Single-nephron pressures, flows, and resistances in hypertensive kidneys with nephrosclerosis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1977-07

AUTHORS

Silvia Azar, Mary Ann Johnson, Bruce Hertel, Louis Tobian

ABSTRACT

Single-nephron pressures, flows, and resistances in hypertensive kidneys with nephrosclerosis. To study the effects of hypertension on a kidney with nephrosclerosis, single-nephron dynamics were determined in rats with one kidney "post-salt" hypertension with nephrosclerosis and in one and two kidney normotensive controls. Hypertension was induced by feeding weanling rats an 8% sodium chloride diet for nine and one half weeks, with a unilateral nephrectomy performed during the fourth week. Thereafter, regular chow was fed, but hypertension persisted. In the rats with hypertension, extensive nephrosclerosis was found, glomerular lesions predominating over arteriolar ones. The sum of afferent and efferent arteriolar resistances (RTA) ( 1010 dynesseccm-5) was decreased in surviving nephrons from hypertensive kidneys with nephrosclerosis and not increased as expected in hypertension. Hypertensive RTA averaged 1.07 0.08, while one and two kidney normotensive rats averaged 1.72 0.13 and 2.77 0.33, respectively. Because resistances were decreased, hypertensive rats had significantly higher glomerular blood flow (GBF) (1324 82 nl/min), and filtration rate (SNGFR) (162 13 nl/min), than the one-kidney normotensive rats: GBF, 583 41; SNGFR, 90 5. Two-kidney normotensive rats were even lower: GBF, 357 55; SNGFR, 60 6. Filtration fraction declined from 0.35 0.03 in two-kidney normotensive rats to 0.25 0.01 in hypertensive rats. The adaptive increase of SNGFR in uninephrectomized normotensive rats results mainly from increased GBF, plus a small increase in transcapillary hydraulic pressure difference (P); in rats having hypertension with nephrosclerosis, a very high P combines with increased flow to increase SNGFR greatly. Reduction of afferent and efferent arteriolar resistances is pivotal in the adaptive response. Greatly increased glomerular capillary pressure may be the pathophysiologic basis for the predominance of glomerular lesions in this model for hypertension. More... »

PAGES

28-40

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ki.1977.76

DOI

http://dx.doi.org/10.1038/ki.1977.76

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1048455888

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/894914


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50 schema:description Single-nephron pressures, flows, and resistances in hypertensive kidneys with nephrosclerosis. To study the effects of hypertension on a kidney with nephrosclerosis, single-nephron dynamics were determined in rats with one kidney "post-salt" hypertension with nephrosclerosis and in one and two kidney normotensive controls. Hypertension was induced by feeding weanling rats an 8% sodium chloride diet for nine and one half weeks, with a unilateral nephrectomy performed during the fourth week. Thereafter, regular chow was fed, but hypertension persisted. In the rats with hypertension, extensive nephrosclerosis was found, glomerular lesions predominating over arteriolar ones. The sum of afferent and efferent arteriolar resistances (RTA) ( 1010 dynesseccm-5) was decreased in surviving nephrons from hypertensive kidneys with nephrosclerosis and not increased as expected in hypertension. Hypertensive RTA averaged 1.07 0.08, while one and two kidney normotensive rats averaged 1.72 0.13 and 2.77 0.33, respectively. Because resistances were decreased, hypertensive rats had significantly higher glomerular blood flow (GBF) (1324 82 nl/min), and filtration rate (SNGFR) (162 13 nl/min), than the one-kidney normotensive rats: GBF, 583 41; SNGFR, 90 5. Two-kidney normotensive rats were even lower: GBF, 357 55; SNGFR, 60 6. Filtration fraction declined from 0.35 0.03 in two-kidney normotensive rats to 0.25 0.01 in hypertensive rats. The adaptive increase of SNGFR in uninephrectomized normotensive rats results mainly from increased GBF, plus a small increase in transcapillary hydraulic pressure difference (P); in rats having hypertension with nephrosclerosis, a very high P combines with increased flow to increase SNGFR greatly. Reduction of afferent and efferent arteriolar resistances is pivotal in the adaptive response. Greatly increased glomerular capillary pressure may be the pathophysiologic basis for the predominance of glomerular lesions in this model for hypertension.
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