Objective: A reduced number of nephrons, whether acquired or congenital, as has been observed in certain inbred rat strains, may lead to systemic hypertension. The present study estimated the total number of glomeruli and mean glomerular size in kidneys of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats.

Methods: Unbiased stereological methods were used on immersion-fixed kidneys from 12-week-old male SHR (n = 9) and age-matched WKY rats (n = 11).

Results: The total number of glomeruli was significantly reduced in the SHR compared with in the WKY rats. Sclerotic glomeruli were not found in either group. No significant difference in mean glomerular volume was observed, but the total glomerular volume was reduced by 25% in the SHR compared with in the WKY rats.

Conclusion: SHR have fewer glomeruli than WKY rats, but of similar size, resulting in a reduced total glomerular volume in adult SHR. These findings are consistent with the hypothesis that the kidney plays an important role in the pathogenesis of genetic hypertension.

Download full-text PDF

Source

Publication Analysis

Top Keywords

wky rats
12
glomerular volume
12
spontaneously hypertensive
8
hypertensive rats
8
total number
8
number glomeruli
8
shr compared
8
compared wky
8
total glomerular
8
shr
6

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!