1. Responses to endothelium-derived nitric oxide (EDNO), indomethacin-sensitive endothelium-derived contracting factor (EDCF) and hyperpolarization by endothelium-derived hyperpolarizing factor (EDHF) and the interaction among these factors in mesenteric arteries from 16-week-old Wistar Kyoto (WKY) rats and age-matched stroke-prone spontaneously hypertensive rats (SHRSP) were studied, observing the time-course of the response to 10-5 mol/L acetylcholine (ACh). 2. The effects of EDNO, EDCF and EDHF were blocked by Nomega-nitro-l-arginine (10-4 mol/L), indomethacin (10-5 mol/L) and a combination of apamin (5 x 10-6 mol/L) and charybdotoxin (10-7 mol/L), respectively. 3. The response to EDNO observed in the absence of EDCF and EDHF was not different between preparations from WKY rats and SHRSP. The response to EDCF observed in the absence of EDNO and EDHF was slightly greater in preparations from SHRSP. The response to EDHF in the absence of EDNO and EDCF was much greater in preparations from WKY rats. 4. Endothelium-derived contracting factor attenuated the relaxation in response to EDNO, the attenuation being greater in preparations from SHRSP. Relaxation in response to EDNO was blocked by EDHF in preparations from WKY rats, but not in preparations from SHRSP. 5. The response to EDCF was augmented by both EDNO and EDHF. The augmentation was greater in preparations from SHRSP. 6. The response to EDHF was attenuated by EDNO in preparations from WKY rats, but not in preparations from SHRSP. The response to EDHF was attenuated by EDCF in preparations from both WKY rats and SHRSP, the attenuation being greater in preparations from SHRSP. 7. These results suggest that there are interactions among these factors in terms of their release or the response to ACh in mesenteric arteries that differ between preparations from WKY rats and SHRSP. In addition, involvement of factors other than these three factors, which also differs between preparations from WKY rats and SHRSP, is suggested.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1046/j.1440-1681.2002.03778.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Granules alleviate brain damage in spontaneously hypertensive rats by modulating the miR-124/STAT3 signaling axis.
Nan Fang Yi Ke Da Xue Xue Bao
January 2025
College of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Objectives: To explore the mechanism of Granules (QDG) for alleviating brain damage in spontaneously hypertensive rats (SHRs).
Methods: Twelve 5-week-old SHRs were randomized into SHR control group and SHR+QDG group treated with QDG by gavage at the daily dose of 0.9 g/kg for 12 weeks.
Rnf40 Exacerbates Hypertension-Induced Cerebrovascular Endothelial Barrier Dysfunction by Ubiquitination and Degradation of Parkin.
CNS Neurosci Ther
January 2025
Hypertension Center, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, Gansu, China.
Aims: We aimed to investigate the role of Rnf40 in hypertension-induced cerebrovascular endothelial barrier dysfunction and cognitive impairment.
Methods: We employed microarray data analysis and integrated bioinformatics databases to identify a novel E3 ligase, Rnf40, that targets Parkin. To understand the role of RNF40 in hypertension-induced cerebrovascular endothelial cell damage, we used pAAV-hFLT1-MCS-EGFP-3×Flag-mir30shRnf40 to establish an Rnf40-deficient model in spontaneously hypertensive rats (SHRs).
NPA7: A Dual Receptor Activating Peptide That Inhibits Cardiac Oxidative Stress.
Hypertension
January 2025
Cardiorenal Research Laboratory, Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN. (Xiaoyu Ma, J.C.M., D.G.M., Xiao Ma, Y.Z., S.P., Y.W., S.J.S., J.C.B.).
Background: Cardiomyocyte oxidative stress significantly contributes to the progression of hypertension-induced heart failure, highlighting the need for targeted therapies. We developed a novel peptide, NPA7, that coactivates the GC-A (guanylyl cyclase A)/cGMP and MasR (Mas receptor)/cAMP pathway. This study aimed to test NPA7's ability to inhibit oxidative stress by modulating the p62-KEAP1 (Kelch-like ECH-associated protein 1)-NRF2 (nuclear factor erythroid 2-related factor 2) pathway in human cardiomyocytes (HCMs) and a rat model of hypertension.
View Article and Find Full Text PDFAlterations in Striatal Architecture and Biochemical Markers' Levels During Postnatal Development in the Rat Model of an Attention Deficit/Hyperactivity Disorder (ADHD).
Int J Mol Sci
December 2024
Department of Human Physiology and Pathophysiology, School of Medicine, Collegium Medicum, University of Warmia and Mazury, Warszawska 30, 10-082 Olsztyn, Poland.
Attention deficit/hyperactivity disorder (ADHD) is defined as a neurodevelopmental condition. The precise underlying mechanisms remain incompletely elucidated. A body of research suggests disruptions in both the cellular architecture and neuronal function within the brain regions of individuals with ADHD, coupled with disturbances in the biochemical parameters.
View Article and Find Full Text PDFBackground: Recent reports suggest increased myocardial iNOS expression leads to excessive protein -nitrosylation, contributing to the pathophysiology of HFpEF. However, the relationship between NO bioavailability, dynamic regulation of protein -nitrosylation by trans- and de-nitrosylases, and HFpEF pathophysiology has not been elucidated. Here, we provide novel insights into the delicate interplay between NO bioavailability and protein -nitrosylation in HFpEF.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!