High salt intake potentiates the renal vascular and glomerular damage caused by low doses of angiotensin II in uni-nephrectomized rats-Reference-Cited by-同舟云学术

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High salt intake potentiates the renal vascular and glomerular damage caused by low doses of angiotensin II in uni-nephrectomized rats

Published:1999-07 Issue:7 Volume:17 Page:923-932
ISSN:0263-6352
Container-title:Journal of Hypertension
language:en
Short-container-title:Journal of Hypertension

Author:

Hirawa Nobuhito,Uehara Yoshio,Kawabata Yukari,Numabe Atsushi,Ogawa Nariaki,Gomi Tomoko,lkeda Toshio,Goto Atsuo,Toyó-oka Teruhiko,Omata Masao

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology,Internal Medicine

Reference30 articles.

1. Role of Genetic Factors in Susceptibility to Experimental Hypertension due to Chronic Excess Salt Ingestion

2. Mechanistic analysis of renal protection by angiotensin converting enzyme inhibitor in Dahl salt-sensitive rats

3. Long-term infusion of kallikrein attenuates renal injury in Dahl salt-sensitive rats.

4. Synergistic Effect of Angiotensin II and a High Sodium Diet on the Vascular Glycosaminoglycan Synthesis of Rats

5. Subpressor dose of angiotensin II increases susceptibility to the haemodynamic injury of blood pressure in Dahl salt-sensitive rats

Cited by 10 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. Impaired response of regulator of Gαq signaling-2 mRNA to angiotensin II and hypertensive renal injury in Dahl salt-sensitive rats;Hypertension Research;2015-11-26

2. Aldosterone Blockade in Chronic Kidney Disease;Seminars in Nephrology;2014-05

3. Salt and Multiorgan Damage in Hypertension: Vascular Stiffening and Cardiorenal Structural Dysfunction Responses;Blood Pressure and Arterial Wall Mechanics in Cardiovascular Diseases;2014

4. Angiotensin II- and Salt-Induced Kidney Injury through Rac1-Mediated Mineralocorticoid Receptor Activation;Journal of the American Society of Nephrology;2012-03-22

5. Salt loading produces severe renal hemodynamic dysfunction independent of arterial pressure in spontaneously hypertensive rats;American Journal of Physiology-Heart and Circulatory Physiology;2007-02

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