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‘Slow Pressor’ Hypertension From Low‐Dose Chronic Angiotensin II Infusion
Author(s) -
Edgley AJ,
Kett MM,
Anderson WP
Publication year - 2001
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2001.03590.x
Subject(s) - angiotensin ii , medicine , endocrinology , blood pressure , renin–angiotensin system , in vivo , kidney , renal artery , pathophysiology of hypertension , lumen (anatomy) , vascular smooth muscle , smooth muscle , biology , microbiology and biotechnology
SUMMARY 1. Angiotensin (Ang) II causes growth‐related effects on vascular smooth muscle cells in vitro and in vivo . 2. Chronic infusions of AngII systemically, at doses that are initially subpressor, result in slowly progressive increases in arterial pressure (‘slow‐pressor’ hypertension). It has been suggested that the hypertension is due to induced growth in systemic resistance vessel walls by the AngII infusions. 3. We report the results of several studies investigating whether there are also induced structural changes in renal resistance vessels during chronic AngII infusions. We have developed models in Sprague‐Dawley rats in which low‐dose AngII infusions, either into the renal artery (thus restricting the effects to the kidney) or systemically, result in hypertension. 5. In both models, we have evidence suggesting that chronic AngII infusions have resulted in apparent structurally induced reductions in renal vasculature lumen upstream to the glomerulus. 6. The role of these renal changes in the development of the hypertension remain to be determined.