Publications by authors named "Daine Alcorn"

3 Publications

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Notice of retraction of article.

Clin Exp Pharmacol Physiol 2004 Sep;31(9):657-8

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http://dx.doi.org/10.1111/j.1440-1681.2004.04047.xDOI Listing
September 2004

Changes in mean arterial pressure predict degranulation of renomedullary interstitial cells.

Clin Exp Pharmacol Physiol 2002 Dec;29(12):1055-9

Departments of Anatomy, University of Melbourne, Parkville, Victoria, Australia.

1. Renomedullary interstitial cells (RMIC) are characterized by numerous intracellular granules thought to contain renal medullary antihypertensive substances. However, the nature of the trigger for RMIC degranulation remains to be elucidated. The present study examines the effects of acute alterations in mean arterial pressure (MAP) and medullary blood flow (MBF) on RMIC granulation. 2. Basal MAP and MBF in anaesthetized Sprague-Dawley rats (n = 4/group) were altered by intravenous infusions of vasoactive agents, including angiotensin II alone or with a nitric oxide (NO) synthase inhibitor (N-omega-nitro-l-arginine) or NO donor (sodium nitroprusside), noradrenaline and by carotid artery clamping. Following these treatments, kidneys were examined by electron microscopy and the absolute volume of granules in the renal medulla was calculated using unbiased stereological methods. 3. Acute increases in MAP, regardless of the treatment causing the increase, were associated with a reduction in the absolute volume of granules in the range of 42-67%. Regression analysis revealed that only increases in MAP, but not MBF, strongly predict RMIC degranulation. 4. Despite previous reports that changes in MBF activate renomedullary antihypertensive activity, we conclude that the change in MAP is an important determinant of the activity of the blood pressure-lowering mechanism of the renal medulla, with the assumption that the medullary lipids mediate the antihypertensive property of the renal medulla.
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http://dx.doi.org/10.1046/j.1440-1681.2002.03780.xDOI Listing
December 2002

Prevention of diabetes-induced albuminuria in transgenic rats overexpressing human aldose reductase.

Endocrine 2002 Jun;18(1):47-56

University of Melbourne Department of Medicine, Royal Melbourne Hospital, Parkville, VIC, Australia.

Studies using pharmacologic inhibitors have implicated the enzyme aldose reductase in the pathogenesis of albuminuria and diabetic renal disease. However, a clear conclusion is not easily drawn from such studies since these pharmacologic inhibitors have nonspecific properties. To examine further the role of aldose reductase, we have overexpressed the human enzyme in a transgenic rat model. Transgene expression in the kidney was predominantly localized to the outer stripe of the outer medulla, compatible with the histotopography of the straight (S3) proximal tubule. The effect of enzyme overexpression on diabetes-induced renal function and structure was then investigated. Contrary to what may have been anticipated from the previous enzyme inhibition studies, diabetes-induced albuminuria was completely prevented by the overexpression of aldose reductase. No effect of overexpression of aldose reductase on renal structure nor on urinary excretion of beta2-microglobulin and N-acetyl-beta-D-glucosaminidase was observed in this transgenic rat model. In conclusion, our study strongly suggests that multiple roles for aldose reductase may give it a more complex place in diabetic nephropathy than is currently recognized.
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http://dx.doi.org/10.1385/ENDO:18:1:47DOI Listing
June 2002