Role of endogenous endothelin on renal functions in rats

1991 ◽  
Vol 260 (1) ◽  
pp. F34-F38
Author(s):  
K. Yamada ◽  
S. Yoshida
Keyword(s):  
Sodium Excretion ◽  
Salt Intake ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Sodium Balance ◽  
High Salt Intake ◽  
Fractional Excretion Of Sodium

This study was conducted to determine the involvement of endogenous endothelin (ET), a novel potent vasoconstricting peptide, in systemic and renal hemodynamics and in the renin-angiotensin system by inhibiting ET action via infusion of a specific ET antiserum at a time of altered sodium balance. Infusion of 1:50 diluted ET antiserum, which completely inhibited renal vasoconstriction by the exogenously administered ET (0.25 to 1.0 nmol/kg), caused an increase in urinary sodium excretion and fractional excretion of sodium and a decrease in plasma renin concentration without significant changes in blood pressure, heart rate, glomerular filtration rate, renal plasma flow, and urine volume compared with the values with nonimmune serum in conscious rats fed a low-salt diet. A time control study showed no significant changes in all parameters. These results suggest that the state of low- compared to high-salt intake causes a relatively stronger activity of endogenous ET, and that the endogenous ET contributes to the adaptative modulations of sodium excretion via renal tubular action and renin release in association with the changed state of sodium balance.

Combined intrarenal blockade of the renin-angiotensin system in the conscious dog

1990 ◽  
Vol 258 (3) ◽  
pp. F522-F529 ◽  
Author(s):  
H. M. Siragy ◽  
N. L. Howell ◽  
M. J. Peach ◽  
R. M. Carey
Keyword(s):  
Renal Function ◽  
Enzyme Inhibitor ◽  
Renal Plasma Flow ◽  
Renin Angiotensin System ◽  
Fractional Excretion ◽  
Random Order ◽  
Sodium Balance ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Fractional Excretion Of Sodium

We produced maximal or near-maximal acute intrarenal blockade of the renin-angiotensin system (RAS) by combining inhibitors. Intrarenal infusion of the renin inhibitor, ACRIP, the converting enzyme inhibitor, teprotide, and saralasin were administered individually or combined in random order. The inhibitors were infused for 20 min in doses that did not produce systemic effects in uninephrectomized conscious dogs in sodium balance at 10 meq/day. Significant increases in urine flow rate (UV; F = 97, P less than 0.0001), urinary sodium excretion (UNaV; F = 220, P less than 0.0001), glomerular filtration rate (GFR; F = 64, P less than 0.0001), and renal plasma flow (RPF; F = 108, P less than 0.0001) were observed with each blocker, whether alone or in combination except that ACRIP alone did not alter GFR or RPF. The increase in renal function was related to the number of blockers (3 greater than 2 greater than 1). With the three blockers combined UV increased approximately sixfold (from 0.5 +/- 0.06 to 2.9 +/- 0.03 ml/min), UNaV approximately 10-fold (from 3 +/- 0.4 to 34 +/- 2.8 mueq/min), GFR from 31 +/- 2 to 49 +/- 2 ml/min, RPF from 59 +/- 1 to 120 +/- 4 ml/min, and fractional excretion of sodium from 0.06 +/- 0.01 to 0.5 +/- 0.4% (all P less than 0.001). These changes did not occur where the inhibitors were infused systemically and the changes during intrarenal blocker administration were blocked completely with co-administration of angiotensin II intrarenally. The intrarenal RAS is a potent physiological regulator of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of nitric oxide synthesis attenuates pressure-induced natriuretic responses in anesthetized dogs

1993 ◽  
Vol 264 (1) ◽  
pp. F79-F87 ◽  
Author(s):  
D. S. Majid ◽  
A. Williams ◽  
L. G. Navar
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Sodium Excretion ◽  
Renin Angiotensin System ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Synthesis Inhibition ◽  
Fractional Excretion Of Sodium ◽  
Anesthetized Dogs ◽  
Pressure Natriuresis

Inhibition of nitric oxide (NO) synthesis by intrarenal administration of nitro-L-arginine (NLA) leads to decreases in urinary sodium excretion (UNaV) in association with the increases in renal vascular resistance (RVR). In the present study, we examined the ability of the kidney to alter its sodium excretion in response to acute changes in renal arterial pressure (RAP) in anesthetized dogs before and during intrarenal infusion of NLA (50 micrograms.kg-1.min-1). NO synthesis inhibition in 11 dogs increased RVR by 32 +/- 4% and decreased renal blood flow (RBF) by 25 +/- 3%, outer cortical blood flow by 25 +/- 6%, urine flow by 37 +/- 14%, UNaV by 71 +/- 5%, and fractional excretion of sodium (FENa) by 71 +/- 4%. Glomerular filtration rate was not significantly changed during NLA infusion. As previously reported, there was suppression of the RBF autoregulation plateau during NO synthesis inhibition. In addition, there was a marked attenuation of urine flow and UNaV responses to reductions in RAP (150 to 75 mmHg), with significant reductions in the slopes of the relationships between RAP vs. UNaV and RAP vs. FENa during NLA infusion. Similar responses were observed in nine other dogs treated with the angiotensin receptor antagonist losartan, indicating that an augmented activity of the renin-angiotensin system is not responsible for attenuation of the slope of the pressure-natriuresis relationship during NLA infusion. These data suggest that NO may participate in the mediation of the pressure-natriuresis response.

Effect of intrarenal renin inhibition on renal hemodynamics and excretory function

1990 ◽  
Vol 259 (1) ◽  
pp. R7-R14 ◽  
Author(s):  
K. M. Verburg ◽  
J. R. Kadam ◽  
G. A. Young ◽  
S. H. Rosenberg ◽  
H. D. Kleinert
Keyword(s):  
Recovery Period ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Electrolyte Excretion ◽  
Angiotensin System ◽  
Excretory Function ◽  
Fractional Excretion Of Sodium ◽  
Renin Inhibition

This study was designed to investigate in sodium-depleted monkeys the renal hemodynamic and excretory effects resulting from blockade of the renin-angiotensin system induced by intrarenal infusion of the primate-selective renin inhibitor A-65317. Intrarenal infusion of A-65317 (n = 6) at a dose of 0.01 micrograms.kg-1.min-1 elicited an increase (P less than 0.05) in renal blood flow (RBF) from 43.5 +/- 2.7 to 49.4 +/- 4.4 ml/min and glomerular filtration rate (GFR) from 6.3 +/- 0.3 to 6.9 +/- 0.4 ml/min, with no significant changes in mean arterial pressure (MAP) or plasma renin activity (PRA). Increases (P less than 0.05) in the urine flow rate (0.18 +/- 0.04 to 0.28 +/- 0.04 ml/min) and the fractional excretion of sodium (0.18 +/- 0.06 to 0.35 +/- 0.13%) were also observed. After a recovery period, the intrarenal infusion dose of A-65317 was increased to 0.1 microgram.kg-1.min-1 and RBF increased (P less than 0.05) from 42.9 +/- 3.9 to 53.0 +/- 3.7 ml/min in conjunction with a significant 85 +/- 4% inhibition of PRA and a 14 +/- 4 mmHg reduction in MAP. GFR and electrolyte excretion remained at control levels. Intrarenal infusion of vehicle (n = 6) had no significant effect on any of the variables studied. In a separate group of monkeys, intravenous (iv) infusion of A-65317 at 0.01 microgram.kg-1.min-1 (n = 5) did not result in significant changes from control.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhanced intrarenal receptor-mediated prorenin activation in chronic progressive anti-thymocyte serum nephritis rats on high salt intake

2012 ◽  
Vol 303 (1) ◽  
pp. F130-F138 ◽  
Author(s):  
Yanjie Huang ◽  
Tatsuo Yamamoto ◽  
Taro Misaki ◽  
Hiroyuki Suzuki ◽  
Akashi Togawa ◽  
...  
Keyword(s):  
Apical Membrane ◽  
Salt Intake ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
High Salt ◽  
Ang Ii ◽  
Kidney Fibrosis ◽  
High Salt Intake ◽  
Collecting Ducts

Despite suppression of the circulating renin-angiotensin system (RAS), high salt intake (HSI) aggravates kidney injury in chronic kidney disease. To elucidate the effect of HSI on intrarenal RAS, we investigated the levels of intrarenal prorenin, renin, (pro)renin receptor (PRR), receptor-mediated prorenin activation, and ANG II in chronic anti-thymocyte serum (ATS) nephritic rats on HSI. Kidney fibrosis grew more severe in the nephritic rats on HSI than normal salt intake. Despite suppression of plasma renin and ANG II, marked increases in tubular prorenin and renin proteins without concomitant rises in renin mRNA, non-proteolytically activated prorenin, and ANG II were noted in the nephritic rats on HSI. Redistribution of PRR from the cytoplasm to the apical membrane, along with elevated non-proteolytically activated prorenin and ANG II, was observed in the collecting ducts and connecting tubules in the nephritic rats on HSI. Olmesartan decreased cortical prorenin, non-proteolytically activated prorenin and ANG II, and apical membranous PRR in the collecting ducts and connecting tubules, and attenuated the renal lesions. Cell surface trafficking of PRR was enhanced by ANG II and was suppressed by olmesartan in Madin-Darby canine kidney cells. These data suggest the involvement of the ANG II-dependent increase in apical membrane PRR in the augmentation of intrarenal binding of prorenin and renin, followed by nonproteolytic activation of prorenin, enhancement of renin catalytic activity, ANG II generation, and progression of kidney fibrosis in the nephritic rat kidneys on HSI. The origin of the increased tubular prorenin and renin remains to be clarified. Further studies measuring the urinary prorenin and renin are needed.

Iso-Oncotic Volume Expansion in the Nephrotic Syndrome

1993 ◽  
Vol 84 (6) ◽  
pp. 627-632 ◽  
Author(s):  
Ton J. Rabelink ◽  
Joost A. Bijlsma ◽  
Hein A. Koomans
Keyword(s):  
Nephrotic Syndrome ◽  
Plasma Volume ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Renin Angiotensin System ◽  
Sodium Balance ◽  
Sodium Retention ◽  
Plasma Volume Expansion ◽  
Humoral Factors

1. In previous studies we found that albumin infusions caused only a modest natriuresis in the nephrotic syndrome, suggesting that hypovolaemia played no part in the sodium retention of these patients. However, this finding was inconclusive, since the hyperoncocity of the infused albumin probably opposed sodium excretion. 2. In the present study, we examined the effect of sustained (68 h) plasma volume expansion (+18%), by means of iso-oncotic albumin infusions, on renal function, blood pressure, humoral factors and sodium balance. 3. Plasma atrial natriuretic peptide levels increased almost threefold and renin-angiotensin system activity was suppressed. Glomerular filtration rate remained unchanged, whereas estimated renal plasma flow increased, resulting in a further decrease in filtration fraction. 4. The increase in plasma volume expansion was accompanied by a modest increase in sodium excretion, which, however, was less than the amount of sodium daily infused with the albumin solutions and consumed with the diet, so that net sodium was retained. 5. This observation supports the concept that an intrinsic renal defect causes the sodium retention in the nephrotic syndrome, and argues against the therapeutic use of albumin infusions.

scholarly journals Haemodynamic and Renal Effects of Dopexamine after Cardiac Surgery in Children

1996 ◽  
Vol 24 (4) ◽  
pp. 435-439 ◽  
Author(s):  
W. Habre ◽  
M. Beghetti ◽  
C. Roduit ◽  
E. Girardin ◽  
M. Vallotton ◽  
...  
Keyword(s):  
Heart Rate ◽  
Renal Function ◽  
Cardiac Surgery ◽  
Renal Plasma Flow ◽  
Stroke Volume Index ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Volume Index ◽  
Renal Effects ◽  
Fractional Excretion Of Sodium

Dopexamine hydrochloride, a synthetic dopamine analog with predominantly beta and delta agonist properties, has been shown to improve cardiac performance and renal function in adults with heart failure. This study was designed to investigate the haemodynamic and renal effects of dopexamine in children after cardiac surgery. Seven children were selected in whom a need for postoperative vasodilation after cardiac surgery was anticipated. Haemodynamics and renal function were determined under baseline conditions and during a continuous infusion of dopexamine at 2 and 6 μg.kg-1.min-1 for 90 minutes, the sequence being randomized for the initial dose. Cardiac output was measured by thermodilution and glomerular filtration rate (GFR) and renal plasma flow (RPF) by the clearances of inulin and para-aminohippurate respectively. Dopexamine induced a dose-related increase in cardiac index (CI) expressed as mean (SD) from 3.5 (0.7) to 3.9 (0.76) and 4.5 (0.8) l.min.-1m-2 (both P<0.05), and in heart rate (HR) from 107 (17) to 122 (17) and 136 (17) beats.min-1 (P<0.05). Stroke volume index (SVI) and mean systemic pressure were unchanged, but pulmonary wedge pressure decreased from 14 (3) to 11 (4) and 12 (3) mmHg (both P<0.05). Systemic vascular resistances (SVR) decreased from 24 (7) to 20 (5) mmHg.l-1.min-1.m-2 (P<0.05), with dopexamine 6 μg.kg-1.min-1. Renal blood flow (RBF) increased from 319 (113) to 441 (230) and 410 (138) ml.min-1.m-2 (both P<0.05), GFR from 115 (32) to 142 (34) and 146 (29) ml.min-1.1.73m-2 (both P<0.05), urine output and fractional excretion of sodium respectively from 3.12 (2) to 7.16 (8) and 7.21 (6) ml.kg-1 (both P<0.05) and from 2.24 (1) to 4.25 (3.4) (P<0.05) and 3.15 (3.1)% (n.s.). The fraction of CI delivered to the kidneys, the fraction of RBF filtered in the kidneys, plasma renin activity and aldosterone levels remained unchanged. In children after cardiac surgery, dopexamine increases CI at the expense of a concomitant increase in heart rate and demonstrates few selective vascular systemic or intrinsic renal actions.

Renal and vascular effects of C-type and atrial natriuretic peptides in humans

1997 ◽  
Vol 273 (4) ◽  
pp. R1457-R1464 ◽  
Author(s):  
Isabelle Pham ◽  
Saïd Sediame ◽  
Geneviève Maistre ◽  
Françoise Roudot-Thoraval ◽  
Pierre-Etienne Chabrier ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Vascular Effects ◽  
Fractional Excretion Of Sodium ◽  
Endocrine Factor ◽  
Normal Men ◽  
Dose Dependent ◽  
Atrial Natriuretic

C-type natriuretic peptide (CNP) may affect renal and vascular functions differently from atrial natriuretic peptide (ANP). The objective of this study was to compare the renal and vascular actions of CNP to those of ANP in normal men. CNP or ANP (0.005, 0.01, and 0.05 μg ⋅ kg−1 ⋅ min−1) were given by infusion to eight healthy volunteers. CNP caused dose-dependent increases in natriuresis (UNa) and in the fractional excretion of sodium (FENa) with no effect on diuresis (UV), renal plasma flow, and glomerular filtration rate (GFR). Fraction of filtration (FF) increased only with the 0.05 μg ⋅ kg−1 ⋅ min−1CNP dose. ANP caused larger increases in UNa, FENa, and FF than CNP and also increased UV at 0.01 and 0.05 μg ⋅ kg−1 ⋅ min−1and GFR at 0.05 μg ⋅ kg−1 ⋅ min−1. Although the ANP and CNP infusions produced similar elevation in the respective peptides plasma levels, urinary and nephrogenous guanosine 3′,5′-cyclic monophosphate increased less in response to CNP than to ANP. Blood pressure, forearm blood flow, plasma renin activity, and aldosterone remained unaffected during the peptides infusion. Plasma ANP increased slightly during CNP infusion. Our data indicate a higher threshold of renal response to CNP than to ANP. In contrast to ANP, CNP probably may not act as an endocrine factor in humans.

Evidence that intrarenal bradykinin plays a role in regulation of renal function

1993 ◽  
Vol 265 (4) ◽  
pp. E648-E654 ◽  
Author(s):  
H. M. Siragy
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Kinin System ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium

Bradykinin (BK) is produced by the kidney, but the role of the renal kallikrein-kinin system (KKS) in the control of renal function is not understood. We studied the effects of intrarenal infusion of the BK antagonist, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-trifluoroacetic acid (BKA, n = 5) and BK (n = 4) alone or combined with antagonist (BKA 0.025 ng.kg-1 x min-1 + BK 0.25 ng.kg-1 x min-1, n = 4) in uninephrectomized conscious dogs in sodium balance at 10 and 80 meq/day. During low sodium intake, administration of BKA (infusions from 0.025 to 2.5 ng.kg-1 x min-1) caused a significant antidiuresis (P < 0.0001) and antinatriuresis (P < 0.0001) and a decrease in fractional sodium excretion (P < 0.0001). There were no changes in estimated renal plasma flow (RPF) or glomerular filtration rate during intrarenal administration of BKA at 0.025 and 0.25 ng.kg-1 x min-1. A dose of 2.5 ng.kg-1 x min-1 BKA caused a significant decrease in RPF. There were no changes in plasma aldosterone concentration, plasma renin activity, or systemic arterial pressure during intrarenal BKA administration. At 80 meq/day sodium balance (n = 5), intrarenal administration of BKA did not cause any systemic or renal effects. Intrarenal administration of BK at 0.25 ng.kg-1 x min-1 during low sodium balance caused an increase in urine flow rate and urinary sodium excretion. Coinfusion of BK with BKA completely abrogated the renal excretory changes induced by BKA. These data suggest that intrarenal KKS plays a role in control of renal function largely by a tubular mechanism during low sodium intake.

Hormonal interactions and renal function during mechanical ventilation and ANF infusion in humans

1991 ◽  
Vol 70 (1) ◽  
pp. 287-292 ◽  
Author(s):  
P. Andrivet ◽  
S. Adnot ◽  
S. Sanker ◽  
P. E. Chabrier ◽  
I. Macquin-Mavier ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Renal Function ◽  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Positive End Expiratory Pressure ◽  
Hormonal Responses ◽  
Fractional Excretion Of Sodium

To investigate the influence of atrial natriuretic factor (ANF) on renal function during mechanical ventilation (MV), we examined the renal and hormonal responses to synthetic human ANF infusion in eight patients during MV with zero (ZEEP) or 10 cmH2O positive end-expiratory pressure (PEEP). Compared with ZEEP, MV with PEEP was associated with a reduction in diuresis (V) from 208 +/- 51 to 68 +/- 11 ml/h (P less than 0.02), in natriuresis (UNa) from 12.4 +/- 3.3 to 6.2 +/- 2.1 mmol/h (P less than 0.02), and in fractional excretion of sodium (FENa) from 1.07 +/- 0.02), 0.21 to 0.67 +/- 0.17% (P less than 0.02) and with an increase in plasma renin activity (PRA) from 4.83 +/- 1.53 to 7.85 +/- 3.02 ng.ml-1.h-1 (P less than 0.05). Plasma ANF levels markedly decreased during PEEP in four patients but showed only minor changes in the other four patients, and mean plasma ANF levels did not change (163 +/- 33 pg/ml during ZEEP and 126 +/- 30 pg/ml during PEEP). Glomerular filtration rate and renal plasma flow were unchanged. Infusion of ANF (5 ng.kg-1.min-1) during PEEP markedly increased V and UNa by 110 +/- 61 and 107 +/- 26%, respectively, whereas PRA decreased from 7.85 +/- 3.02 to 4.40 +/- 1.5 ng.ml-1.min-1 (P less than 0.05). In response to a 10 ng.kg-1.min-1 ANF infusion, V increased to 338 +/- 79 ml/h during ZEEP but only to 134 +/- 45 ml/h during PEEP (P less than 0.02), whereas UNa increased, respectively, to 23.8 +/- 5.3 and 11.3 +/- 3.3 mmol/h (P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The natriuretic and diuretic response to dopamine is maintained during rat pregnancy

2008 ◽  
Vol 294 (6) ◽  
pp. F1342-F1344 ◽  
Author(s):  
Jennifer M. Sasser ◽  
Chris Baylis
Keyword(s):  
Blood Pressure ◽  
Collecting Duct ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Fractional Excretion ◽  
Sprague Dawley ◽  
Plasma Volume Expansion ◽  
Pregnant Rats ◽  
Dopamine Infusion ◽  
Fractional Excretion Of Sodium

During pregnancy, there is a marked plasma volume expansion due to renal sodium retention. Pregnant rats exhibit a blunted response to natriuretic stimuli that signal via cGMP, and expression and activity of the cGMP phosphodiesterase PDE-5 are upregulated in the inner medullary collecting duct during pregnancy. Here, we tested the hypothesis that the natriuretic response to a cAMP agonist, dopamine, is maintained during pregnancy. Anesthetized pregnant ( day 16) and age-matched virgin Sprague-Dawley rats were used to determine whether dopamine-cAMP-mediated natriuresis remains intact in pregnant rats. Blood pressure, renal clearances of inulin and p-aminohippuric acid, and excretion of sodium were measured during baseline and dopamine infusion periods. Pregnant rats had a lower blood pressure and hematocrit at baseline than their age-matched virgin counterparts. Dopamine infusion decreased blood pressure and increased glomerular filtration rate and renal plasma flow in virgin but not pregnant rats. Dopamine infusion also increased urine volume, sodium excretion, and the fractional excretion of sodium to a similar extent in virgin and pregnant rats. These results indicate that a cAMP-mediated natriuresis and diuresis (stimulated by dopamine) persists in pregnant rats.

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