Effects of renal arterial angiotensin I infusion on glomerular dynamics in sodium replete dogs

Effects of renal arterial angiotensin I infusion on glomerular dynamics in sodium replete dogs. During intrarenal infusion of angiotensin I (AI), conversion to angiotensin II (AII) within the kidney has been shown to occur early enough to decrease glomerular filtration rate (GFR). To evaluate further the mechanism by which AI decreases GFR, micropuncture studies were conducted in sodium replete dogs. Feedbackmediated alterations in glomerular function were minimized by reducing renal arterial pressure to 90 mm Hg. During infusion of AI (0.82 ± 0.01 µg min -1 ), renal blood flow (3.91 ± 0.25 ml min -1 g -1 ) and GFR (0.63 ± 0.04 ml min -1 g -1 ) decreased by 36.7 ± 6.1% and 18.9 ± 6.1%, respectively. Similarly, single nephron GFR decreased from 66.4 ± 3.8 to 40.0 ± 3.2 nl min -1 and estimated glomerular plasma flow (280 ± 49 nl min -1 ) decreased by 55 ± 6%. Stop-flow pressure (40.5 ± 3.6 mm Hg) did not change significantly, while proximal tubular (21.8 ± 1.4 mm Hg) and peritubular capillary pressures (13.2 ± 1.8 mm Hg) decreased by 25.5 ± 2.8% and 49.4% ± 5.1%, respectively. Glomerular capillary and effective filtration pressures were not altered significantly. There were increases in both preglomerular (168%) and efferent (203%) arteriolar resistances, along with a decrease in the glomerular filtration coefficient (K f ) from 4.6 ± 0.6 to 2.5 ± 0.5 nl mm Hg -1 min -1 . These data indicate that augmented intrarenal conversion of circulating AI reduces GFR as a consequence of decreases in K f as well as in glomerular plasma flow, the latter being due to concomitant increases in preglomerular and efferent arteriolar resistances. Effets d'une perfusion arterielle renale d'angiotensine I sur la dynamique glomerulaire ches des chiens en repletion sodee. Pendant une perfusion intrarenale d'angiotensine I (AI), il a ete montre que la conversion en angiotensine II (AII) dans le rein survient suffisamment tot pour diminuer le debit de filtration glomerulaire (GFR). Afin de preciser plus le mecanisme par lequel AI diminue GFR, des etudes de microponction ont ete entreprises chez des chiens en repletion sodee. Les alterations de la fonction glomerulaire par mecanisme de retrocontrole ont ete minimisees en reduisant la pression arterielle renale a 90 mm Hg. Pendant la perfusion d'AI (0,82 ± 0,01 pg min -1 ), le debit sanguin renal (3,91 ± 0,25 ml min -1 g -1 ), et GFR (0,63 ± 0,04 ml min -1 g -1 ) ont diminue de 36,7 ± 6,1% et 18,9 ± 6,1%, respectivement. De meme, GFR nephronique individuel a diminue de 66,4 ± 3,8 a 40,0 ± 3,2 nl min -1 et le debit plasmatique glomerulaire estime (280 ± 49 nl min -1 ) a diminue de 55 ± 6%. La pression d'occlusion (40,5 ± 3,6 mm Hg) ne s'est pas modifiee significativement alors que les pressions tubulaires proximales (21,8 ± 1,4 mm Hg) et capillaires peritubulaires (13,2 ± 1,8 mm Hg) ont baisse de 25,5 ± 2,8% et 49,4 ± 5,1%, respectivement. La pression capillaire glomerulaire et la pression de filtration efficace n'ont pas ete significativement modifiees. Il y a eu une elevation des resistances arteriolaires preglomerulaires (168%) et efferentes (203%), en meme temps qu'une diminution du coefficient de filtration glomerulaire (K f ) de 4,6 ± 0,6 a 2,5 ± 0,5 nl mm Hg -1 . Ces donnees indiquent que l'augmentation de la conversion intrarenale de l'AI circulante diminue GFR par des baisses de K f et du debit plasmatique glomerulaire, cette derniere etant due a des elevations concomitantes des resistances arteriolaires preglomerulaires et efferentes.