Atrial Natriuretic Peptide Administered as Intravenous Infusion or Bolus Injection to Patients with Liver Cirrhosis and Ascites

Petrillo, Antonio; Scherrer, Urs; Jj, Gonvers; Nussberger, Jürg; Marder, Harold K.; P, de Vane; Waeber, Bernard; Hofstetter,; Hr, Brunner

doi:10.1097/00005344-198809000-00004

Cited by 18 publications

(5 citation statements)

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“…When continuous intravenous infusion of ANP in pharmacological doses was used, an inverse correlation between the natriuretic effect and the dose was observed [17]. Petrillo ef al.…”

Section: Discussionmentioning

confidence: 99%

“…found the same natriuretic effect of ANP bolus injection in doses of 1.0 p g kg-' and 2.0 p g kg-' in only three patients with liver cirrhosis and ascites [ 171. When continuous intravenous infusion of ANP in pharmacological doses was used, an inverse correlation between the natriuretic effect and the dose was observed [17]. Our group has previously found a clear dose-dependent natriuretic and diuretic effect of an ANP analogue given as a bolus injection in doses of 0.3, 1.5, and 3.0 p g kg-' in healthy subjects [ 181.…”

Section: Discussionmentioning

confidence: 99%

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Dose‐response study of atrial natriuretic peptide bolus injection in healthy man

Eiskjer

Pedersen

1993

Eur J Clin Investigation

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The effects of human atrial natriuretic peptide (ANP) on glomerular filtration rate (GFR), renal plasma flow (RPF), urinary flow rate, urinary sodium excretion, tubular function estimated by lithium clearance, and plasma levels of sodium and water homeostatic hormones were studied in a dose-response study with 50 healthy subjects. Placebo or ANP 0.5, 1.0, 1.5, or 2.0 micrograms kg-1 bwt was given as an intravenous bolus injection to five different groups. GFR rose after ANP, whereas no immediate change in RPF was observed. Significant increases with no distinct additional effect of ANP doses higher than 1.0 microgram kg-1 were detected in filtration fraction, urinary flow rate and urinary excretion rate of sodium. Both proximal and distal fractional reabsorption of sodium was reduced and the effect seemed to flatten out at doses higher than 1.0 microgram kg-1. Dose-dependent increases in cyclic guanosine monophosphate in urine and plasma were found after ANP bolus injection, and the rise in both was correlated with the increase in urinary sodium excretion. ANP caused a dose-dependent decrease in blood pressure and an increase in pulse rate. Plasma concentrations of angiotensin II and arginine vasopressin did not change after ANP. In summary, we found that ANP bolus injection caused a natriuresis and diuresis in healthy man with a threshold at a dose of 1.0 microgram kg-1. No distinct further renal effects were observed with higher doses despite dose-dependent increases in urinary cGMP excretion and plasma cGMP. Inhibition of both proximal and distal tubular fractional sodium reabsorption by ANP contributed to the natriuretic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…When continuous intravenous infusion of ANP in pharmacological doses was used, an inverse correlation between the natriuretic effect and the dose was observed [17]. Petrillo ef al.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Dose‐response study of atrial natriuretic peptide bolus injection in healthy man

Eiskjer

Pedersen

1993

Eur J Clin Investigation

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“…Although published data on ANF infusion in patients with cirrhosis are relatively limited, the available reports indicate that many (but not all) patients manifested a blunted natriuretic response to sustained infusion of the peptide [65][66][67][68][69]. Although significant increases in so dium excretion were noted in one study [67], a compar ison was not made with normal subjects having compa rable baseline sodium excretion rates.…”

Section: Renal Responsiveness To Infusion Of Exogenous Peptidementioning

confidence: 99%

Atrial Natriuretic Factor in Patients with Liver Disease

Epstein

1989

Am J Nephrol

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“…However, in animal models and patients with cirrhosis, particularly those with ascites, the renal response to ANF seems to be blunted (31,32). This might be due to alterations in renal ANF receptors (33) as well as to a decrease in mean arterial pressure following ANF administration in cirrhotic subjects (34). Thus, low-dose infusions of ANF may induce greater natriuresis than high-dose infusions.…”

Section: Atrial Natriuretic Factor (Anf)mentioning

confidence: 99%

Medical treatment of ascites in cirrhosis

Gerbes¹

1993

Journal of Hepatology

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Medical treatment of cirrhotic ascites is essentially supportive, dictated by the patient's discomfort, impaired cardiovascular or respiratory function and potential for infection. Treatment of'simple' ascites (moderate fluid accumulation, serum albumin > 3.5 g/dl, serum creatinine < 1.5 mg/di, no electrolyte disturbance) is implemented sequentially. Only 10% of patients respond to dietary sodium restriction and bed rest; most require pharmacotherapy consisting of spironolactone, which increases the proportion of responding patients to 65% and loop diuretics, which may produce clinical improvement in an additional 20% (85% in all); in the remaining 15% of refractory patients, use of novel adjunctive therapies may be attempted. Patients with tense ascites, impaired renal function and electrolyte disturbances merit special consideration before diuretics are introduced. Spironolactone has long been a standard for the treatment of cirrhotic ascites because it directly antagonizes aldosterone. The loop diuretic most frequently added to spironolactone has been furosemide. However, there is preliminary evidence that torasemide may be more effective in some patients. Other investigational agents that may play a role in treatment of patients resistant to conventional drugs include ornipressin (a vasopressin analogue) and atrial natriuretic factor.Key words: Ascites; Atrial natriuretic peptide; Cirrhosis; Diuretics; Liver disease; Ornipressin; Spironolactone; Torasemide A brief overview of the pathophysiology of ascites formation in hepatic cirrhosis (1) can facilitate understanding both of the available therapeutic options and of the rationale for development of new therapeutic approaches. Traditionally, the initiating event of renal sodium and water retention in cirrhosis was considered to be ascites formation (underfilling hypothesis) or primary renal dysfunction due to a hepatorenal reflex (overflow hypothesis) (2). The alterations of systemic, splanchnic and renal haemodynamics, as well as increases in circulating levels of substances that cause sodium retention (3-6), are compatible with a decrease in effective blood volume as suggested by the underfilling hypothesis. These alterations, however, precede ascites formation. The recently introduced vasodilation hypothesis (7) reconciles many aspects of the underfilling theory and the overflow theory; it proposes that peripheral arterial vasodilation is the initiating event leading to decreased effective blood volume and renal sodium retention ( Table 1) and suggests that haemodynamic, hormonal and renal changes are augmented as liver disease becomes more severe. Peripheral arterial vasodilation leads to a decrease in effective arterial blood volume and, in compensation, increases in circulating levels of renin, aldosterone, noradrenaline and vasopressin, which result in renal vasoconstriction with sodium and water retention. With increasing severity of cirrhosis, the activation of these stimulants of sodium retention cannot restore effective blood volume. This, togethe...

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Atrial Natriuretic Peptide Administered as Intravenous Infusion or Bolus Injection to Patients with Liver Cirrhosis and Ascites

Cited by 18 publications

References 0 publications

Dose‐response study of atrial natriuretic peptide bolus injection in healthy man

Dose‐response study of atrial natriuretic peptide bolus injection in healthy man

Atrial Natriuretic Factor in Patients with Liver Disease

Medical treatment of ascites in cirrhosis

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