The 3-month old SHR differ from the WKY rats in that the former have an increased osmolality, concentration of albumins, activity (but not the concentration) of sodium and a reduced activity of potassium. The shifts in the albumins concentration occur, mainly, on account of the amino acid phenylalanine. The gradient increase of the sodium and potassium concentration between the plasma and muscular tissue in followed by a slight hyperpolarisation of the muscle fibers, a drop in the lability and a increase in pO2. The above shifts of homeostatic parameters were not revealed in the SHR and WKY rats of 1.5 and 6.0 months of age.

Download full-text PDF

Source

Publication Analysis

Top Keywords

wky rats
8
[the age-related
4
age-related characteristics
4
characteristics changes
4
changes osmotic
4
osmotic ionic
4
ionic homeostasis
4
homeostasis spontaneously
4
spontaneously hypertensive
4
hypertensive rats]
4

Similar Publications

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 PDF

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.

View Article and Find Full Text PDF

Background: Prostaglandin E (PGE) in the rostral ventrolateral medulla (RVLM) has been recognized as a pivotal pressor substance in hypertension, yet understanding of its effects and origins in the RVLM remains largely elusive. This study aimed to elucidate the pivotal enzymes and molecular mechanisms underlying PGE synthesis induced by central Ang II (angiotensin II) and its implications in the heightened oxidative stress and sympathetic outflow in hypertension.

Methods And Results: RVLM microinjections of PGE and Tempol were administered in Wistar-Kyoto rats.

View Article and Find Full Text PDF

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).

View Article and Find Full Text PDF

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 PDF

Want 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!