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February 1, 1993Hypertension104 citations

Regional angiotensin II production in essential hypertension and renal artery stenosis.

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PAP J AdmiraalADA.H. Jan DanserMJMartina Sura–de Jong

Key Result

Systemic infusion of 125I-angiotensin I or II demonstrated 30-50% extraction of angiotensin II in limbs and 80-100% in renal and hepatomesenteric beds, indicating circulating angiotensin II derives solely from blood-borne angiotensin I.

Key Points

  • This research investigates the production and metabolism of angiotensin II in different vascular regions related to essential hypertension and renal artery stenosis.
  • Measured steady-state plasma levels of 125I-angiotensin I and II in various veins during systemic infusion.
  • Examined extraction rates of angiotensin II in limbs, renal, and hepatomesenteric vascular beds in participants.
  • Analyzed the conversion of angiotensin I to II across vascular sites in both conditions.
  • Extraction of angiotensin II ranged from 30-50% in limbs to 80-100% in the renal and hepatomesenteric areas.
  • 20-30% conversion of angiotensin I to II in limbs was observed, with no conversion in renal and hepatomesenteric beds.
  • No circulating source of angiotensin II was identified other than blood-borne angiotensin I.

Study Design

Type

Observational (n=20)

Structured PICO

P
Population
20 patients with essential hypertension (n=13) or unilateral renal artery stenosis (n=7) undergoing physiological assessment of regional angiotensin metabolism.
E
Exposure
Systemic infusion of 125I-angiotensin I or II for physiological measurement.
O
Outcome
Steady-state plasma levels of 125I-angiotensin I and II and endogenous angiotensin I and II in the aorta and the antecubital, femoral, renal, and hepatic veins.surrogate

The study demonstrates a high degree of compartmentalization in angiotensin I and II production, indicating that circulating angiotensin II is primarily derived from blood-borne angiotensin I rather than regional tissue production.

Abstract

To study regional metabolism and production of angiotensin II, we measured steady-state plasma levels of 125I-angiotensin I and II and endogenous angiotensin I and II in the aorta and the antecubital, femoral, renal, and hepatic veins during systemic infusion of 125I-angiotensin I or II. Extraction of arterially delivered angiotensin II ranged from 30-50% in the limbs to 80-100% in the renal and hepatomesenteric vascular beds both in essential hypertension (n = 13) and in unilateral renal artery stenosis (n = 7). Across the limbs, 20-30% of arterially delivered angiotensin I was converted to angiotensin II in both groups, and there was no arteriovenous gradient in endogenous angiotensin II. No conversion of arterially delivered angiotensin I was detected across the renal and hepatomesenteric beds, and there was net extraction of angiotensin II from the systemic circulation by these beds. Although regional production of angiotensin I at tissue sites made a significant contribution to its level in the veins, little of this locally produced angiotensin I reached the regional veins in the form of angiotensin II, even in the kidney with artery stenosis, where the venous levels of locally produced angiotensin I were particularly high. These results provide no evidence for a source of circulating angiotensin II other than blood-borne angiotensin I and illustrate the high degree of compartmentalization of angiotensin I and II production.

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Cite This Study

Admiraal et al. (1993) conducted an observational in Essential hypertension and unilateral renal artery stenosis (n=20). Systemic infusion of 125I-angiotensin I or II was evaluated on Regional extraction and conversion of angiotensin I and II. Systemic infusion of 125I-angiotensin I or II demonstrated 30-50% extraction of angiotensin II in limbs and 80-100% in renal and hepatomesenteric beds, indicating circulating angiotensin II derives solely from blood-borne angiotensin I.

synapsesocial.com/papers/6a6eea0fe71d69abee07d29ehttps://doi.org/10.1161/01.hyp.21.2.173
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