Relationship between Plasma Concentrations of Angiotensin I, Angiotensin II and Plasma Renin Activity during Cardio‐Pulmonary Bypass in Man*

Favre, L.; Vallotton, Michel B.; Müller, Alex F.

doi:10.1111/j.1365-2362.1974.tb00384.x

Cited by 39 publications

(3 citation statements)

References 20 publications

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“…It has been reported that the plasma Ang II-to-I concentration ratio is not reduced in human subjects during extrapulmonary bypass with extracorporeal circulation, which may suggest that extrapulmonary conversion of arterially delivered Ang I is the most important source of circulating Ang II. 19 It should be noted, however, that the Ang II-to-I concentration ratio in plasma is not only dependent on the degree of conversion of blood-borne Ang I; it also depends on Ang I and II degradation and Ang I production, as well as on Ang II production from sources other than conversion of blood-borne Ang I.…”

Section: Discussionmentioning

confidence: 99%

“…Regional venous Ang I derived from regional production by circulating PRA was calculated as Ang I out from PRA=PRA x blood transit time (19) This equation does not take into account the regional metabolism of Ang I and therefore leads to an overestimation of the level of regional venous Ang I that is regionally produced by circulating PRA. Endogenous Ang II in regional venous plasma also originates from arterial delivery and de novo production.…”

Section: Calculationsmentioning

confidence: 99%

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

et al. 1993

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To study regional metabolism and production of angiotensin II, we measured steady-state plasma levels of 12S I-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 125 I-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. sin system, circulating renin acts on circulating .Z \ -angiotensinogen to form the decapeptide angiotensin I (Ang I). During the passage of blood through the lungs, Ang I is converted to the octapeptide angiotensin II (Ang II) by angiotensin converting enzyme (ACE) that is bound to the luminal surface of the pulmonary vascular endothelium. Ang II is then transported by the bloodstream to peripheral target sites to exert its physiological actions.This view of the renin-angiotensin system, however, is an oversimplification. Observations in animals and humans have clearly demonstrated that considerable conversion of plasma Ang I occurs in organs other than the lungs,'-6 but particularly in humans, it is not known to what extent extrapulmonary conversion of Ang I to Ang II contributes to the circulating levels of Ang II.Moreover, the concept of the renin-angiotensin system as a circulating endocrine system is now being challenged.7 -10 Animal studies, in which pharmacological doses of Ang II were systemically infused, have

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Section: Discussionmentioning

confidence: 99%

Section: Calculationsmentioning

confidence: 99%

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

et al. 1993

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“…Angiotensin I generation was calculated as total angiotensinogen − intact angiotensinogen (Figure 1). Angiotensin I levels were interpreted as plasma renin activity (PRA) [21,22].…”

Section: Determination Of Renin Activitymentioning

confidence: 99%

Evidence for Impaired Renin Activity in Postural Orthostatic Tachycardia Syndrome

Spahic

Mattisson

Hamrefors

et al. 2023

JCM

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Background: Postural orthostatic tachycardia syndrome (POTS) is a heterogeneous condition predominantly affecting autonomic control of the cardiovascular system. Its extensive symptom diversity implies multi-organ involvement that interacts in ways still requiring full exploration. Current understanding of POTS pathophysiology suggests alterations in the renin–angiotensin–aldosterone system as a possible contributing factor. Therefore, we investigated the relationship between the activity of the renin–angiotensin–aldosterone system and hemodynamic parameters in a cohort of POTS patients and controls recruited at a tertiary referral center. Methods: The case-control study included 46 patients with POTS (27 ± 9 years), and 48 healthy controls (30 ± 9 years) without orthostatic intolerance. Plasma renin activity, expressed as angiotensin I generation, and plasma aldosterone were measured by enzyme-linked immunosorbent assay and were correlated with hemodynamic parameters obtained during active standing tests. Results: Renin activity was significantly downregulated in POTS patients compared to healthy individuals (median, 3406 ng/mL vs. 9949 ng/mL, p < 0.001), whereas aldosterone concentration did not differ between POTS and healthy controls (median, 218 pmol/L vs. 218 pmol/L, p = 0.26). A significant inverse correlation between renin activity and supine and orthostatic blood pressure levels was observed in healthy individuals (p < 0.05 for all), but not in POTS patients. Conclusions: Renin activity, but not aldosterone concentration, is downregulated in patients with POTS. Moreover, renin activity in POTS is dissociated from supine and standing blood pressure levels in contrast to healthy individuals. These findings suggest impaired renin function in POTS, which may direct future therapeutic approaches.

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Angiotensin-Converting Enzyme Activity

et al. 1985

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Relationship between Plasma Concentrations of Angiotensin I, Angiotensin II and Plasma Renin Activity during Cardio‐Pulmonary Bypass in Man*

Cited by 39 publications

References 20 publications

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

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

Evidence for Impaired Renin Activity in Postural Orthostatic Tachycardia Syndrome

Angiotensin-Converting Enzyme Activity

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