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Reduced Reactivity of Renal Microvessels to Pressure and Angiotensin II in Fawn-Hooded Rats

 

作者: William,   van Rodijnen Ton,   van Lambalgen Geert-Jan,   Tangelder Richard,   van Dokkum Abraham,   Provoost Piet,  

 

期刊: Hypertension: Journal of The American Heart Association  (OVID Available online 2002)
卷期: Volume 39, issue 1  

页码: 111-115

 

ISSN:0194-911X

 

年代: 2002

 

出版商: OVID

 

关键词: rats, Fawn-hooded;hydronephrosis;renal circulation;pressure;angiotensin II;vasoconstriction

 

数据来源: OVID

 

摘要:

Fawn-Hooded rats possess an increased risk to develop glomerular damage. Both an impaired control of preglomerular resistance and an elevated postglomerular resistance have been implicated. In the present study, we directly assessed the myogenic reactivity of distal interlobular arteries and afferent arterioles from hypertensive and normotensive Fawn-Hooded rats compared with Sprague-Dawley and Wistar rats, which are known to be resistant for developing renal disease. Pressure-response curves were made in isolated perfused hydronephrotic kidneys from these rats. In addition, increasing concentrations of angiotensin II were added to the perfusate to determine the reactivity of interlobular arteries, afferent arterioles, and efferent arterioles to this peptide. Preglomerular vessels from hypertensive and normotensive Fawn-Hooded rats exhibited an impaired reactivity to both pressure and angiotensin II compared with that of Sprague-Dawley and Wistar rats. Basal efferent arteriolar diameters were similar among the 4 strains of rat. In addition, efferent arterioles from hypertensive and normotensive Fawn-Hooded rats displayed a reduced sensitivity to angiotensin II. Our observations demonstrate that in Fawn-Hooded rats, 2 components of preglomerular resistance control are impaired: the myogenic and the angiotensin II response. In addition, efferent arteriolar reactivity to angiotensin II is not elevated but lowered in these rats. Therefore, a deficit in preglomerular resistance control is the most important intrinsic factor involved in the increased susceptibility of Fawn-hooded rats to develop renal disease.

 

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