Atrial Natriuretic Peptide-Induced Decreases in Renal Blood Flow in Man: Implications for the Natriuretic Mechanism

1989 ◽  
Vol 77 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Wilbert M. T. Janssen ◽  
Dick de Zeeuw ◽  
Gjalt K. van der Hem ◽  
Paul E. de Jong
Keyword(s):  
Blood Flow ◽  
Atrial Natriuretic Peptide ◽  
Renal Blood Flow ◽  
Natriuretic Peptide ◽  
Vascular Resistance ◽  
Sodium Excretion ◽  
Renal Vascular Resistance ◽  
Urinary Osmolality ◽  
Renal Vascular ◽  
Atrial Natriuretic

1. We studied the effect of a low-dose infusion of atrial natriuretic peptide (ANP) on renal blood flow in healthy volunteers. We additionally investigated the effect of ANP on renal haemodynamic function and on urinary sodium excretion. 2. ANP induced a rise in packed cell volume and a slight increase (but no decrease) in the renal extraction of hippuran. These changes did not offset the observed fall in effective renal plasma flow. Renal blood flow thus truly decreased and renal vascular resistance increased. 3. ANP induced an increase in glomerular filtration rate and a decrease in urinary osmolality in the first hour of ANP infusion, whereas absolute and fractional sodium excretion increased significantly only in the second hour of ANP infusion. The decrease in urinary osmolality in the first hour of ANP infusion correlated with the induced natriuresis. The changes in urinary osmolality and sodium excretion both correlated with the changes in plasma ANP levels. 4. These data indicate that ANP may cause a decrease in renal blood flow and an increase of renal vascular resistance in man. Our results suggest a role for ANP-induced (intra)renal haemodynamic changes in ANP-induced natriuresis, possibly through an increase in the filtered load of sodium into a washed-out medullary interstitium.

scholarly journals Abnormal glomerular response to atrial natriuretic peptide in rats with aortocaval fistulas.

1996 ◽  
Vol 7 (7) ◽  
pp. 1038-1044
Author(s):  
L L Norling ◽  
B A Thornhill ◽  
R L Chevalier
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Renal Blood Flow ◽  
Natriuretic Peptide ◽  
Vascular Resistance ◽  
Sprague Dawley ◽  
And Control ◽  
Atrial Natriuretic

Heart failure is characterized by a blunted natriuretic and diuretic response to atrial natriuretic peptide (ANP). To investigate this, a rat model of compensated high-output heart failure was used to determine whether glomerular response to ANP differs in animals with high cardiac output compared with control animals. An aortocaval (AC) fistula was made below the level of the renal arteries in male Sprague-Dawley rats. At 6 wk, one group of AC fistula (N = 6) and control rats (N = 6) was injected with radiolabeled microspheres for determination of hemodynamic parameters, including cardiac output, renal blood flow, and vascular resistance. Rats with AC fistulas had significant changes in cardiac output (218 +/- 17 versus 57 +/- 11 mL/min, P < or = 0.0001), renal blood flow (3.4 +/-0.7 versus 8.4 +/- 1.9 mL/min Left, P < or = 0.05; 3.0 +/- 0.4 versus 7.2 +/- 1.9 mL/min Right, P < or = 0.05), and total vascular resistance (0.6 +/- 0.1 versus 2.7 +/- 0.4 mm Hg/mL per min, P < 0.001) compared with control animals, respectively. In another group of animals, after 6 wk, glomeruli were isolated from kidneys. Extracellular (EC) and intracellular (IC) cGMP was measured as an indication of glomerular response to ANP. Early glomerular response to ANP (10(-8)mol/L) showed a similar acute 13- to 18-fold rise in IC cGMP after 30 sec exposure to ANP (P < or = 0.0001 versus no ANP; N = 4 AC fistula rats and N = 4 control rats). During 1-h incubations with ANP, glomerular response was characterized by a five- to sevenfold increase in EC cGMP. However, glomeruli of AC fistula rats produced significantly less EC cGMP than did those of control animals (21.3 +/- 2.5 versus 44 +/- 4.9 fMol cGMP/2000 glomeruli, P < = 0.005; N = 5 AC fistula rats and N = 5 control rats, respectively). Probenecid-sensitive transport of EC cGMP between AC fistula and control rats (86% decrease versus 82% decrease) was similar. However, glomeruli from AC fistula animals had significantly less phosphodiesterase activity compared with control animals (3.6 +/- 0.4 versus 5.4 +/- 0.7 nMol cGMP/mg protein per min, P < or = 0.01; N = 4 AC fistula rats and N = 5 control rats, respectively). It is speculated that reduced glomerular generation of cGMP in response to ANP contributes to sodium retention in heart failure, but may be compensated for in part by decreased phosphodiesterase-mediated hydrolysis of cGMP.

Effects of volume expansion on renal nerve activity, renal blood flow, and sodium and water excretion in conscious dogs

1985 ◽  
Vol 249 (5) ◽  
pp. F680-F687 ◽  
Author(s):  
H. Morita ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Renal Vascular Resistance ◽  
Conscious Dogs ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity ◽  
Renal Vascular

Effects of acute volume expansion with isotonic isoncotic 3% dextran in saline were examined on renal nerve activity (RNA), renal blood flow, vascular resistance, and sodium and water excretion in conscious dogs. In intact dogs, acute volume expansion increased mean arterial pressure 15 +/- 3 mmHg, left atrial pressure 5.5 +/- 0.6 mmHg, and decreased RNA 88 +/- 2%, whereas renal blood flow did not change and renal vascular resistance increased slightly. When renal perfusion pressure was maintained at control levels, volume expansion decreased RNA 87 +/- 2% and renal vascular resistance 15 +/- 4%. During the 80-min period after volume expansion, urine flow rate increased 0.66 +/- 0.13 ml/min and sodium excretion rose 3.89 +/- 0.54 mueq X min-1 X kg-1, whereas RNA remained depressed. Arterial baroreceptor denervation (ABD) did not diminish responses of RNA, renal blood flow, renal vascular resistance, or sodium and water excretion to volume expansion. After ABD plus bilateral cervical vagotomy, volume expansion did not decrease RNA, and diuretic and natriuretic responses were significantly attenuated (P less than 0.025). However, responses of renal blood flow to volume expansion were not altered significantly. In conscious dogs with renal denervation, responses of renal blood flow to volume expansion were not impaired, whereas diuretic and natriuretic responses were attenuated (P less than 0.025). Thus, in intact conscious dogs, vagally mediated reflex decreases in RNA induced by acute volume expansion exerted a significant effect on sodium and water excretion but little control of renal blood flow and renal vascular resistance.

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

scholarly journals Losartan does not decrease renal oxygenation and norepinephrine effects in rats after resuscitated hemorrhage

2018 ◽  
Vol 315 (2) ◽  
pp. F241-F246
Author(s):  
Sofia Jönsson ◽  
Jacqueline M. Melville ◽  
Mediha Becirovic-Agic ◽  
Michael Hultström
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Oxygen Tension ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Renal Oxygen Consumption ◽  
Significant Difference ◽  
Renal Vascular

Renin-angiotensin-system blockers are thought to increase the risk of acute kidney injury after surgery and hemorrhage. We found that losartan does not cause renal cortical hypoxia after hemorrhage in rats because of decreased renal vascular resistance, but we did not evaluate resuscitation. We aimed to study losartan’s effect on renal cortical and medullary oxygenation, as well as norepinephrine’s vasopressor effect in a model of resuscitated hemorrhage. After 7 days of losartan (60 mg·kg−1·day−1) or control treatment, male Wistar rats were hemorrhaged 20% of their blood volume and resuscitated with Ringerʼs acetate. Mean arterial pressure, renal blood flow, and kidney tissue oxygenation were measured at baseline and after resuscitation. Finally, the effect of norepinephrine on mean arterial pressure and renal blood flow was investigated. As expected, losartan lowered mean arterial pressure but not renal blood flow. Losartan did not affect renal oxygen consumption and oxygen tension. Mean arterial pressure and renal blood flow were lower after resuscitated hemorrhage. A smaller increase of renal vascular resistance in the losartan group translated to a smaller decrease in cortical oxygen tension, but no significant difference was seen in medullary oxygen tension, either between groups or after hemorrhage. The effect of norepinephrine on mean arterial pressure and renal blood flow was similar in control- and losartan-treated rats. Losartan does not decrease renal oxygenation after resuscitated hemorrhage because of a smaller increase in renal vascular resistance. Further, losartan does not decrease the efficiency of norepinephrine as a vasopressor, indicating that blood pressure may be managed effectively during losartan treatment.

Long-Term versus Short-Term Effects of Hydrochlorothiazide on Renal Haemodynamics in Essential Hypertension

1979 ◽  
Vol 56 (5) ◽  
pp. 463-469 ◽  
Author(s):  
P. Van Brummelen ◽  
M. Woerlee ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Blood Flow ◽  
Essential Hypertension ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Vanillylmandelic Acid ◽  
Plasma Renin Concentration ◽  
Renal Vascular

1. Renal blood flow, glomerular filtration rate, renal vascular resistance and filtration fraction were studied in ten patients with essential hypertension, during placebo, and after 1 week, 3, 6 and 9 months of hydrochlorothiazide. Plasma renin concentration and urinary excretion of vanillylmandelic acid were also measured. 2. Mean arterial pressure was lowered significantly during hydrochlorothiazide, the long-term effect being slightly more pronounced than the short-term effect. 3. The decrease in renal blood flow during the first week (P < 0·01) was followed by a progressive rise. After 9 months renal blood flow was above placebo level in eight of the ten patients. After an initial decrease, glomerular filtration rate returned gradually to its original value. Renal vascular resistance and filtration fraction increased during the first week and declined thereafter. After 3, 6 and 9 months renal vascular resistance was significantly lower compared with placebo values. 4. Plasma renin concentration and urinary excretion of vanillylmandelic acid increased significantly during the first week of hydrochlorothiazide. Subsequently, vanillylmandelic acid fell to below pretreatment amounts (P < 0·05), whereas plasma renin concentration remained elevated. 5. Long-term treatment of essential hypertension with hydrochlorothiazide has a favourable effect on abnormal renal haemodynamics. Besides the influence of blood pressure reduction per se, humoral and neural factors may be involved.

Renal vascular effects of epinephrine infusion in the halothane-anesthetized piglet

1994 ◽  
Vol 72 (4) ◽  
pp. 394-396 ◽  
Author(s):  
Keith J. Harrington ◽  
Robert G. Allen ◽  
Jay W. Dewald
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Renal Vascular Resistance ◽  
Epinephrine Infusion ◽  
Arterial Blood ◽  
Renal Vascular

The objective of this study was to determine the dose–response effects of epinephrine, given by systemic intravenous infusion to the halothane-anesthetized newborn piglet, on renal blood flow, mean arterial blood pressure, and renal vascular resistance. Seven newborn piglets were acutely instrumented. A transit-time ultrasound flow probe was placed around the renal artery and a femoral arterial catheter was placed for blood pressure monitoring. Epinephrine was infused in doubling doses from 0.2 to 3.2 μg∙kg−1∙min−1. Mean arterial blood pressure increased from 54 mmHg (1 mmHg = 133.3 Pa) to an average of 96 mmHg at 3.2 μg∙kg−1∙min−1 of epinephrine. Renal blood flow increased from 165 mL∙min−1∙100 g−1 at baseline to 185 mL∙min−1∙100 g−1 at a dose of 0.2 μg∙kg−1∙min−1 and increased further at 0.4 and 0.8 μg∙kg−1∙min−1 to reach 261 mL∙min−1∙100 g−1. Renal blood flow began to fall at a dose of 3.2 μg∙kg−1∙min−1, remaining however, significantly above baseline (211 mL∙min−1∙100 g−1). Consequently, calculated renal vascular resistance fell as the dose was increased from 0.2 to 0.8 μg∙kg−1∙min−1 and then rose again at 1.6 and 3.2 μg∙kg−1∙min−1, being significantly above baseline at 3.2 μg∙kg−1∙min−1. These results demonstrate that epinephrine when given by systemic infusion to the halothane-anesthetized newborn pig is a renal vasodilator at low doses and causes renal vasoconstriction at moderate to high doses. Renal blood flow remained above baseline at all doses tested, and thus, within the dosage range tested, epinephrine infusion should not cause renal ischemia.Key words: epinephrine, kidney blood flow, piglet, renal vascular resistance.

Canine renal vascular response to hyperoncotic dextran in kidneys with or without glomerular filtration

1983 ◽  
Vol 245 (6) ◽  
pp. F687-F690
Author(s):  
R. W. Gotshall
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Tubuloglomerular Feedback ◽  
Vascular Response ◽  
Anesthetized Dogs ◽  
Tubular Flow ◽  
Renal Vascular

The effect of intrarenal arterial infusion of hyperoncotic dextran on renal hemodynamics and excretion was studied in anesthetized dogs. To examine the role of glomerular filtration and tubular flow in the hemodynamic response, several kidney models were employed. Nonfiltering kidneys (NFK) were produced by combined ischemia and ureteral obstruction (UO). Additionally, kidneys with only UO and a lack of filtration as well as kidneys with only ischemia and glomerular filtration were studied. Renal blood flow in normal kidneys was increased by hyperoncotic dextran from 357 +/- 47 to 486 +/- 65 ml X min-1 X 100 g-1, with a corresponding decrease in renal vascular resistance. Ischemic kidneys responded likewise to the dextran infusion, increasing renal blood flow from 261 +/- 31 to 339 +/- 29 ml X min-1 X 100 g-1. Glomerular filtration rate was reduced by the dextran infusion from 80.1 +/- 7.9 to 60.7 +/- 6.6 in normal kidneys and from 31.8 +/- 9.6 to 20.2 +/- 5.8 ml X min-1 X 100 g-1 in ischemic kidneys. Urine flow and sodium excretion were also reduced in these kidneys. In contrast, both NFK and UO, which lacked filtration and tubular flow, did not vasodilate in response to dextran. Renal blood flow remained unchanged from control values (NFK: 146 +/- 6, UO: 111 +/- 22 ml X min-1 X 100 g-1) in these kidneys. These experiments show that the renal vascular response to hyperoncotic dextran is not due to a change in blood volume or viscosity nor to a direct pharmacologic action of dextran. The most likely explanation is that hyperoncotic dextran alters tubuloglomerular feedback control of renal vascular resistance by decreasing filtration and altering tubular flow and/or composition. However, the involvement of another intrarenal vasodilatory system cannot be discounted.

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