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Proceedings of the Symposium ‘Angiotensin AT 1 Receptors: From Molecular Physiology to Therapeutics’: STRUCTURAL CHANGES IN THE RENAL VASCULATURE IN THE SPONTANEOUSLY HYPERTENSIVE RAT: NO EFFECT OF ANGIOTENSIN II BLOCKADE
Author(s) -
Kett Michelle M,
Anderson Warwick P,
Bertram John F,
Alcorn Daine
Publication year - 1996
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 - 10.1111/j.1440-1681.1996.tb03074.x
Subject(s) - medicine , angiotensin ii , endocrinology , muscle hypertrophy , angiotensin ii receptor type 1 , blood pressure , glomerulus , renal artery , renin–angiotensin system , pathophysiology of hypertension , kidney , spontaneously hypertensive rat
SUMMARY1 There is strong evidence for a renal basis to the development of hypertension in the spontaneously hypertensive rat (SHR). Alterations of the SHR renal vasculature, including the glomerulus, may be involved in the initiation and maintenance of hypertension in this animal model. 2 The arterial walls of pre‐glomerular vessels of the SHR are hypertrophied compared with WKY vessels. Unlike other vascular beds in the SHR, this hypertrophy is independent of angiotensin II (AngII). 3 Glomerular number and volume are similar between SHR and the normotensive Wistar‐Kyoto (WKY) rats. These results provide no support for the theory that a reduced filtration surface area within the kidneys of the SHR contributes to the elevated blood pressure in these animals. 4 Intrarenal hypertrophy may have similar haemodynamic consequences to clipping of the main renal artery, as in Goldblatt hypertension. Further analysis of the role of pre‐glomerular arterial hypertrophy is warranted to determine its involvement in the initiation and maintenance of hypertension in the SHR.