Endogenous prostaglandins limit angiotensin-II induced regional vasoconstriction in conscious rats

Charles L Stebbins, J. David Symons, K. Sue Hageman, Timothy I. Musch

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

In conscious rats, we tested the hypothesis that prostaglandins attenuate regional vasoconstriction caused by acute infusion of angiotensin II. Mean arterial pressure, regional blood flow, and vascular conductance in response to 2-minute infusions of 0.05 or 1 μg/kg/min Ang II were assessed before and during indomethacin treatment (5 mg/kg). Effects of the lower dose of Ang II (n = 8) on regional blood flow were not altered by indomethacin, but conductance in the kidney (2.98 ± 0.35 vs. 2.19 ± 0.32), stomach (1.15 ± 0.13 vs. 0.83 ± 0.13), and white gastrocnemius muscle (0.11 ± 0.02 vs. 0.07 ± 0.01 mL/min/100g/mm Hg) were reduced. Changes in conductance were not seen in the pancreas or spleen. In response to the higher dose of Ang II (n = 7), indomethacin reduced blood flow in the kidney, red and white gastrocnemius, and soleus muscles. Reductions in conductance were found in the kidney, stomach and small intestine, and in the red and white gastrocnemius, and soleus muscles (2.27 ± 0.9 vs. 1.79 ± 0.14, 0.44 ± 0.07 vs. 0.27 ± 0.03, 0.68 ± 0.11 vs. 0.60 ± 0.07, 0.43 ± 0.08 vs. 0.16 ± 0.03, 0.10 ± 0.02 vs. 0.05 ± 0.01, and 0.26 ± 0.03 vs. 0.15 ± 0.02 mL/min/100g, respectively). No changes occurred in the pancreas and spleen. Indomethacin had no effect on baseline blood flow or conductance in any of these organs. These results suggest that prostaglandins attenuate vasoconstriction caused by Ang II in a manner that is organ-specific and dependent on the dose of Ang II. Consequently, prostaglandins may limit vasoconstriction and potential ischemia caused by elevated levels of this hormone.

Original languageEnglish (US)
Pages (from-to)10-16
Number of pages7
JournalJournal of Cardiovascular Pharmacology
Volume42
Issue number1
DOIs
StatePublished - Jul 1 2003

Fingerprint

Vasoconstriction
Angiotensin II
Prostaglandins
Skeletal Muscle
Indomethacin
Regional Blood Flow
Kidney
Pancreas
Stomach
Spleen
Small Intestine
Blood Vessels
Arterial Pressure
Ischemia
Hormones

Keywords

  • Blood pressure
  • Conscious rats
  • Indomethacin
  • Regional blood flow
  • Vascular conductance

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Endogenous prostaglandins limit angiotensin-II induced regional vasoconstriction in conscious rats. / Stebbins, Charles L; Symons, J. David; Hageman, K. Sue; Musch, Timothy I.

In: Journal of Cardiovascular Pharmacology, Vol. 42, No. 1, 01.07.2003, p. 10-16.

Research output: Contribution to journalArticle

Stebbins, Charles L ; Symons, J. David ; Hageman, K. Sue ; Musch, Timothy I. / Endogenous prostaglandins limit angiotensin-II induced regional vasoconstriction in conscious rats. In: Journal of Cardiovascular Pharmacology. 2003 ; Vol. 42, No. 1. pp. 10-16.
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N2 - In conscious rats, we tested the hypothesis that prostaglandins attenuate regional vasoconstriction caused by acute infusion of angiotensin II. Mean arterial pressure, regional blood flow, and vascular conductance in response to 2-minute infusions of 0.05 or 1 μg/kg/min Ang II were assessed before and during indomethacin treatment (5 mg/kg). Effects of the lower dose of Ang II (n = 8) on regional blood flow were not altered by indomethacin, but conductance in the kidney (2.98 ± 0.35 vs. 2.19 ± 0.32), stomach (1.15 ± 0.13 vs. 0.83 ± 0.13), and white gastrocnemius muscle (0.11 ± 0.02 vs. 0.07 ± 0.01 mL/min/100g/mm Hg) were reduced. Changes in conductance were not seen in the pancreas or spleen. In response to the higher dose of Ang II (n = 7), indomethacin reduced blood flow in the kidney, red and white gastrocnemius, and soleus muscles. Reductions in conductance were found in the kidney, stomach and small intestine, and in the red and white gastrocnemius, and soleus muscles (2.27 ± 0.9 vs. 1.79 ± 0.14, 0.44 ± 0.07 vs. 0.27 ± 0.03, 0.68 ± 0.11 vs. 0.60 ± 0.07, 0.43 ± 0.08 vs. 0.16 ± 0.03, 0.10 ± 0.02 vs. 0.05 ± 0.01, and 0.26 ± 0.03 vs. 0.15 ± 0.02 mL/min/100g, respectively). No changes occurred in the pancreas and spleen. Indomethacin had no effect on baseline blood flow or conductance in any of these organs. These results suggest that prostaglandins attenuate vasoconstriction caused by Ang II in a manner that is organ-specific and dependent on the dose of Ang II. Consequently, prostaglandins may limit vasoconstriction and potential ischemia caused by elevated levels of this hormone.

AB - In conscious rats, we tested the hypothesis that prostaglandins attenuate regional vasoconstriction caused by acute infusion of angiotensin II. Mean arterial pressure, regional blood flow, and vascular conductance in response to 2-minute infusions of 0.05 or 1 μg/kg/min Ang II were assessed before and during indomethacin treatment (5 mg/kg). Effects of the lower dose of Ang II (n = 8) on regional blood flow were not altered by indomethacin, but conductance in the kidney (2.98 ± 0.35 vs. 2.19 ± 0.32), stomach (1.15 ± 0.13 vs. 0.83 ± 0.13), and white gastrocnemius muscle (0.11 ± 0.02 vs. 0.07 ± 0.01 mL/min/100g/mm Hg) were reduced. Changes in conductance were not seen in the pancreas or spleen. In response to the higher dose of Ang II (n = 7), indomethacin reduced blood flow in the kidney, red and white gastrocnemius, and soleus muscles. Reductions in conductance were found in the kidney, stomach and small intestine, and in the red and white gastrocnemius, and soleus muscles (2.27 ± 0.9 vs. 1.79 ± 0.14, 0.44 ± 0.07 vs. 0.27 ± 0.03, 0.68 ± 0.11 vs. 0.60 ± 0.07, 0.43 ± 0.08 vs. 0.16 ± 0.03, 0.10 ± 0.02 vs. 0.05 ± 0.01, and 0.26 ± 0.03 vs. 0.15 ± 0.02 mL/min/100g, respectively). No changes occurred in the pancreas and spleen. Indomethacin had no effect on baseline blood flow or conductance in any of these organs. These results suggest that prostaglandins attenuate vasoconstriction caused by Ang II in a manner that is organ-specific and dependent on the dose of Ang II. Consequently, prostaglandins may limit vasoconstriction and potential ischemia caused by elevated levels of this hormone.

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