Renal interstitial hydrostatic pressure and natriuretic response to high doses of angiotensin II in pregnant rats

Tianzheng Yu, Ali A. Khraibi

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background: Administration of high doses of angiotensin II (Ang II) results in natriuretic and diuretic responses that are mediated by increases in renal perfusion pressure (RPP). Elevations in renal interstitial hydrostatic pressure (RIHP) caused by increases in mean arterial pressure (MAP) or RPP are associated with significant increases in urinary sodium excretion (UNaV) and urine flow rate (V). In pregnant rats the renin-angiotensin system (RAS) is activated and basal RIHP is reduced. The exact relationship among MAP, RIHP, UNaV, and V in response to a high pressor dose of Ang II during normal pregnancy is not known. Methods: The objective of this study was to evaluate the relationship between MAP and RIHP, and determine the role of RIHP in the natriuretic and diuretic responses to administration of high dose of Ang II in midterm pregnant (MP) and nonpregnant (NP) Sprague-Dawley (SD) rats. Results: Intravenous infusion of Ang II (200 ng/kg/min) significantly increased MAP (ΔMAP), ΔUNaV, and ΔV in anesthetized MP and NP rats. The ΔMAP, ΔUNaV, and ΔV were 12 ± 2 mm Hg, 27.9 ± 2.7 μEq/min, and 197 ± 23 μL/min for MP rats and were similar (15 ± 3 mm Hg, 34.1 ± 4.3 μEq/min, and 242 ± 34 μL/min, respectively) for NP rats. The RIHP decreased significantly (P < .05) with Ang II infusion in NP (from 6.1 ± 0.2 to 3.9 ± 0.4 mm Hg) but not in MP (from 3.3 ± 0.3 to 4.1 ± 0.4 mm Hg) groups of rats. Acute renal decapsulation eliminated the change in RIHP mediated by high doses of Ang II infusion in the NP group, but did not affect MAP or the natriuretic and diuretic responses to Ang II in either the MP or NP groups of rats. Conclusions: The natriuretic and diuretic responses to high doses of Ang II are not mediated by changes in RIHP in pregnant or nonpregnant rats.

Original languageEnglish (US)
Pages (from-to)300-305
Number of pages6
JournalAmerican journal of hypertension
Volume19
Issue number3
DOIs
StatePublished - Mar 1 2006

Fingerprint

Hydrostatic Pressure
Angiotensin II
Kidney
Arterial Pressure
Diuretics
Perfusion
Pressure
Renin-Angiotensin System
Intravenous Infusions
Sprague Dawley Rats
Sodium
Urine

Keywords

  • Angiotensin II infusion
  • Pregnancy
  • Proximal tubular reabsorption
  • Renal interstitial hydrostatic pressure
  • Sodium excretion

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Renal interstitial hydrostatic pressure and natriuretic response to high doses of angiotensin II in pregnant rats. / Yu, Tianzheng; Khraibi, Ali A.

In: American journal of hypertension, Vol. 19, No. 3, 01.03.2006, p. 300-305.

Research output: Contribution to journalArticle

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abstract = "Background: Administration of high doses of angiotensin II (Ang II) results in natriuretic and diuretic responses that are mediated by increases in renal perfusion pressure (RPP). Elevations in renal interstitial hydrostatic pressure (RIHP) caused by increases in mean arterial pressure (MAP) or RPP are associated with significant increases in urinary sodium excretion (UNaV) and urine flow rate (V). In pregnant rats the renin-angiotensin system (RAS) is activated and basal RIHP is reduced. The exact relationship among MAP, RIHP, UNaV, and V in response to a high pressor dose of Ang II during normal pregnancy is not known. Methods: The objective of this study was to evaluate the relationship between MAP and RIHP, and determine the role of RIHP in the natriuretic and diuretic responses to administration of high dose of Ang II in midterm pregnant (MP) and nonpregnant (NP) Sprague-Dawley (SD) rats. Results: Intravenous infusion of Ang II (200 ng/kg/min) significantly increased MAP (ΔMAP), ΔUNaV, and ΔV in anesthetized MP and NP rats. The ΔMAP, ΔUNaV, and ΔV were 12 ± 2 mm Hg, 27.9 ± 2.7 μEq/min, and 197 ± 23 μL/min for MP rats and were similar (15 ± 3 mm Hg, 34.1 ± 4.3 μEq/min, and 242 ± 34 μL/min, respectively) for NP rats. The RIHP decreased significantly (P < .05) with Ang II infusion in NP (from 6.1 ± 0.2 to 3.9 ± 0.4 mm Hg) but not in MP (from 3.3 ± 0.3 to 4.1 ± 0.4 mm Hg) groups of rats. Acute renal decapsulation eliminated the change in RIHP mediated by high doses of Ang II infusion in the NP group, but did not affect MAP or the natriuretic and diuretic responses to Ang II in either the MP or NP groups of rats. Conclusions: The natriuretic and diuretic responses to high doses of Ang II are not mediated by changes in RIHP in pregnant or nonpregnant rats.",
keywords = "Angiotensin II infusion, Pregnancy, Proximal tubular reabsorption, Renal interstitial hydrostatic pressure, Sodium excretion",
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AU - Khraibi, Ali A.

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N2 - Background: Administration of high doses of angiotensin II (Ang II) results in natriuretic and diuretic responses that are mediated by increases in renal perfusion pressure (RPP). Elevations in renal interstitial hydrostatic pressure (RIHP) caused by increases in mean arterial pressure (MAP) or RPP are associated with significant increases in urinary sodium excretion (UNaV) and urine flow rate (V). In pregnant rats the renin-angiotensin system (RAS) is activated and basal RIHP is reduced. The exact relationship among MAP, RIHP, UNaV, and V in response to a high pressor dose of Ang II during normal pregnancy is not known. Methods: The objective of this study was to evaluate the relationship between MAP and RIHP, and determine the role of RIHP in the natriuretic and diuretic responses to administration of high dose of Ang II in midterm pregnant (MP) and nonpregnant (NP) Sprague-Dawley (SD) rats. Results: Intravenous infusion of Ang II (200 ng/kg/min) significantly increased MAP (ΔMAP), ΔUNaV, and ΔV in anesthetized MP and NP rats. The ΔMAP, ΔUNaV, and ΔV were 12 ± 2 mm Hg, 27.9 ± 2.7 μEq/min, and 197 ± 23 μL/min for MP rats and were similar (15 ± 3 mm Hg, 34.1 ± 4.3 μEq/min, and 242 ± 34 μL/min, respectively) for NP rats. The RIHP decreased significantly (P < .05) with Ang II infusion in NP (from 6.1 ± 0.2 to 3.9 ± 0.4 mm Hg) but not in MP (from 3.3 ± 0.3 to 4.1 ± 0.4 mm Hg) groups of rats. Acute renal decapsulation eliminated the change in RIHP mediated by high doses of Ang II infusion in the NP group, but did not affect MAP or the natriuretic and diuretic responses to Ang II in either the MP or NP groups of rats. Conclusions: The natriuretic and diuretic responses to high doses of Ang II are not mediated by changes in RIHP in pregnant or nonpregnant rats.

AB - Background: Administration of high doses of angiotensin II (Ang II) results in natriuretic and diuretic responses that are mediated by increases in renal perfusion pressure (RPP). Elevations in renal interstitial hydrostatic pressure (RIHP) caused by increases in mean arterial pressure (MAP) or RPP are associated with significant increases in urinary sodium excretion (UNaV) and urine flow rate (V). In pregnant rats the renin-angiotensin system (RAS) is activated and basal RIHP is reduced. The exact relationship among MAP, RIHP, UNaV, and V in response to a high pressor dose of Ang II during normal pregnancy is not known. Methods: The objective of this study was to evaluate the relationship between MAP and RIHP, and determine the role of RIHP in the natriuretic and diuretic responses to administration of high dose of Ang II in midterm pregnant (MP) and nonpregnant (NP) Sprague-Dawley (SD) rats. Results: Intravenous infusion of Ang II (200 ng/kg/min) significantly increased MAP (ΔMAP), ΔUNaV, and ΔV in anesthetized MP and NP rats. The ΔMAP, ΔUNaV, and ΔV were 12 ± 2 mm Hg, 27.9 ± 2.7 μEq/min, and 197 ± 23 μL/min for MP rats and were similar (15 ± 3 mm Hg, 34.1 ± 4.3 μEq/min, and 242 ± 34 μL/min, respectively) for NP rats. The RIHP decreased significantly (P < .05) with Ang II infusion in NP (from 6.1 ± 0.2 to 3.9 ± 0.4 mm Hg) but not in MP (from 3.3 ± 0.3 to 4.1 ± 0.4 mm Hg) groups of rats. Acute renal decapsulation eliminated the change in RIHP mediated by high doses of Ang II infusion in the NP group, but did not affect MAP or the natriuretic and diuretic responses to Ang II in either the MP or NP groups of rats. Conclusions: The natriuretic and diuretic responses to high doses of Ang II are not mediated by changes in RIHP in pregnant or nonpregnant rats.

KW - Angiotensin II infusion

KW - Pregnancy

KW - Proximal tubular reabsorption

KW - Renal interstitial hydrostatic pressure

KW - Sodium excretion

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