The myogenic response is the tendency of certain vessels, most notably small arteries and arterioles, to constrict in response to an increase in intravascular pressure. The effects of propofol on the myogenic response of the isolated pressurized rabbit ear artery were studied in segments preconstricted either with norepinephrine or 5-hydroxytryptamine and subjected to pressure increases from 60 to 100 mm Hg applied either rapidly (jumps over 500 ms) or slowly (ramps over 120 s). In the control experiments the preconstricted vessels initially dilated, then rapidly returned toward their initial diameter. In response to pressure ramps, vessels slowly dilated, but closely retained their resting diameter. Administration of propofol (1.6 x 10(-4) to 1.6 x 10(-3) M) resulted in dilation of the constricted vessels. With pressure jumps vessels had a reduced capacity to recover their initial diameters, and with pressure ramps vessels dilated to greater diameters. When the concentration of vasoconstrictor was increased to antagonize the propofol-induced dilation the myogenicity was not restored. This attenuation of myogenicity, distinct from the drug's vasodilator effect may represent a further mechanism by which anesthetic agents can affect cardiovascular function.
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http://dx.doi.org/10.1213/00000539-199304000-00025 | DOI Listing |
Eur J Appl Physiol
January 2025
Department of Kinesiology, Health Promotion, and Recreation, University of North Texas, Denton, TX, USA.
Physical activity (PA) and exercise elicit adaptations and physiological responses in skeletal muscle, which are advantageous for preserving health and minimizing chronic illnesses. The complicated atmosphere of the exercise response can be attributed to hereditary and environmental variables. The primary cause of these adaptations and physiological responses is the transcriptional reactions that follow exercise, whether endurance- (ET) or resistance- training (RT).
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Biochemistry, Dongguk University College of Medicine, 123 Dongdae-ro, Gyeongju 38066, Republic of Korea.
Cortactin (CTTN) is an actin-binding protein regulating actin polymerization and stabilization, which are vital processes for maintaining skeletal muscle homeostasis. Despite the established function of CTTN in actin cytoskeletal dynamics, its role in the myogenic differentiation of progenitor cells remains largely unexplored. In this study, we investigated the role of CTTN in the myogenic differentiation of C2C12 myoblasts by analyzing its effects on actin cytoskeletal remodeling, myocardin-related transcription factor A (MRTFA) nuclear translocation, serum response factor (SRF) activation, expression of myogenic transcription factors, and myotube formation.
View Article and Find Full Text PDFEar Hear
December 2024
Department of Communication Sciences and Disorders, James Madison University, Harrisonburg, Virginia, USA.
Objectives: Cervical vestibular evoked myogenic potentials (cVEMPs) reflect saccular stimulation that results in an inhibitory muscle reflex recorded over the sternocleidomastoid muscle. These responses are utilized to study basic vestibular functions and are also applied clinically. Traditionally, cVEMPs have utilized transient stimuli such as clicks and tonebursts to evoke onset responses.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Clinical Nutrition Service Center, Department of General Surgery, Nanjing Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Background: Skeletal muscle remodelling can cause clinically important changes in muscle phenotypes. Satellite cells (SCs) myogenic potential underlies the maintenance of muscle plasticity. Accumulating evidence shows the importance of succinate in muscle metabolism and function.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Sprott Centre for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Canada.
Background: Duchenne muscular dystrophy (DMD) is a devastating disease characterized by progressive muscle wasting that leads to diminished lifespan. In addition to the inherent weakness of dystrophin-deficient muscle, the dysfunction of resident muscle stem cells (MuSC) significantly contributes to disease progression.
Methods: Using the mdx mouse model of DMD, we performed an in-depth characterization of disease progression and MuSC function in dystrophin-deficient skeletal muscle using immunohistology, isometric force measurements, transcriptomic analysis and transplantation assays.
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