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

L. Rosivall, P. K. Carmines, L. G. Navar

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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. Feedback-mediated 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 225 ± 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.

Original languageEnglish
Pages (from-to)263-268
Number of pages6
JournalKidney International
Volume26
Issue number3
Publication statusPublished - 1984

Fingerprint

Angiotensin I
Glomerular Filtration Rate
Sodium
Dogs
Kidney
Pressure
Renal Circulation
Nephrons
Punctures
Angiotensin II
Arterial Pressure

ASJC Scopus subject areas

  • Nephrology

Cite this

Effects of renal arterial angiotensin I infusion on glomerular dynamics in sodium replete dogs. / Rosivall, L.; Carmines, P. K.; Navar, L. G.

In: Kidney International, Vol. 26, No. 3, 1984, p. 263-268.

Research output: Contribution to journalArticle

@article{b8e3c26596164dbb8573728e6acf1afe,
title = "Effects of renal arterial angiotensin I infusion on glomerular dynamics in sodium replete dogs",
abstract = "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. Feedback-mediated 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 225 ± 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.",
author = "L. Rosivall and Carmines, {P. K.} and Navar, {L. G.}",
year = "1984",
language = "English",
volume = "26",
pages = "263--268",
journal = "Kidney International",
issn = "0085-2538",
publisher = "Nature Publishing Group",
number = "3",

}

TY - JOUR

T1 - Effects of renal arterial angiotensin I infusion on glomerular dynamics in sodium replete dogs

AU - Rosivall, L.

AU - Carmines, P. K.

AU - Navar, L. G.

PY - 1984

Y1 - 1984

N2 - 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. Feedback-mediated 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 225 ± 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.

AB - 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. Feedback-mediated 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 225 ± 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.

UR - http://www.scopus.com/inward/record.url?scp=0021146292&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021146292&partnerID=8YFLogxK

M3 - Article

VL - 26

SP - 263

EP - 268

JO - Kidney International

JF - Kidney International

SN - 0085-2538

IS - 3

ER -