Literature DB >> 3670111

The effect of hypertension on glomerular structures and capillary permeability in passive Heymann glomerulonephritis.

B M Iversen1, J Ofstad.   

Abstract

In glomerulonephritic and normal kidneys hypertension has been shown to increase the urinary protein excretion and the thickness of the glomerular basement membrane and to reduce the glomerular filtration rate. We have studied the effect of desoxycorticosterone acetate (DOCA)-salt hypertension on the glomerular anatomy and function in normal control rats and rats with passive Heymann nephritis. Standard methods for measurements of glomerular filtration rate and urinary protein excretion were used and the results were correlated to morphometrical measurements in randomly selected glomeruli in all groups. In control rats, DOCA-salt hypertension increased the kidney weight (P less than 0.001), the glomerular volume (P less than 0.05), and the surface of peripheral glomerular basement membrane (P less than 0.01). The thickness of peripheral glomerular basement membrane and the length of glomerulary capillaries were not affected. In glomerulonephritic rats, DOCA-salt hypertension did not change the kidney weight and glomerular capillary diameter. The thickness of the peripheral basement membrane increased (P less than 0.05), while the length of glomerular capillaries and the surface of peripheral basement membrane were reduced (P less than 0.05). Glomerular filtration rate per unit peripheral basement membrane was not significantly different among the groups while protein excretion per unit peripheral basement membrane increased significantly both in the hypertensive and in the glomerulonephritic groups. The estimated hydraulic conductivity of the glomerular capillaries was reduced both in rats with DOCA-salt hypertension and glomerulonephritic rats with and without DOCA-salt hypertension. In conclusion, DOCA-salt hypertension seems to decrease hydraulic conductivity and increase protein excretion both in normal and in glomerulonephritic kidneys although the effect on glomerular morphology is different.

Entities:  

Mesh:

Substances:

Year:  1987        PMID: 3670111     DOI: 10.1016/0026-2862(87)90049-5

Source DB:  PubMed          Journal:  Microvasc Res        ISSN: 0026-2862            Impact factor:   3.514


  4 in total

1.  Mechanical and structural changes in human thoracic aortas with age.

Authors:  Majid Jadidi; Mahmoud Habibnezhad; Eric Anttila; Kaspars Maleckis; Anastasia Desyatova; Jason MacTaggart; Alexey Kamenskiy
Journal:  Acta Biomater       Date:  2019-12-23       Impact factor: 8.947

2.  Activation of the Cholinergic Anti-inflammatory Pathway Attenuated Angiotension II-Dependent Hypertension and Renal Injury.

Authors:  Shu-Jie Wu; Zhe-Wei Shi; Xue Wang; Fang-Fang Ren; Zuo-Yi Xie; Li Lei; Peng Chen
Journal:  Front Pharmacol       Date:  2021-03-17       Impact factor: 5.810

3.  Podocyte damage is a critical step in the development of glomerulosclerosis in the uninephrectomised-desoxycorticosterone hypertensive rat.

Authors:  M Kretzler; I Koeppen-Hagemann; W Kriz
Journal:  Virchows Arch       Date:  1994       Impact factor: 4.064

4.  Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis.

Authors:  Qiulun Lu; Zejun Ma; Ye Ding; Tatiana Bedarida; Liming Chen; Zhonglin Xie; Ping Song; Ming-Hui Zou
Journal:  Nat Commun       Date:  2019-05-13       Impact factor: 14.919

  4 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.