title: Effects of uninephrectomy on renal structural properties in spontaneously hypertensive rats.
abstract: 1. To investigate effects of a reduction in nephron numbers on renal structural properties in hypertension, either unilateral nephrectomy (UNX) or sham operation (SO) was performed at 5 weeks of age in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats (n = 9 for each operation for each strain). 2. At 10-12 weeks of age, flow-pressure (F-P) and pressure-glomerular filtration rate (P-GFR) relationships were determined for maximally vasodilated, perfused kidneys. Kidneys were then perfusion fixed for histological analysis. 3. In the SO groups, the slope of F-P (minimal renal vascular resistance, reflecting overall luminal dimensions of pre- and post-glomerular vasculature) was greater in SHR than in WKY rats. The threshold pressure for beginning filtration at P-GFR (preglomerular to post-glomerular vascular resistance ratio) was higher in SHR than in WKY rats, but the slope of P-GFR (glomerular filtration capacity) did not differ between the two strains. These results suggest that vascular narrowing occurred, especially in the preglomerular resistance vessels in the kidneys of SHR, although glomerular filtration capacity was normal. 4. In UNX animals, the following results were obtained: (i) the slope of F-P was not affected in either strain; (ii) the pressure for beginning filtration at P-GFR was unchanged in WKY rats, but was decreased in SHR; (iii) the slope of P-GFR increased in WKY rats, but a compensatory adaptive increase was missing in SHR; and (iv) histologically, small increases in the luminal cross-sectional area of interlobular arteries and glomerular tuft area were observed in both strains. However, the increase in vascular lumen was more pronounced in SHR, whereas glomerular enlargement was greater in WKY rats. 5. These results suggested that UNX attenuates vascular narrowing of the preglomerular resistance vessels and glomerular structural adaptations to UNX (i.e. increased filtering capacity and glomerular enlargement) are impaired in SHR.
authors.affiliation: Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan.
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kinuno
authors.forename: Fumihiro
authors.initials: F
authors.lastname: Tomoda
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Koike
authors.forename: Masanobu
authors.initials: M
authors.lastname: Takata
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Inoue
mesh_terms: D000818:Animals; D001794:Blood Pressure; D003404:Creatinine / Q000652:urine; D005919:Glomerular Filtration Rate; D006973:Hypertension / Q000473:pathology* / Q000503:physiopathology; D066298:In Vitro Techniques; D007668:Kidney / Q000098:blood supply / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009392:Nephrectomy; D009929:Organ Size; D011507:Proteinuria / Q000652:urine; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012079:Renal Circulation; D014655:Vascular Resistance; D014664:Vasodilation
chemical_list: D003404:Creatinine