What question did this study set out to answer?

To determine the intrarenal role of angiotensin II in regulating renal hemodynamics during normal, sodium-depleted, and vena-caval-constricted states.

June 1, 1973Circulation ResearchOpen Access

Intrarenal Role of Angiotensin II

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Why the study?

Does intrarenal infusion of an angiotensin II antagonist alter renal blood flow and resistance in normal, sodium-depleted, and vena caval constricted dogs?

Population

Normal dogs, sodium-depleted dogs (n=5), and dogs with thoracic vena caval constriction (n=5).

Comparison

l-sarcosine-8-alanine-angiotensin II infused… vs Baseline control values prior to infusion.

Design

Preclinical

Follow-up

40 minutes

Authors

RFRonald H. FreemanMonsanto (United States)JDJames O. DavisUniversity of Alberta SVStephen J. VitaleUniversity of Missouri

Discussion

Member takes

Implication

Supports intrarenal angiotensin II role in sodium-depleted hemodynamics; leaves open clinical translation from this animal model.

Key Points

To determine the intrarenal role of angiotensin II in regulating renal hemodynamics during normal, sodium-depleted, and vena-caval-constricted states.
Administered the specific competitive antagonist 1-sarcosine-8-alanine-angiotensin II via intrarenal infusion into normal dogs, sodium-depleted dogs (N=5), and dogs with thoracic vena caval constriction (N=5).
Measured renal blood flow, renal vascular resistance, and mean arterial blood pressure during graded antagonist infusions at 0.2 µg/kg/min and 2.0 µg/kg/min.
In sodium-depleted dogs (N=5), antagonist infusion at 0.2 µg/kg/min increased renal blood flow from 196 ± 5 to 246 ± 12 ml/min at 40 minutes (P < 0.005) and decreased renal resistance from 0.71 ± 0.03 to 0.54 ± 0.03 mm Hg/ml min⁻¹ (P < 0.005).
In dogs with vena caval constriction (N=5), the 0.2 µg/kg/min infusion increased renal blood flow from 143 ± 16 to 190 ± 19 ml/min at 40 minutes (P < 0.005) and reduced renal resistance from 0.90 ± 0.14 to 0.64 ± 0.10 mm Hg/ml min⁻¹ without significantly altering arterial pressure.
The 0.2 µg/kg/min dose produced no hemodynamic changes in normal dogs, whereas a higher dose (2.0 µg/kg/min) reduced arterial pressure and renal resistance in sodium-depleted (N=5) and vena-caval-constricted (N=3) dogs.

Structured PICO

Does intrarenal infusion of an angiotensin II antagonist alter renal blood flow and resistance in normal, sodium-depleted, and vena caval constricted dogs?

Population

Normal dogs, sodium-depleted dogs (n=5), and dogs with thoracic vena caval constriction (n=5).

Intervention

l-sarcosine-8-alanine-angiotensin II (angiotensin II antagonist) infused into the renal artery at 0.2 µg/kg min-1 and 2.0 µg/kg min-1 for up to 40 minutes.

Comparator

Baseline control values prior to infusion.

Outcome

Renal blood flow and renal resistance.surrogate

Angiotensin II plays an important intrarenal role in the homeostatic regulation of renal blood flow during sodium depletion and vena caval constriction.

Cite This Study

Freeman et al. (1973) studied this question.

synapsesocial.com/papers/6a7160ed439bab0cabc38e38 https://doi.org/10.1161/01.res.32.6.692

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June 1, 1973Circulation ResearchOpen Access

Intrarenal Role of Angiotensin II

View Full Paper

Ask AI

Bookmark

Why the study?

Does intrarenal infusion of an angiotensin II antagonist alter renal blood flow and resistance in normal, sodium-depleted, and vena caval constricted dogs?

Population

Normal dogs, sodium-depleted dogs (n=5), and dogs with thoracic vena caval constriction (n=5).

Comparison

l-sarcosine-8-alanine-angiotensin II infused… vs Baseline control values prior to infusion.

Design

Preclinical

Follow-up

40 minutes

Authors

RFRonald H. FreemanMonsanto (United States)JDJames O. DavisUniversity of Alberta SVStephen J. VitaleUniversity of Missouri

Discussion

Member takes

Implication

Supports intrarenal angiotensin II role in sodium-depleted hemodynamics; leaves open clinical translation from this animal model.

Key Points

To determine the intrarenal role of angiotensin II in regulating renal hemodynamics during normal, sodium-depleted, and vena-caval-constricted states.
Administered the specific competitive antagonist 1-sarcosine-8-alanine-angiotensin II via intrarenal infusion into normal dogs, sodium-depleted dogs (N=5), and dogs with thoracic vena caval constriction (N=5).
Measured renal blood flow, renal vascular resistance, and mean arterial blood pressure during graded antagonist infusions at 0.2 µg/kg/min and 2.0 µg/kg/min.
In sodium-depleted dogs (N=5), antagonist infusion at 0.2 µg/kg/min increased renal blood flow from 196 ± 5 to 246 ± 12 ml/min at 40 minutes (P < 0.005) and decreased renal resistance from 0.71 ± 0.03 to 0.54 ± 0.03 mm Hg/ml min⁻¹ (P < 0.005).
In dogs with vena caval constriction (N=5), the 0.2 µg/kg/min infusion increased renal blood flow from 143 ± 16 to 190 ± 19 ml/min at 40 minutes (P < 0.005) and reduced renal resistance from 0.90 ± 0.14 to 0.64 ± 0.10 mm Hg/ml min⁻¹ without significantly altering arterial pressure.
The 0.2 µg/kg/min dose produced no hemodynamic changes in normal dogs, whereas a higher dose (2.0 µg/kg/min) reduced arterial pressure and renal resistance in sodium-depleted (N=5) and vena-caval-constricted (N=3) dogs.

Structured PICO

Does intrarenal infusion of an angiotensin II antagonist alter renal blood flow and resistance in normal, sodium-depleted, and vena caval constricted dogs?

Population

Normal dogs, sodium-depleted dogs (n=5), and dogs with thoracic vena caval constriction (n=5).

Intervention

l-sarcosine-8-alanine-angiotensin II (angiotensin II antagonist) infused into the renal artery at 0.2 µg/kg min-1 and 2.0 µg/kg min-1 for up to 40 minutes.

Comparator

Baseline control values prior to infusion.

Outcome

Renal blood flow and renal resistance.surrogate

Angiotensin II plays an important intrarenal role in the homeostatic regulation of renal blood flow during sodium depletion and vena caval constriction.

Cite This Study

Freeman et al. (1973) studied this question.

synapsesocial.com/papers/6a7160ed439bab0cabc38e38 https://doi.org/10.1161/01.res.32.6.692

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