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      Renal Hemodynamics during Development of Hypertension in Young Spontaneously Hypertensive Rats

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          Background/Aims: Cross-transplantation studies between animals with genetic hypertension and normotensive animals indicate a key role of the kidney in development of hypertension, and studies in young spontaneously hypertensive rats (SHR) have shown reduced glomerular filtration rate (GFR) and renal blood flow (RBF) for a short period at the age of 4–6 weeks during blood pressure increase. We tested the hypothesis that a decline in GFR during development of hypertension in SHR might be more pronounced in juxtamedullary cortex than other cortical zones. Methods: By use of the aprotinin method, total and zonal cortical GFR was measured in anaesthetized Wistar-Kyoto (WKY) rats and SHR at the ages of 2, 4, 6, 8 and 10 weeks. RBF was measured by a transit time flowmeter. Results: Body and kidney weights in SHR and WKY were not significantly different in any age group (p >0.05). Mean arterial blood pressure (MAP) was not different at the age of 2 weeks (79 ± 6 mm Hg in SHR and 74 ± 5 mm Hg in WKY, p > 0.05), but was significantly higher in 4-week-old SHR (104 ± 1 mm Hg) compared to 4-week-old WKY (77 ± 3 mm Hg) (p < 0.01). The difference in blood pressure increased with age from 4 to 10 weeks. RBF, total GFR, and outer, middle, and inner cortical GFR increased with age but were not different in SHR and WKY in any age group (p >0.05). Renal vascular resistance was increased from 4 weeks of age in SHR (21.5 ± 1.8), significantly higher than WKY (14.4 ± 0.9 mm Hg·ml<sup>–1</sup>·min·g) (p < 0.01) and stayed at higher values in older age groups (p ≤ 0.01). Conclusion: RBF, total and zonal GFR are not significantly different in anaesthetized SHR compared to WKY at ages from 2 to 10 weeks and GFR in juxtamedullary cortex is not decreased in SHR during onset of hypertension. The results from the present study indicate that development of hypertension cannot be explained by a temporary decline in RBF or total or zonal GFR.

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          Renal Hemodynamics in Young and Old Spontaneously Hypertensive Rats during Intrarenal Infusion of Arginine Vasopressin

          Background/Aims: To gain insight into the effect of arginine vasopressin (AVP) on renal hemodynamics in hypertensive rats, we investigated the vasoconstrictive response to AVP on total renal blood flow (RBF) and total and zonal glomerular filtration rate (GFR) in young and old spontaneously hypertensive rats (SHR). A hypothesis of increased AVP sensitivity in the juxtamedullary cortex of SHR was tested. Methods: Total RBF and total and zonal GFR were studied in 10- and 40-week-old SHR and normotensive Wistar-Kyoto rats (WKY). RBF was recorded by a flowmeter before infusion of AVP and immediately after injection of a bolus dose of 10 ng AVP. Whole kidney GFR and its intracortical distribution was measured by the tubular uptake of 125 I- and 131 I-labelled aprotinin before and during a continuous infusion of AVP 5 ng/min. Ligand binding measurements of preglomerular V 1a receptors were performed in young and old rats. Results: RBF decreased by 43 ± 3% in 10-week SHR (9.2 ± 0.5 vs. 5.2 ± 0.3 ml·min –1 ·g –1 ), significantly more than 10-week WKY where RBF decreased by 35 ± 3% (9.6 ± 0.7 vs. 6.5 ± 0.5 ml·min –1 ·g –1 ) (p 0.05). GFR decreased by 6 ± 3% (1.03 ± 0.04 vs. 0.96 ± 0.04 ml·min –1 ·g –1 , p –1 ·g –1 , p > 0.10). GFR decreased by 11 ± 10% in 40-week SHR and by 4 ± 4% in 40-week WKY (p > 0.05). AVP infusion significantly increased filtration fraction in all groups except 40-week SHR, indicating that AVP has the strongest vasoconstrictive effect on postglomerular vessels. The intrarenal distribution of GFR was unchanged in the normotensive and hypertensive groups. V 1a receptor density was upregulated in young SHR compared to young WKY (p 1a receptors.

            Author and article information

            Kidney Blood Press Res
            Kidney and Blood Pressure Research
            S. Karger AG
            28 November 2002
            : 25
            : 5
            : 322-328
            aRenal Research Group, Institute of Medicine, and bDepartment of Physiology, University of Bergen, Norway
            66792 Kidney Blood Press Res 2002;25:322–328
            © 2002 S. Karger AG, Basel

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            Figures: 6, Tables: 1, References: 39, Pages: 7
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