Post-stenotic arterial pressures, renal haemodynamics and sodium excretion during graded pressure reduction in conscious rats with one- and two-kidney coarctation hypertension

Stephen C Textor, L. Smith-Powell

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Abstract

Study of rat models of renovascular hypertension has been limited by the difficulty in measuring the post-stenotic pressures in conscious animals. We studied a model using inter-renal aortic coarctation (0.33 mm clip) in which post-stenotic (iliac) and systemic (carotid) pressures could be measured chronically. One-kidney-coarctation (1K-coarctation) rats (analogous to one-kidney, one clip hypertension) were compared to two-kidney-coarctation (2K-coarctation) and 1K-sham-coarctation groups. After coarctation, post-stenotic pressures fell to 40±4 mmHg then rose to normal over 5 days, concomitantly with a rise in systemic pressure to 141±6 mmHg. 1K-coarctation animals developed consistently higher post-stenotic pressures than 2K-coarctation rats after 6 weeks. Reduction of systemic pressures to normal with sodium nitroprusside induced major decrements in renal function in 1K-coarctation rats [effective renal plasma flow (ERPF): 4.32±0.40 to 1.41±0.28 ml/min; P<0.01; glomerular filtration rate (GFR), 1.56±0.18 to 0.42±0.33 ml/min, P<0.01], but not in 2K-coarctation or 1K-sham-coarctation groups. This produced an abrupt decrease in filtered sodium load, which combined with a decline in fractional sodium excretion during pressure reduction to make 1K-coarctation rats especially sensitive to fluctuations in renal artery pressure. We propose that a marked dependence upon post-stenotic perfusion pressures to maintain sodium homeostasis may be involved in sustaining hypertension in 1K-renovascular models. Inter-renal coarctation provides a valuable model for studying post-stenotic haemodynamic changes in chronically instrumented rats.

Original languageEnglish (US)
Pages (from-to)311-319
Number of pages9
JournalJournal of Hypertension
Volume6
Issue number4
StatePublished - 1988
Externally publishedYes

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Arterial Pressure
Hemodynamics
Sodium
Hypertension
Kidney
Pressure
Surgical Instruments
Effective Renal Plasma Flow
Renovascular Hypertension
Aortic Coarctation
Nitroprusside
Renal Artery
Glomerular Filtration Rate
Homeostasis
Perfusion

ASJC Scopus subject areas

  • Endocrinology
  • Internal Medicine

Cite this

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title = "Post-stenotic arterial pressures, renal haemodynamics and sodium excretion during graded pressure reduction in conscious rats with one- and two-kidney coarctation hypertension",
abstract = "Study of rat models of renovascular hypertension has been limited by the difficulty in measuring the post-stenotic pressures in conscious animals. We studied a model using inter-renal aortic coarctation (0.33 mm clip) in which post-stenotic (iliac) and systemic (carotid) pressures could be measured chronically. One-kidney-coarctation (1K-coarctation) rats (analogous to one-kidney, one clip hypertension) were compared to two-kidney-coarctation (2K-coarctation) and 1K-sham-coarctation groups. After coarctation, post-stenotic pressures fell to 40±4 mmHg then rose to normal over 5 days, concomitantly with a rise in systemic pressure to 141±6 mmHg. 1K-coarctation animals developed consistently higher post-stenotic pressures than 2K-coarctation rats after 6 weeks. Reduction of systemic pressures to normal with sodium nitroprusside induced major decrements in renal function in 1K-coarctation rats [effective renal plasma flow (ERPF): 4.32±0.40 to 1.41±0.28 ml/min; P<0.01; glomerular filtration rate (GFR), 1.56±0.18 to 0.42±0.33 ml/min, P<0.01], but not in 2K-coarctation or 1K-sham-coarctation groups. This produced an abrupt decrease in filtered sodium load, which combined with a decline in fractional sodium excretion during pressure reduction to make 1K-coarctation rats especially sensitive to fluctuations in renal artery pressure. We propose that a marked dependence upon post-stenotic perfusion pressures to maintain sodium homeostasis may be involved in sustaining hypertension in 1K-renovascular models. Inter-renal coarctation provides a valuable model for studying post-stenotic haemodynamic changes in chronically instrumented rats.",
author = "Textor, {Stephen C} and L. Smith-Powell",
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AU - Textor, Stephen C

AU - Smith-Powell, L.

PY - 1988

Y1 - 1988

N2 - Study of rat models of renovascular hypertension has been limited by the difficulty in measuring the post-stenotic pressures in conscious animals. We studied a model using inter-renal aortic coarctation (0.33 mm clip) in which post-stenotic (iliac) and systemic (carotid) pressures could be measured chronically. One-kidney-coarctation (1K-coarctation) rats (analogous to one-kidney, one clip hypertension) were compared to two-kidney-coarctation (2K-coarctation) and 1K-sham-coarctation groups. After coarctation, post-stenotic pressures fell to 40±4 mmHg then rose to normal over 5 days, concomitantly with a rise in systemic pressure to 141±6 mmHg. 1K-coarctation animals developed consistently higher post-stenotic pressures than 2K-coarctation rats after 6 weeks. Reduction of systemic pressures to normal with sodium nitroprusside induced major decrements in renal function in 1K-coarctation rats [effective renal plasma flow (ERPF): 4.32±0.40 to 1.41±0.28 ml/min; P<0.01; glomerular filtration rate (GFR), 1.56±0.18 to 0.42±0.33 ml/min, P<0.01], but not in 2K-coarctation or 1K-sham-coarctation groups. This produced an abrupt decrease in filtered sodium load, which combined with a decline in fractional sodium excretion during pressure reduction to make 1K-coarctation rats especially sensitive to fluctuations in renal artery pressure. We propose that a marked dependence upon post-stenotic perfusion pressures to maintain sodium homeostasis may be involved in sustaining hypertension in 1K-renovascular models. Inter-renal coarctation provides a valuable model for studying post-stenotic haemodynamic changes in chronically instrumented rats.

AB - Study of rat models of renovascular hypertension has been limited by the difficulty in measuring the post-stenotic pressures in conscious animals. We studied a model using inter-renal aortic coarctation (0.33 mm clip) in which post-stenotic (iliac) and systemic (carotid) pressures could be measured chronically. One-kidney-coarctation (1K-coarctation) rats (analogous to one-kidney, one clip hypertension) were compared to two-kidney-coarctation (2K-coarctation) and 1K-sham-coarctation groups. After coarctation, post-stenotic pressures fell to 40±4 mmHg then rose to normal over 5 days, concomitantly with a rise in systemic pressure to 141±6 mmHg. 1K-coarctation animals developed consistently higher post-stenotic pressures than 2K-coarctation rats after 6 weeks. Reduction of systemic pressures to normal with sodium nitroprusside induced major decrements in renal function in 1K-coarctation rats [effective renal plasma flow (ERPF): 4.32±0.40 to 1.41±0.28 ml/min; P<0.01; glomerular filtration rate (GFR), 1.56±0.18 to 0.42±0.33 ml/min, P<0.01], but not in 2K-coarctation or 1K-sham-coarctation groups. This produced an abrupt decrease in filtered sodium load, which combined with a decline in fractional sodium excretion during pressure reduction to make 1K-coarctation rats especially sensitive to fluctuations in renal artery pressure. We propose that a marked dependence upon post-stenotic perfusion pressures to maintain sodium homeostasis may be involved in sustaining hypertension in 1K-renovascular models. Inter-renal coarctation provides a valuable model for studying post-stenotic haemodynamic changes in chronically instrumented rats.

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