In this study, myography was used to determine the effect of arterial size on nitric oxide (NO) vasodilatory mechanisms in the hindlimb vasculature of the toad . Immunohistochemical analysis showed NO synthase (NOS) 1 immunoreactivity in perivascular nitrergic nerves in the iliac and sciatic arteries. Furthermore, NOS3 immunoreactivity was observed in the vascular smooth muscle of the sciatic artery, but not the endothelium. Acetylcholine (ACh) was used to facilitate intracellular Ca signaling to activate vasodilatory pathways in the arteries. In the iliac artery, ACh-mediated vasodilation was abolished by blockade of the soluble guanylate cyclase pathway with the soluble guanylate cyclase inhibitor ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, 10 M) and blockade of the prostaglandin signaling pathway with indomethacin (10 M). Furthermore, disruption of the endothelium had no effect on the ACh-mediated vasodilation in the iliac artery, and generic inhibition of NOS with -nitro-l-arginine (3 × 10 M) significantly inhibited the vasodilation, indicating NO signaling. In contrast to the iliac artery, ACh-mediated vasodilation of the sciatic artery had a significant endothelium-dependent component. Interestingly, the vasodilation was not significantly affected by -nitro-l-arginine, but it was significantly inhibited by the specific NOS1 inhibitor -(1-imino-3-butenyl)-l-ornithine (vinyl-l-NIO, 10 M). ODQ mostly inhibited the ACh-mediated vasodilation. In addition, indomethacin also significantly inhibited the ACh-mediated vasodilation, indicating a role for prostaglandins in the sciatic artery. This study found that the mechanisms of vasodilation in the hindlimb vasculature of vary with vessel size and that the endothelium is involved in vasodilation in the smaller sciatic artery.
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http://dx.doi.org/10.1152/ajpregu.00319.2018 | DOI Listing |
J Physiol
November 2024
Department of Physiology, Pharmacology & Toxicology, Health Sciences Center, West Virginia University, Morgantown, WV, USA.
Alarmins are classified by their release from damaged or ruptured cells. Many alarmins have been found to increase vascular tone and oppose endothelium-dependent dilatation (EDD). Interleukin (IL)-33 plays a prominent role in lung injury and can be released during vascular injury and in chronic studies found to be cardioprotective.
View Article and Find Full Text PDFInt J Mol Sci
October 2024
Department of Pharmaceutical Sciences, Thomas J. Long School of Pharmacy, University of the Pacific, Stockton, CA 95211, USA.
Several reports, including our previous studies, indicate that hyperglycemia and diabetes mellitus exert differential effects on vascular function in males and females. This study examines sex differences in the vascular effects of type 2 diabetes (T2D) in an established monogenic model of obesity-induced T2D, Zucker Diabetic Fatty (ZDF) rats. Acetylcholine (ACh) responses were assessed in phenylephrine pre-contracted rings before and after apocynin, a NADPH oxidase (NOX) inhibitor.
View Article and Find Full Text PDFAdv Mater
November 2024
State Key Laboratory of Analytical Chemistry for Life Science, School of Chemistry and Chemical Engineering, Nanjing University, Nanjing, 210023, China.
Reproducing human nervous systems with endogenous mechanisms has attracted increasing attention, driven by its great potential in streamlining the neuro-electronic interfaces with bilateral signaling. Here, an artificial aquatic autonomic nervous system (ANS) with switchable excitatory/inhibitory characteristics and acetylcholine (ACh)-mediated plasticity is reported based on the newly emerged organic photoelectrochemical transistor (OPECT). Under the modulation of spatial light and ACh, the system exhibits an immediate switch between excitation and inhibition, and many pulse patterns as well as advanced ANS functions are mimicked.
View Article and Find Full Text PDFShock
November 2024
Division of Pediatric Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
Cardiopulmonary bypass (CPB), an extracorporeal method necessary for the surgical correction of complex congenital heart defects, incites significant inflammation that affects vascular function. These changes are associated with alterations in cellular metabolism that promote energy production to deal with this stress. Utilizing laser Doppler perfusion monitoring coupled with iontophoresis in patients undergoing corrective heart surgery, we hypothesized that temporal, untargeted metabolomics could be performed to assess the link between metabolism and vascular function.
View Article and Find Full Text PDFCells
June 2024
Institute of Physiology, Federal State Autonomous Educational Institution of Higher Education "N.I. Pirogov, Russian National Research Medical University" Ministry of Health, 117997 Moscow, Russia.
This manuscript explores the intricate role of acetylcholine-activated inward rectifier potassium (K) channels in the pathogenesis of atrial fibrillation (AF), a common cardiac arrhythmia. It delves into the molecular and cellular mechanisms that underpin AF, emphasizing the vital function of K channels in modulating the atrial action potential and facilitating arrhythmogenic conditions. This study underscores the dual nature of K activation and its genetic regulation, revealing that specific variations in potassium channel genes, such as Kir3.
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