Response to atrial natriuretic peptide in dogs with hypovolemic acute pancreatitis

1989 ◽  
Vol 256 (2) ◽  
pp. F211-F217
Author(s):  
M. Levy ◽  
P. Cernacek
Keyword(s):  
Blood Pressure ◽  
Acute Pancreatitis ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Sodium Excretion ◽  
Fractional Excretion ◽  
Fractional Excretion Of Sodium ◽  
Acute Renal Insufficiency ◽  
Atrial Natriuretic

The ability of atrial natriuretic peptide (ANP) to preserve renal function in dogs with hypovolemic acute renal insufficiency was tested in anesthetized dogs 4 h after the induction of acute pancreatitis. Plasma volume had decreased by 21.5% and glomerular filtration rate (GFR) by 43.2%. Blood pressure had declined by 30 mmHg. ANP was given intravenously at 50 and 150 ng.kg-1.min-1. With the lower dose, blood pressure (BP), GFR, and clearance of p-aminohippuric acid (CPAH) did not change but urine flow (V) and sodium excretion (UNaV) increased. With the higher dose, BP declined by 25 mmHg, GFR declined, but V and UNaV still increased. When plasma volume was maintained with 4% colloid during the progression of pancreatitis and ANP 50 ng.kg-1.min-1 given, BP declined, GFR did not change, and there was a magnified increment in V and UNaV. The administration of glucagon (5 micrograms/min iv) to dogs with hypovolemic pancreatitis caused BP to decline by 17 mmHg. Despite a major increment in GFR, fractional excretion of sodium increased only slightly, compared with that obtained with ANP. We conclude that glucagon preserves GFR more effectively than ANP in hypovolemia, but ANP is more effective in protecting urinary water and sodium excretion.

Atrial natriuretic peptide and adaptation of sodium urinary excretion in patients with chronic renal failure

1988 ◽  
Vol 75 (3) ◽  
pp. 243-249 ◽  
Author(s):  
Stanislas Czekalski ◽  
Catherine Michel ◽  
Jean-Claude Dussaule ◽  
Philippe Touraine ◽  
Francoise Mignon ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Mean Blood Pressure ◽  
Group Iii ◽  
Sodium Load ◽  
Atrial Natriuretic

1. In order to examine the potential role of endogenous atrial natriuretic peptide (ANP) in modulating the increased sodium excretion per nephron in chronic renal failure, we studied healthy subjects with normal renal function (group I) and patients with moderate (group II) or severe chronic renal failure (group III) before, during and after administration of an intravenous sodium load. All subjects had been on a controlled diet containing 120 mmol of sodium per day for 5 days before the study. 2. Under basal conditions, plasma ANP and fractional excretion of sodium (FENa) were highest in group III. Both parameters increased in response to the sodium load in the three groups studied (P < 0.001). Changes with time differed from group to group (P < 0.05), the more marked response for both parameters being observed in group III. After adjustment with respect to plasma ANP (analysis of covariance), FENa was no longer modified in response to the sodium load, whereas adjustment of FENa with respect to mean blood pressure was without consequence on the significance of its change with time. This demonstrates that plasma ANP, but not mean blood pressure, represents the main factor producing variation in FENa during and after the sodium load. 3. These results suggest an important role for plasma ANP in promoting adaptation of short-term sodium excretion in response to an acute sodium load in patients with chronic renal failure who ingest a normal sodium intake.

Evaluation of SQ 28 603, an inhibitor of neutral endopeptidase, in conscious monkeys

1991 ◽  
Vol 69 (10) ◽  
pp. 1609-1617 ◽  
Author(s):  
Andrea A. Seymour ◽  
Benoni Abboa-Offei ◽  
Magdi M. Asaad ◽  
W. Lynn Rogers
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Neutral Endopeptidase ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Excretory Function ◽  
Plasma Atrial Natriuretic Peptide ◽  
Atrial Natriuretic

The potent neutral endopeptidase inhibitor SQ 28 603 (N-(2-(mercaptomethyl)-1-oxo-3-phenylpropyl)-β-alanine) significantly increased excretion of sodium from 4.9 ± 2.3 to 14.3 ± 2.1 μequiv./min and cyclic 3′,5′-guanosine monophosphate from 118 ± 13 to 179 ± 18 pmol/min after intravenous administration of 300 μmol/kg (~80 mg/kg) in conscious female cynomolgus monkeys. SQ 28 603 did not change blood pressure or plasma atrial natriuretic peptide concentrations in the normal monkeys. In contrast, 1-h infusions of 3, 10, or 30 pmol∙kg−1∙min−1 of human atrial natriuretic peptide lowered blood pressure by −3 ± 4, −9 ± 4, and −27 ± 3 mmHg (1 mmHg = 133.322 Pa), increased cyclic guanosine monophosphate excretion from 78 ± 11 to 90 ± 6, 216 ± 33, and 531 ± 41 pmol/min, and raised plasma atrial natriuretic peptide from 7.2 ± 0.7 to 21 ± 4, 62 ± 12, and 192 ± 35 fmol/mL without affecting sodium excretion. In monkeys receiving 10 pmol∙kg−1∙min−1 of atrial natriuretic peptide, 300 μmol/kg of SQ 28 603 reduced mean arterial pressure by −13 ± 5 mmHg and increased sodium excretion from 6.6 ± 3.2 to 31.3 ± 6.0 μequiv./min, cyclic guanosine monophosphate excretion from 342 ± 68 to 1144 ± 418 pmol/min, and plasma atrial natriuretic peptide from 124 ± 8 to 262 ± 52 fmol/mL. In conclusion, SQ 28 603 stimulated renal excretory function in conscious monkeys, presumably by preventing the degradation of atrial natriuretic peptide by neutral endopeptidase.Key words: atrial natriuretic peptide, neutral endopeptidase, natriuresis, cyclic guanosine monophosphate.

Response of atrial natriuretic peptide to acute saline loading in essential hypertension

1988 ◽  
Vol 255 (6) ◽  
pp. F1085-F1090 ◽  
Author(s):  
A. Mimran ◽  
J. Nussberger ◽  
J. Ribstein ◽  
B. Waeber ◽  
H. R. Brunner
Keyword(s):  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Fractional Excretion ◽  
Normal Subjects ◽  
Saline Loading ◽  
Fractional Excretion Of Sodium ◽  
Atrial Natriuretic

To further investigate the mechanism(s) of the exaggerated natriuretic response of hypertensives to volume expansion (VE; 1,800 ml iv isotonic saline over 3 h), the plasma levels of immunoreactive atrial natriuretic peptide (ANP) were measured in 11 normal subjects (NT) and 12 patients with mild essential hypertension (HT). NT and HT groups were similar with respect to age and basal levels of renin, aldosterone and ANP (34.5 +/- 5.5 in NT and 32.5 +/- 6.3 pg/ml in HT, mean +/- SE). In response to VE, ANP increased to the same extent in both groups (a change of 19.3 +/- 5.2 in NT and of 22.2 +/- 7.1 pg/ml in HT) despite the finding of an exaggerated natriuretic response to VE in essential hypertension (36 +/- 3.5 in NT and 54.9 +/- 6.3 nmol/3 h in HT, P less than 0.02). In addition, the fall in hematocrit and serum protein associated with saline infusion was less marked in HT than NT. The change in ANP induced by VE was inversely correlated with the percent fall in hematocrit and the increment in the fractional excretion of sodium in both groups. These observations suggest that ANPs may participate in the control of the renal response to isotonic VE; however they do not support an unequivocal influence of ANP in the exaggerated natriuretic response to VE of patients with essential hypertension.

Low dose infusion of atrial natriuretic peptide causes salt and water excretion in normal man

1988 ◽  
Vol 74 (4) ◽  
pp. 359-363 ◽  
Author(s):  
Alyn Morice ◽  
Joanna Pepke-Zaba ◽  
Elena Loysen ◽  
Ruth Lapworth ◽  
Michael Ashby ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Low Dose ◽  
Volume Index ◽  
Urinary Volume ◽  
Dose Infusion ◽  
Atrial Natriuretic

1. The effects of low dose infusion of atrial natriuretic peptide (ANP) were observed in a double-blind, placebo-controlled study in six fluid-loaded volunteers. After baseline observations, hourly increments of 0.4, 2 and 10 pmol min−1 kg−1 were infused with continuous observation of heart rate, blood pressure and cardiac output. Plasma ANP, aldosterone, and catecholamines, and urinary volume and sodium excretion, were estimated at half-hourly intervals. 2. ANP infusion resulted in an increase of 35, 98 and 207% in urinary sodium excretion and of 10, 20 and 71% in urinary volume when compared with placebo. Plasma ANP was markedly elevated above placebo levels only during infusion of 10 pmol of ANP min−1 kg−1. 3. No change in heart rate or blood pressure was noted during the study, but a significant fall in stroke volume index was observed during active treatment. Plasma levels of aldosterone and catecholamines were not significantly different on the 2 treatment days. 4. The potent natriuretic and diuretic effects of this peptide at plasma concentrations not significantly elevated from physiological suggest a hormonal role for ANP in the homoeostasis of salt and water balance.

Atrial Natriuretic Peptide as a Regulator of Transvascular Fluid Balance

Physiology ◽  
1996 ◽  
Vol 11 (3) ◽  
pp. 138-143 ◽  
Author(s):  
EM Renkin ◽  
VL Tucker
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Fluid Balance ◽  
Interstitial Fluid ◽  
Fluid Volume ◽  
Interstitial Fluid Volume ◽  
Atrial Natriuretic

Unlike other natriuretics, which act via the kidneys to reduce interstitial fluid volume with little change in plasma volume, atrial natriuretic peptide has important extrarenal actions that enable it to reduce plasma volume preferentially.

Atrial Natriuretic Peptide, Altitude and Acute Mountain Sickness

1989 ◽  
Vol 77 (5) ◽  
pp. 509-514 ◽  
Author(s):  
J. S. Milledge ◽  
J. M. Beeley ◽  
S. McArthur ◽  
A. H. Morice
Keyword(s):  
Body Weight ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Packed Cell Volume ◽  
Sodium Excretion ◽  
Acute Mountain Sickness ◽  
Urine Volume ◽  
Symptom Scores ◽  
Mountain Sickness ◽  
Atrial Natriuretic

1. To investigate the mechanisms of acute mountain sickness, 22 subjects travelled to 3100 m by road and the following day walked to 4300 m on Mount Kenya. Control measurements were made over 2 days at 1300 m before ascent and for 2 days after arrival at 4300 m. These included body weight, 24 h urine volume, 24 h sodium and potassium excretion, blood haemoglobin, packed cell volume, and symptom score for acute mountain sickness. In 15 subjects blood samples were taken for assay of plasma aldosterone and atrial natriuretic peptide. 2. Altitude and the exercise in ascent resulted in a marked decrease in 24 h urine volume and sodium excretion. Aldosterone levels were elevated on the first day and atrial natriuretic peptide levels were higher on both altitude days compared with control. 3. Acute mountain sickness symptom scores showed a significant negative correlation with 24 h urinary sodium excretion on the first altitude day. Aldosterone levels tended to be lowest in subjects with low symptom scores and higher sodium excretion. No correlation was found between changes in haemoglobin concentration, packed cell volume, 24 h urine volume or body weight and acute mountain sickness symptom score. 4. Atrial natriuretic peptide levels at low altitude showed a significant inverse correlation with acute mountain sickness symptom scores on ascent.

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