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Hydronephrosis causes salt-sensitive hypertension and impaired renal concentrating ability in mice
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi.
Vise andre og tillknytning
2007 (engelsk)Inngår i: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 189, nr 3, s. 293-301Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Aim: Hypertension is a common disease in the industrialized world and approximately 5% of all cases are secondary to kidney malfunction. We have recently shown that hydronephrosis due to partial unilateral ureteral obstruction (PUUO) causes salt-sensitive hypertension in rats. The mechanisms are still unclear, but appear to be intrarenal and primarily located to the diseased kidney. In the present study, we have developed a model for PUUO to study if hydronephrotic mice develop salt-sensitive hypertension.

Methods: PUUO was created in 3-week-old mice (C57bl/6J). Blood pressure and heart rate were measured telemetrically in adult animals on normal and high salt diets. Metabolism cages were used to study the renal excretion of electrolytes and water. Plasma samples for renin analysis were collected and renal histological changes were evaluated.

Results: All hydronephrotic animals developed salt-sensitive hypertension that correlated to the degree of hydronephrosis. In hydronephrotic animals, blood pressure increased from 114 ± 1 mmHg on normal salt diet to 120 ± 2 mmHg on high salt diet, compared with 103 ± 1 to 104 ± 1 in controls. Hydronephrotic animals showed increased diuresis and reduced ability to regulate electrolyte concentration. No differences in plasma renin concentration were found between the groups. The parenchymal weight and glomerular area of contralateral kidneys were significantly increased in the hydronephrotic animals. Histopathology of the hydronephrotic kidneys displayed areas with fibrosis, inflammation and glomerular changes.

Conclusion: This study provides a model for PUUO in mice and demonstrates the presence of salt-sensitive hypertension and an impaired renal concentrating ability in mice which has not been described before.

sted, utgiver, år, opplag, sider
2007. Vol. 189, nr 3, s. 293-301
Emneord [en]
hydronephrosis, hypertension, nitric oxide, oxidative stress, partial ureteral obstruction, renin, salt sensitivity, telemetry
HSV kategori
Identifikatorer
URN: urn:nbn:se:uu:diva-96933DOI: 10.1111/j.1748-1716.2006.01637.xISI: 000244226300008PubMedID: 17305709OAI: oai:DiVA.org:uu-96933DiVA, id: diva2:171672
Tilgjengelig fra: 2008-03-28 Laget: 2008-03-28 Sist oppdatert: 2017-12-14bibliografisk kontrollert
Inngår i avhandling
1. Development of Salt-Sensitive Hypertension in Hydronephrosis
Åpne denne publikasjonen i ny fane eller vindu >>Development of Salt-Sensitive Hypertension in Hydronephrosis
2008 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Hydronephrosis, due to ureteropelvic junction obstruction, is a common condition in infants with an incidence of approximately 0.5-1%. During the last decade, the surgical management of non-symptomatic hydronephrosis has become more conservative, and the long-term physiological consequences of this new policy are unclear. The overall aim of this thesis was to determine whether there is a link between hydronephrosis and the development of hypertension. Hydronephrosis was induced by partial ureteral obstruction in 3-week old rats or mice. In the adult animals, blood pressure was measured telemetrically during different sodium conditions and the renal function was evaluated. Both species developed salt-sensitive hypertension and histopathological changes (i.e. fibrosis, inflammation, glomerular and tubular changes) that correlated with the degree of hydronephrosis. An abnormal renal excretion pattern with increased diuresis and impaired urine concentrating ability was observed in hydronephrosis. The mechanisms were primarily located to the diseased kidney, as relief of the obstruction attenuated blood pressure and salt-sensitivity. Increased renin angiotensin system activity, due to ureteral obstruction, might be involved in the development but not necessary the maintenance of hypertension. Hydronephrotic animals displayed reduced nitric oxide availability, which might be due to increased oxidative stress in the diseased kidney. Renal nitric oxide deficiency and subsequent resetting of the tubuloglomerular feedback mechanism, appeared to have an important role in the development of hypertension. In conclusion, experimental hydronephrosis, induced by partial ureteral obstruction, provides a new model for studies of salt-sensitive hypertension. Furthermore, the new findings imply that the current conservative treatment strategy in hydronephrosis should be reconsidered in favour of treatment that is more active, in order to prevent the development of renal injury and hypertension in later life.

sted, utgiver, år, opplag, sider
Uppsala: Acta Universitatis Upsaliensis, 2008. s. 77
Serie
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 324
Emneord
Physiology, blood pressure, nephrectomy, nitric oxide, oxidative stress, renal function, renin angiotensin system, salt-sensitivity, telemetry, tubuloglomerular feedback, ureteral obstruction, Fysiologi
Identifikatorer
urn:nbn:se:uu:diva-8586 (URN)978-91-554-7137-8 (ISBN)
Disputas
2008-04-18, BMC / B21, Uppsala Biomedical Center, Husargatan 3, Uppsala, 13:00
Opponent
Veileder
Tilgjengelig fra: 2008-03-28 Laget: 2008-03-28bibliografisk kontrollert

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