Ageing reduces endothelium-dependent vasodilatation in humans and animals, and in humans, exercise training reverses the ageing-associated reduction in endothelium-dependent vasodilatation. The purpose of this study was to determine the mechanism(s) by which 10-12 weeks of treadmill exercise enhances endothelium-dependent vasodilatation in muscles of differing fibre composition from young and old rats. Three- and 22-month-old male Fischer 344 rats were assigned to young sedentary, young exercise-trained, old sedentary, or old exercise-trained groups. Arterioles were isolated from the soleus and gastrocnemius muscles; luminal diameter changes were determined in response to the endothelium-dependent vasodilator acetylcholine (ACh, 10(-9)-10(-4) mol l(-1)) alone and in the presence of the nitric oxide synthase (NOS) inhibitor l-NAME (10(-5) mol l(-1)) or the combination of l-NAME and the cyclooxygenase inhibitor indomethacin (10(-5) mol l(-1)). Training ameliorated the ageing-induced reduction in endothelium-dependent vasodilatation in soleus muscle arterioles. Treatment with l-NAME alone and in combination with indomethacin abolished differences in ACh vasodilatation occurring with ageing and training. Expression of endothelial NOS (eNOS) mRNA in soleus arterioles was unaltered by ageing, whereas eNOS protein was increased with age; training elevated both eNOS mRNA and protein. In gastrocnemius muscle arterioles, ageing did not alter maximal vasodilatation, but ageing and training increased maximal arteriolar diameter. These results demonstrate that ageing-induced reductions and training-induced enhancement of endothelial vasodilatation both occur through the nitric oxide signalling mechanism in highly oxidative skeletal muscle, but ageing and training do not appear to act on the same portion of the signalling cascade.
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http://dx.doi.org/10.1113/jphysiol.2003.060301 | DOI Listing |
Receptors for the vasoactive adipokine apelin, termed APJ receptors, are G-protein-coupled receptors and are widely expressed throughout the cardiovascular system. APJ receptors can also signal via G-protein-independent pathways, including G-protein-coupled-receptor kinase 2 (GRK2), which inhibits nitric oxide synthase (eNOS) activity and nitric oxide (NO) production in endothelial cells. Apelin causes endothelium-dependent, NO-mediated relaxation of coronary arteries from normotensive animals, but the effects of activating APJ receptor signaling pathways in hypertensive coronary arteries are largely unknown.
View Article and Find Full Text PDFNutrients
December 2024
Institute of Medical Science, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.
Background: There is compelling evidence of an inverse association between potassium intake and blood pressure (BP). A potential mechanism for this effect may be dietary potassium-mediated augmentation of endothelium-dependent relaxation. To date, studies have investigated potassium intake supplementation over several weeks in healthy volunteers with variable results on vascular function.
View Article and Find Full Text PDFChem Biol Interact
January 2025
College of Chemistry and Materials, Key Laboratory of Green Catalysis of Jiangxi Education Institutes, Jiangxi Normal University, Nanchang, 330022, China. Electronic address:
As a replacement of bisphenol A, bisphenol S (BPS) is commonly used in the wrappers and food containers of daily life. Epidemiological studies demonstrate a close link between BPS exposure and vascular diseases, where the biological activities of BPS remain scarcely known. Herein, the effects of BPS on endothelial function as well as the underlying mechanism were investigated in human umbilical vein endothelial cells (HUVECs) and mouse arteries.
View Article and Find Full Text PDFBiomedicines
December 2024
Department of Thermophysiology, Institute for Translational Medicine, Medical School, University of Pecs, 7624 Pecs, Hungary.
Hydrogen sulfide (HS) is a gasotransmitter that modulates vascular tone, causing either vasodilation or vasoconstriction depending on the vascular bed, species, and experimental conditions. The cold-sensitive transient receptor potential ankyrin-1 (TRPA1) channel mediates HS-induced effects; however, its contribution to the vasomotor responses of different arteries at different temperatures has remained unclear. Here, we aimed to fill this gap by comparing the effects of sodium sulfide (NaS), which is a fast-releasing HS donor, on the isolated carotid and tail skin arteries of rats and mice at cold and normal body temperature with wire myography.
View Article and Find Full Text PDFBiomedicines
November 2024
Department of Physiology and Immunology, Faculty of Medicine Osijek, J. J. Strossmayer University of Osijek, J. Huttlera 4, 31000 Osijek, Croatia.
: Increased sodium chloride (NaCl) intake led to leukocyte activation and impaired vasodilatation via increased oxidative stress in human/animal models. Interestingly, subpressor doses of angiotensin II (AngII) restored endothelium-dependent vascular reactivity, which was impaired in a high-salt (HS) diet in animal models. Therefore, the present study aimed to assess the effects of AngII exposure following high salt (HS) loading on endothelial cells' (ECs') viability, activation, and reactive oxygen species (ROS) production.
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