Angiotensin II in arterial and renal venous plasma and renal lymph in the dog

Abstract

A B S T R A C T Angiotensin II was determined by radioimmunoassay in systemic arterial, pulmonary arterial, and renal venous plasma and in renal hilar lymph in dogs. Levels of the peptide were determined prior to and during progressive graded hemorrhage or reduction in renal perfusion pressure. Levels of angiotensin II in plasma consistently rose during transit through the lung indicating pulmonary conversion of angiotensin I to angiotensin II. On the other hand, angiotensin II in the renal vein plasma was less than that in arterial plasma indicating renal extraction of the peptide from plasma. When renal hilar lymph was sampled under similar conditions, angiotensin II in lymph was consistently higher than that in arterial or renal venous plasma. Furthermore, in some experiments angiotensin II in lymph increased at a time when the concentration in plasma was undetectable. No evidence was found to indicate that angiotensin II in plasma entered renal lymph. It was concluded that angiotensin II levels in lymph reflected the concentration of angiotensin II in renal tissue. The data further suggested that angiotensin II is partially removed from arterial plasma by hydrolysis during transit through the -kidney. INTRODUCTIONSeveral investigators have proposed models in which angiotensin II (AII) is a critical mediator for the control of glomerular filtration rate (1), renal autoregulation (2), and tubular sodium reabsorption (3,4). It is not clear whether the AII postulated to mediate these control mechanisms is produced within the kidney or reaches the kidney from the systemic circulation.

Review: Intrarenal angiotensin II levels in normal and hypertensive states

“…Earlier measurements of renal lymph, considered a reflection of renal interstitial fluid, suggested that interstitial fluid Ang II concentrations were much higher than plasma concentrations. [45][46][47] These results were consistent with the notion that Ang II is formed locally and added to the interstitial compartment. However, it was not clear how much of renal lymph Ang II concentrations were due to continued Ang II formation within the lymphatic compartment, since lymph also contains ample quantities of renin and renin substrate.…”

Compartmentalization of angiotensin II generation in the dog heart. Evidence for independent mechanisms in intravascular and interstitial spaces.

“…Danser et al demonstrated rapid ANG I degradation within the cardiac and systemic vasculature of the pig in vivo, and an increased ANG I degradation rate during captopril administration, most likely due to aminopeptidase and endopeptidase action on increased concentrations of ANG I substrate (35). Previous studies by Bailie et al demonstrated that, after injection into the renal artery of the dog, significant amounts of 14 C ANG II did not appear in the renal lymph or the urine, suggesting that metabolism of circulating ANG peptide occurs primarily in the vascular compartment (36). In a related fashion, the endothelial cell has been shown to metabolize very actively adenosine, and thus function as a physiological barrier for passage of adenosine into the ISF (37).…”

Evidence for tissue-specific activation of renal angiotensinogen mRNA expression in chronic stable experimental heart failure.

“…Indeed, it has recently been demonstrated that the majority of angiotensin I found in renal venous blood is of intrarenal origin (35). Evidence for predominent intrarenal production of angiotensin II has been suggested by the demonstration that angiotensin II concentrations in the renal lymph (36), and the proximal tubule (37) greatly exceeded the plasma concentrations. A body of data suggests that the intrarenal RAS may be involved in the alterations in sodium and fluid balance observed in chronic HF via direct tubular effect or hemodynamic changes ( 19,38).…”