Renal effects of acute endothelial-derived relaxing factor blockade are not mediated by angiotensin II

1993 ◽  
Vol 264 (1) ◽  
pp. F74-F78 ◽  
Author(s):  
C. Baylis ◽  
K. Engels ◽  
L. Samsell ◽  
P. Harton
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Conscious Rat ◽  
Relaxing Factor ◽  
Renal Hemodynamic ◽  
Renal Vascular

The renal responses to acute blockade of the endothelial-derived relaxing factor (EDRF) resemble the renal actions of angiotensin II (ANG II), and the present studies were conducted to establish what role, if any, the endogenous renin-angiotensin system plays in mediating the renal response to acute EDRF blockade. These studies were conducted in the conscious chronically catheterized rat. In control experiments we observed that acute blockade of ANG II synthesis with converting-enzyme inhibition (CEI) led to a fall in blood pressure (BP) and a slight renal vasodilation but no significant change in glomerular filtration rate (GFR) or renal plasma flow (RPF). Urine flow and sodium excretion were unchanged by CEI. Use of the nonpeptide ANG II receptor antagonist losartan had no effect on BP, renal vascular resistance (RVR), GFR, or RPF; however, urine flow and sodium excretion did rise significantly. Because of the high specificity of losartan, this suggests that, in the normal conscious rat, endogenous ANG II does not control renal vascular tone but does enhance renal sodium reabsorption. ANG II blockade with either CEI or losartan had little effect on BP and no effect on the renal hemodynamic responses to acute EDRF blockade. The marked natriuretic and diuretic response to acute EDRF blockade persists during concomitant losartan but is abolished by CEI. These studies suggest that in the conscious rat the renal hemodynamic response to EDRF blockade is not mediated by endogenous ANG II.

Angiotensin II inhibition on blood pressure and renal hemodynamics in pregnant rats

1986 ◽  
Vol 250 (2) ◽  
pp. F308-F314 ◽  
Author(s):  
C. Baylis ◽  
R. C. Collins
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Urine Flow ◽  
Ang Ii ◽  
Pregnant Rats ◽  
Acute Surgery ◽  
Arterial Blood ◽  
Renal Vascular

Late-pregnant (18-20 days) and virgin rats were studied under anesthesia or while awake to investigate the effect of acute angiotensin II (ANG II) inhibition (with saralasin or captopril) on mean arterial blood pressure (AP) and renal hemodynamics. ANG II inhibition had no effect on AP in either anesthetized or awake virgin rats. Saralasin produced no effect on renal hemodynamics although with captopril small increases in renal plasma flow rate (RPF) and decreases in renal vascular resistance (RVR) occurred in virgins. In anesthetized pregnant rats, ANG II inhibition evoked marked decreases in AP. In some rats receiving saralasin, AP was only mildly depressed and RVR fell, leading to increases in glomerular filtration rate and RPF. In others, saralasin produced large decreases in AP, and indices of renal function became unmeasurable because of near cessation of urine flow. All late-pregnant anesthetized rats receiving captopril showed increased RPF irrespective of the magnitude of the fall in AP. In awake pregnant rats no effect on AP was seen with ANG II inhibition. Saralasin had no effect on renal hemodynamics although with captopril a small increase in RPF was observed. These data indicate that the stress of acute surgery and anesthesia produces a dependence of AP on ANG II in the pregnant but not the virgin rat. Under normal pregnant (awake) conditions, however, ANG II inhibition has no net effect on AP.

Mechanisms of angiotensin II natriuresis and antinatriuresis

1985 ◽  
Vol 249 (2) ◽  
pp. F299-F307 ◽  
Author(s):  
M. E. Olsen ◽  
J. E. Hall ◽  
J. P. Montani ◽  
A. C. Guyton ◽  
H. G. Langford ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Distal Tubule ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Sodium Load ◽  
Proximal Tubular ◽  
Anesthetized Dogs

The aim of this study was to determine the role of changes in renal arterial pressure (RAP), renal hemodynamics, and tubular reabsorption in mediating the natriuretic and antinatriuretic actions of angiotensin II (ANG II). In seven anesthetized dogs, endogenous ANG II formation was blocked with captopril, and ANG II was infused intravenously at rates of 5-1,215 ng X kg-1 X min-1 while RAP was either servo-controlled at the preinfusion level or permitted to increase. When RAP was servo-controlled, ANG II infusion at all rates from 5-1,215 ng X kg-1 X min-1 decreased urinary sodium excretion (UNaV) and fractional sodium excretion (FENa) while increasing fractional reabsorption of lithium (FRLi) (an index of proximal tubular fractional sodium reabsorption) and causing no change in calculated distal tubule fractional sodium reabsorption (FRDNa). When RAP was permitted to increase, ANG II infusion rates up to 45 ng X kg-1. min-1 also decreased UNaV and FENa while increasing FRLi and causing no change in FRDNa. However, at 135 ng X kg-1 X min-1 and above, UNaV and FENa increased while FRLi and FRDNa decreased when RAP was allowed to rise, even though renal blood flow and filtration fraction were not substantially different from the values observed when RAP was servo-controlled. Filtered sodium load was slightly higher when RAP was permitted to increase during ANG II infusion compared with when RAP was servo-controlled, although the differences were not statistically significant. Thus, even very large doses of ANG II cause antinatriuresis when RAP is prevented from increasing.(ABSTRACT TRUNCATED AT 250 WORDS)

Natriuretic response to renal interstitial hydrostatic pressure during angiotensin II blockade

1994 ◽  
Vol 266 (1) ◽  
pp. F117-F119 ◽  
Author(s):  
J. A. Haas ◽  
J. C. Lockhart ◽  
T. S. Larson ◽  
T. Henrikson ◽  
F. G. Knox
Keyword(s):  
Angiotensin Ii ◽  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Renin Angiotensin System ◽  
Urinary Sodium Excretion ◽  
Treated Group ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Angiotensin System ◽  
Before And After

Increases in renal interstitial hydrostatic pressure (RIHP) increase urinary sodium excretion (UNaV). Experimentally increasing RIHP by direct renal interstitial volume expansion (DRIVE) has been shown to decrease proximal tubule sodium reabsorption. The purpose of the present study was to investigate whether the renin-angiotensin system modulates the natriuretic response to DRIVE. Unilateral nephrectomy and implantation of two polyethylene matrices were performed 3 wk before the acute experiment. Fractional sodium excretion (FENa), RIHP, and glomerular filtration rate (GFR) were measured before and after DRIVE in control rats (n = 9) and in rats receiving the angiotensin II (ANG II) receptor antagonist, losartan potassium (10 mg/kg i.v.; n = 10). DRIVE was achieved by infusing 100 microliters of 2.5% albumin solution directly into the renal interstitium. GFR remained unchanged by DRIVE in both groups. In control animals, DRIVE significantly increased both RIHP (delta 3.8 +/- 0.5 mmHg) and FENa (delta 0.92 +/- 0.19%). In the losartan-treated group, RIHP (delta 2.8 +/- 0.4 mmHg) and FENa (delta 1.93 +/- 0.41%) also significantly increased. The natriuretic response to DRIVE was significantly enhanced during ANG II receptor blockade compared with control animals (delta UNaV/delta RIHP = 2.01 +/- 0.67 vs. 0.44 +/- 0.17 mu eq.min-1 x mmHg-1, respectively; P < 0.05). These results suggest that the blockade of angiotensin enhances the natriuretic response to increased RIHP during DRIVE.

scholarly journals Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaohua Huang ◽  
Shereen M. Hamza ◽  
Wenqing Zhuang ◽  
William A. Cupples ◽  
Branko Braam
Keyword(s):  
Angiotensin Ii ◽  
Ace Inhibitor ◽  
Venous Pressure ◽  
Ace Inhibition ◽  
Hemodynamic Response ◽  
Systemic Effect ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Renal Hemodynamic ◽  
Renal Vascular

Elevated central venous pressure increases renal venous pressure (RVP) which can affect kidney function. We previously demonstrated that increased RVP reduces renal blood flow (RBF), glomerular filtration rate (GFR), and renal vascular conductance (RVC). We now investigate whether the RAS and RBF autoregulation are involved in the renal hemodynamic response to increased RVP. Angiotensin II (ANG II) levels were clamped by infusion of ANG II after administration of an angiotensin-converting enzyme (ACE) inhibitor in male Lewis rats. This did not prevent the decrease in ipsilateral RBF (−1.9±0.4ml/min, p&lt;0.05) and GFR (−0.77±0.18ml/min, p&lt;0.05) upon increased RVP; however, it prevented the reduction in RVC entirely. Systemically, the RVP-induced decline in mean arterial pressure (MAP) was more pronounced in ANG II clamped animals vs. controls (−22.4±4.1 vs. −9.9±2.3mmHg, p&lt;0.05), whereas the decrease in heart rate (HR) was less (−5±6bpm vs. −23±4bpm, p&lt;0.05). In animals given vasopressin to maintain a comparable MAP after ACE inhibition (ACEi), increased RVP did not impact MAP and HR. RVC also did not change (0.018±0.008ml/minˑmmHg), and the reduction of GFR was no longer significant (−0.54±0.15ml/min). Furthermore, RBF autoregulation remained intact and was reset to a lower level when RVP was increased. In conclusion, RVP-induced renal vasoconstriction is attenuated when ANG II is clamped or inhibited. The systemic effect of increased RVP, a decrease in HR related to a mild decrease in blood pressure, is attenuated also during ANG II clamp. Last, RBF autoregulation remains intact when RVP is elevated and is reduced to lower levels of RBF. This suggests that in venous congestion, the intact RBF autoregulation could be partially responsible for the vasoconstriction.

scholarly journals Intrarenal transfer of an intracellular fluorescent fusion of angiotensin II selectively in proximal tubules increases blood pressure in rats and mice

2011 ◽  
Vol 300 (5) ◽  
pp. F1076-F1088 ◽  
Author(s):  
Xiao C. Li ◽  
Julia L. Cook ◽  
Isabelle Rubera ◽  
Michel Tauc ◽  
Fan Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Sodium Excretion ◽  
Proximal Tubules ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Contralateral Kidney ◽  
Adenoviral Transfer ◽  
Rats And Mice

The present study tested the hypothesis that intrarenal adenoviral transfer of an intracellular cyan fluorescent fusion of angiotensin II (ECFP/ANG II) selectively in proximal tubules of the kidney increases blood pressure by activating AT1 (AT1a) receptors. Intrarenal transfer of ECFP/ANG II was induced in the superficial cortex of rat and mouse kidneys, and the sodium and glucose cotransporter 2 (sglt2) promoter was used to drive ECFP/ANG II expression selectively in proximal tubules. Intrarenal transfer of ECFP/ANG II induced a time-dependent, proximal tubule-selective expression of ECFP/ANG II in the cortex, which peaked at 2 wk and was sustained for 4 wk. ECFP/ANG II expression was low in the glomeruli and the entire medulla and was absent in the contralateral kidney or extrarenal tissues. At its peak of expression in proximal tubules at day 14, ANG II was increased by twofold in the kidney ( P < 0.01) and more than threefold in proximal tubules ( P < 0.01), but remained unchanged in plasma or urine. Systolic blood pressure was increased in ECFP/ANG II-transferred rats by 28 ± 6 mmHg ( P < 0.01), whereas fractional sodium excretion was decreased by 20% ( P < 0.01) and fractional lithium excretion was reduced by 24% ( P < 0.01). These effects were blocked by losartan and prevented in AT1a knockout mice. Transfer of a scrambled ECFP/ANG IIc had no effects on blood pressure, kidney, and proximal tubule ANG II, or sodium excretion. These results provide evidence that proximal tubule-selective transfer of an intracellular ANG II fusion protein increases blood pressure by activating AT1a receptors and increasing sodium reabsorption in proximal tubules.

Renal response to atrial natriuretic factor is modulated by intrarenal angiotensin II

1988 ◽  
Vol 254 (3) ◽  
pp. R453-R456 ◽  
Author(s):  
C. J. Showalter ◽  
R. S. Zimmerman ◽  
T. R. Schwab ◽  
B. S. Edwards ◽  
T. J. Opgenorth ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Ang Ii ◽  
Natriuretic Factor ◽  
Renal Hemodynamic ◽  
Atrial Natriuretic

The present study in anesthetized dogs (n = 8) was designed to test the hypothesis that intrarenal angiotensin II (ANG II) attenuates the increase in sodium excretion in response to atrial natriuretic factor (ANF). To test this hypothesis, renal hemodynamic and excretory responses to systemically administered ANF (0.3 micrograms.kg-1.min-1) were assessed in the presence of ANG II infusion into the left kidney (ANG II K) at a nonpressor dose (1.5 ng.kg-1.min-1) and with an infusion of saline into the right kidney, the latter which served as control (CK). During ANF infusion, absolute increases in urinary sodium excretion (delta + 160.8 +/- 44.7 vs. delta + 369.4 +/- 56.9 mu eq/min, P less than 0.005) and fractional sodium excretion (delta + 2.55 +/- 0.62 vs. delta + 4.26 +/- 0.82%, P less than 0.03) were markedly attenuated in the ANG II K compared with CK. Glomerular filtration rate increased only in the CK. Urine osmolality decreased in both the ANG II K and CK. These studies demonstrate an attenuated natriuresis to ANF in the presence of intrarenally infused ANG II, which is associated with a blunted increase in glomerular filtration rate. These studies support the hypothesis that the renal hemodynamic and excretory responses to ANF are modulated by intrarenal ANG II.

Role of endothelium-derived nitric oxide in the renal hemodynamic response to amino acid infusion

1992 ◽  
Vol 263 (3) ◽  
pp. R510-R516 ◽  
Author(s):  
C. Chen ◽  
K. D. Mitchell ◽  
L. G. Navar
Keyword(s):  
Nitric Oxide ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Urine Flow ◽  
Nitric Oxide Synthesis ◽  
Synthesis Inhibitor ◽  
Acid Infusion ◽  
Amino Acid Infusion ◽  
Renal Hemodynamic

The present study was performed in anesthetized rats to compare the renal hemodynamic responses to mixed amino acids (M-AA) with those to L-arginine (L-Arg) and to examine the effect of endothelium-derived nitric oxide (EDNO) synthesis blockade on the M-AA-induced rise in renal plasma flow (RPF) and glomerular filtration rate (GFR). Intravenous infusion of both M-AA (Ser, Gly, Ala, and Pro, 0.71 mmol.100 g-1.min-1) and L-Arg (0.71 mmol.100 g-1.min-1) increased RPF and GFR. Peak increases in RPF for M-AA and L-Arg were 39.7% (P less than 0.05) and 63.4% (P less than 0.01), whereas GFR increases were 33.6% (P less than 0.05) and 46.7% (P less than 0.01, respectively). Outer cortical blood flow (OCBF) was increased with both treatments. Sodium excretion and urine flow were increased more with L-Arg than M-AA (both P less than 0.01). Infusion of the nitric oxide synthesis inhibitor, nitro-L-arginine (N-L-Arg, 20 micrograms.100 g-1.min-1) increased mean arterial pressure but decreased RPF 48.4% (P less than 0.001), OCBF 39.5% (P less than 0.001), GFR 37.8% (P less than 0.01), urine flow 29.8% (P less than 0.01), and sodium excretion 40.9% (P less than 0.01). When M-AA was administered after N-L-Arg, significant increases in OCBF, RPF, and GFR were observed (P less than 0.01); there was also an enhancement of sodium excretion and urine flow (both P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Vasopressor-Induced Natriuresis and Altered Intrarenal Haemodynamics in Cirrhotic Man

1973 ◽  
Vol 45 (1) ◽  
pp. 19-34 ◽  
Author(s):  
R. A. Gutman ◽  
A. W. Forrey ◽  
W. P. Fleet ◽  
R. E. Cutler
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Flow Distribution ◽  
Systemic Hypertension ◽  
Sodium Reabsorption ◽  
Physical Factors ◽  
Filtration Fraction ◽  
Intrarenal Blood Flow ◽  
Induced Changes

1. The influence of two intravenous vasopressors (angiotensin II and norepinephrine) on renal function and intrarenal blood flow distribution was studied in thirteen cirrhotic subjects and the results compared with those from eight non-cirrhotics. 2. Increased sodium excretion occurred in four of eight cirrhotics with ascites who received comparable pressor doses of angiotensin II and one of five similar subjects who received norepinephrine. In contrast, sodium excretion fell or remained the same in all eight non-cirrhotics. 3. Renal plasma flow fell and filtration fraction rose in nearly all subjects who did not respond to vasopressors with a natriuresis but changed little in those who did. 4. Vasopressor-induced changes of the multicompartmental 133xenon washout curve were qualitatively different in the group who responded with a natriuresis in comparison to the others. Whereas the distribution of flow to the fastest component fell in the non-responder, it remained the same or rose in those who developed a natriuresis. 5. We interpret these results as suggesting a state of relative renal vasopressor resistance allowing the induced systemic hypertension to reduce tubular sodium reabsorption in some cirrhotics by influencing peritubular ‘physical factors’.

Renal blood flow, early distal sodium, and plasma renin concentrations during osmotic diuresis

2000 ◽  
Vol 279 (4) ◽  
pp. R1268-R1276 ◽  
Author(s):  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou ◽  
Ole Skøtt
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urine Flow ◽  
Sodium Reabsorption ◽  
Osmotic Diuresis ◽  
Nacl Concentration ◽  
Proximal Tubular ◽  
Distal Tubules

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.

Angiotensin II regulates nephrogenesis and renal vascular development

1995 ◽  
Vol 269 (1) ◽  
pp. F110-F115 ◽  
Author(s):  
A. Tufro-McReddie ◽  
L. M. Romano ◽  
J. M. Harris ◽  
L. Ferder ◽  
R. A. Gomez
Keyword(s):  
Angiotensin Ii ◽  
Kidney Development ◽  
Rana Catesbeiana ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Ang Ii ◽  
Newborn Rats ◽  
Sprague Dawley ◽  
Renal Growth ◽  
Glomerular Size ◽  
Renal Vascular

To test the hypothesis that angiotensin II (ANG II) is necessary for normal embryonic and postnatal kidney development, the effect of angiotensin receptor blockade or angiotensin converting enzyme inhibition on nephrovascular development was studied in newborn Sprague-Dawley rats and in Rana catesbeiana tadpoles undergoing prometamorphosis. Blockade of ANG II type 1 receptor (AT1) in newborn rats induced an arrest in nephrovascular maturation and renal growth, resulting in altered kidney architecture, characterized by fewer, thicker, and shorter afferent arterioles, reduced glomerular size and number, and tubular dilatation. Inhibition of ANG II generation in tadpoles induced even more marked developmental renal abnormalities. Blockade of ANG II type 2 receptor (AT2) in newborn rats did not alter renal growth or morphology. Results indicate that ANG II regulates nephrovascular development, a role that is conserved across species.

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