Pre-glomerular structural changes in the renal vasculature in hypertension.

W. P. Anderson, M. M. Kett, R. G. Evans, D. Alcorn

Research output: Contribution to journalReview ArticleResearchpeer-review

Abstract

This paper reviews the evidence for the occurrence of hypertrophy of the renal arterial vessels in experimental and human hypertension. In spontaneously hypertensive rats (SHR), the walls of the interlobar, arcuate and interlobular arteries appear to be hypertrophied in both the "pre-hypertensive phase" and in established hypertension. The lumen diameter of the afferent arteriole in SHR is reduced, but this is probably not due to wall hypertrophy. The renal arterial hypertrophy is not reversed by chronic angiotensin converting enzyme inhibition in SHR, in contrast to findings in other vascular beds. Renal arterial hypertrophy also occurs in other forms of hypertension including in the kidney contralateral to a renal artery stenosis, and in hypertension following sino-aortic denervation. Whilst it is not possible to document changes in wall dimensions of intrarenal arteries during the development of human hypertension, renal haemodynamic abnormalities currently attributed to renal vasoconstriction in early human hypertension are also compatible with renal arterial hypertrophy. These abnormalities include increased resting renal vascular resistance and augmented renal vascular resistance responses to vasoconstrictor agents. It is argued that hypertrophy of renal vasculature to increase pre-glomerular resistance will have dual effects: it will increase total peripheral resistance (the kidneys account for about 20% of total peripheral resistance), and it will effect renal haemodynamics distally in a manner similar to narrowing of the main renal artery. It remains to be shown experimentally whether renal arterial hypertrophy could be the primary cause of some forms of hypertension.

Original languageEnglish
Pages (from-to)74-80
Number of pages7
JournalBlood pressure. Supplement
Volume2
Publication statusPublished - 1995
Externally publishedYes

Cite this

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title = "Pre-glomerular structural changes in the renal vasculature in hypertension.",
abstract = "This paper reviews the evidence for the occurrence of hypertrophy of the renal arterial vessels in experimental and human hypertension. In spontaneously hypertensive rats (SHR), the walls of the interlobar, arcuate and interlobular arteries appear to be hypertrophied in both the {"}pre-hypertensive phase{"} and in established hypertension. The lumen diameter of the afferent arteriole in SHR is reduced, but this is probably not due to wall hypertrophy. The renal arterial hypertrophy is not reversed by chronic angiotensin converting enzyme inhibition in SHR, in contrast to findings in other vascular beds. Renal arterial hypertrophy also occurs in other forms of hypertension including in the kidney contralateral to a renal artery stenosis, and in hypertension following sino-aortic denervation. Whilst it is not possible to document changes in wall dimensions of intrarenal arteries during the development of human hypertension, renal haemodynamic abnormalities currently attributed to renal vasoconstriction in early human hypertension are also compatible with renal arterial hypertrophy. These abnormalities include increased resting renal vascular resistance and augmented renal vascular resistance responses to vasoconstrictor agents. It is argued that hypertrophy of renal vasculature to increase pre-glomerular resistance will have dual effects: it will increase total peripheral resistance (the kidneys account for about 20{\%} of total peripheral resistance), and it will effect renal haemodynamics distally in a manner similar to narrowing of the main renal artery. It remains to be shown experimentally whether renal arterial hypertrophy could be the primary cause of some forms of hypertension.",
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year = "1995",
language = "English",
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journal = "Blood pressure. Supplement",
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Pre-glomerular structural changes in the renal vasculature in hypertension. / Anderson, W. P.; Kett, M. M.; Evans, R. G.; Alcorn, D.

In: Blood pressure. Supplement, Vol. 2, 1995, p. 74-80.

Research output: Contribution to journalReview ArticleResearchpeer-review

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AU - Anderson, W. P.

AU - Kett, M. M.

AU - Evans, R. G.

AU - Alcorn, D.

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N2 - This paper reviews the evidence for the occurrence of hypertrophy of the renal arterial vessels in experimental and human hypertension. In spontaneously hypertensive rats (SHR), the walls of the interlobar, arcuate and interlobular arteries appear to be hypertrophied in both the "pre-hypertensive phase" and in established hypertension. The lumen diameter of the afferent arteriole in SHR is reduced, but this is probably not due to wall hypertrophy. The renal arterial hypertrophy is not reversed by chronic angiotensin converting enzyme inhibition in SHR, in contrast to findings in other vascular beds. Renal arterial hypertrophy also occurs in other forms of hypertension including in the kidney contralateral to a renal artery stenosis, and in hypertension following sino-aortic denervation. Whilst it is not possible to document changes in wall dimensions of intrarenal arteries during the development of human hypertension, renal haemodynamic abnormalities currently attributed to renal vasoconstriction in early human hypertension are also compatible with renal arterial hypertrophy. These abnormalities include increased resting renal vascular resistance and augmented renal vascular resistance responses to vasoconstrictor agents. It is argued that hypertrophy of renal vasculature to increase pre-glomerular resistance will have dual effects: it will increase total peripheral resistance (the kidneys account for about 20% of total peripheral resistance), and it will effect renal haemodynamics distally in a manner similar to narrowing of the main renal artery. It remains to be shown experimentally whether renal arterial hypertrophy could be the primary cause of some forms of hypertension.

AB - This paper reviews the evidence for the occurrence of hypertrophy of the renal arterial vessels in experimental and human hypertension. In spontaneously hypertensive rats (SHR), the walls of the interlobar, arcuate and interlobular arteries appear to be hypertrophied in both the "pre-hypertensive phase" and in established hypertension. The lumen diameter of the afferent arteriole in SHR is reduced, but this is probably not due to wall hypertrophy. The renal arterial hypertrophy is not reversed by chronic angiotensin converting enzyme inhibition in SHR, in contrast to findings in other vascular beds. Renal arterial hypertrophy also occurs in other forms of hypertension including in the kidney contralateral to a renal artery stenosis, and in hypertension following sino-aortic denervation. Whilst it is not possible to document changes in wall dimensions of intrarenal arteries during the development of human hypertension, renal haemodynamic abnormalities currently attributed to renal vasoconstriction in early human hypertension are also compatible with renal arterial hypertrophy. These abnormalities include increased resting renal vascular resistance and augmented renal vascular resistance responses to vasoconstrictor agents. It is argued that hypertrophy of renal vasculature to increase pre-glomerular resistance will have dual effects: it will increase total peripheral resistance (the kidneys account for about 20% of total peripheral resistance), and it will effect renal haemodynamics distally in a manner similar to narrowing of the main renal artery. It remains to be shown experimentally whether renal arterial hypertrophy could be the primary cause of some forms of hypertension.

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