, calcium-dependent force, vascular tone, or pathway-specific responses involving calcium channels, cyclic nucleotides, endothelin, and nitric oxide. These observations connect cellular mechanisms with pharmacological effects on pulmonary vascular resistance and support evaluation of targeted treatments.
Research using pulmonary artery smooth muscle cells can address pulmonary hypertension and vascular remodeling, two settings in which altered smooth-muscle behavior is pharmacologically important. By examining contraction, relaxation, and signaling responses, investigators can explore mechanisms contributing to abnormal pulmonary vascular resistance and determine how candidate therapies may modify those processes.
Cellular findings identify signaling processes that drugs might modify to reduce excessive pulmonary vascular resistance. Responses involving calcium channels, cyclic nucleotide pathways, endothelin signaling, or nitric oxide-mediated relaxation can indicate which mechanisms support contraction or relaxation. This information helps connect molecular targets with therapeutic strategies designed to improve pulmonary vascular function in pulmonary hypertension.