Renal and Hemodynamic Effects of Atrial Natriuretic Peptide in Patients with Cirrhosis

Fried, T. A.; Aronoff, George R.; Benabe, Julio E.; Brunner, Hans R.; DiBona, Gerald F.; Fleischhauer, Thomas; Lam, Mildred; Lawton, William J.; Luft, Friedrich C.; Martínez‐Maldonado, Manuel; McCullough, Arthur J.; Petrillo, Antonio

doi:10.1097/00000441-199001000-00002

Cited by 16 publications

(4 citation statements)

References 22 publications

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“…ANF appears to play a central role in the deranged sodium homeostasis of cirrhosis, from the early phase of compensated cirrhosis to the late stage of refractory ascites (10,27,28). In the advanced stage of cirrhosis, massive refractory ascites is present, the renin angiotensin aldosterone system and sympathetic nervous system are markedly activated and ANF, even when infused at pharmacological doses, cannot override their effects (11,13,28). In this study, the response to mannitol infusion in a group of ANF nonresponders enabled us to subclassify those patients.…”

Section: Discussionmentioning

confidence: 99%

Refractory Ascites: Modulation of Atrial Natriuretic Factor Unresponsiveness by Mannitol

et al. 1992

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We have previously shown that unresponsiveness to atrial natriuretic factor is a marker of the severity of ascites. The tubular mechanisms are unknown, but it seems that increased reabsorption of sodium proximal to the main site of action of atrial natriuretic factor (i.e., the inner medullary collecting duct) plays an important role. We attempted to decrease the proximal reabsorption of sodium with mannitol in patients unresponsive to atrial natriuretic factor. The results of mannitol in such a group of patients has previously been conflicting. We studied 10 patients with massive, resistant ascites who were off diuretics and on a 20-mmol/day sodium diet for 7 days. Atrial natriuretic factor unresponsiveness was confirmed by failure of a 2-hr atrial natriuretic factor infusion to induce a natriuresis. The next day all patients received an infusion of 40 gm of mannitol and subsequently a combined infusion of mannitol and atrial natriuretic factor. Proximal reabsorption of sodium and water were evaluated by lithium clearance, and glomerular filtration rate and renal blood flow were evaluated by inulin clearance and p-aminohippurate clearances, respectively. Six patients responded to mannitol alone with an increased diuresis (from 39 +/- 7 to 148 +/- 35 ml/hr) and natriuresis (from 0.27 +/- 0.05 mmol/hr to 1.65 +/- 0.53 mmol/hr; p less than 0.05) (responders), whereas four did not (nonresponders). The combination of atrial natriuretic factor and mannitol induced a further significant increase in sodium excretion (3.28 +/- 0.68 mmol/hr) but not in urine excretion, compared with mannitol alone.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Refractory Ascites: Modulation of Atrial Natriuretic Factor Unresponsiveness by Mannitol

et al. 1992

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“…Some of the limitations were foretold in previous studies. For example, in 1990 Fried and colleagues concluded that anaritide-induced decreases in mean arterial pressure may “limit its therapeutic potential” (Fried et al 1990). Concerns were voiced again in 2000, when Lewis and colleagues concluded that anaritide “may be beneficial if the hypotension could be avoided” (Lewis et al 2000).…”

Section: Therapeutics Of Natriuretic Peptidesmentioning

confidence: 99%

Natriuretic Peptides: Their Structures, Receptors, Physiologic Functions and Therapeutic Applications

Potter

Yoder

Flora

et al. 2009

Handbook of Experimental Pharmacology

509

449

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Natriuretic peptides are a family of three structurally related hormone/paracrine factors. Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are secreted from the cardiac atria and ventricles, respectively. ANP signals in an endocrine and paracrine manner to decrease blood pressure and cardiac hypertrophy. BNP acts locally to reduce ventricular fibrosis. C-type natriuretic peptide (CNP) primarily stimulates long bone growth but likely serves unappreciated functions as well. ANP and BNP activate the transmembrane guanylyl cyclase, natriuretic peptide receptor-A (NPR-A). CNP activates a related cyclase, natriuretic peptide receptor-B (NPR-B). Both receptors catalyze the synthesis of cGMP, which mediates most known effects of natriuretic peptides. A third natriuretic peptide receptor, natriuretic peptide receptor-C (NPR-C), clears natriuretic peptides from the circulation through receptor-mediated internalization and degradation. However, a signaling function for the receptor has been suggested as well. Targeted disruptions of the genes encoding all natriuretic peptides and their receptors have been generated in mice, which display unique physiologies. A few mutations in these proteins have been reported in humans. Synthetic analogs of ANP (anaritide and carperitide) and BNP (nesiritide) have been investigated as potential therapies for the treatment of decompensated heart failure and other diseases. Anaritide and nesiritide are approved for use in acute decompensated heart failure, but recent studies have cast doubt on their safety and effectiveness. New clinical trials are examining the effect of nesiritide and novel peptides, like CD-NP, on these critical parameters. In this review, the history, structure, function, and clinical applications of natriuretic peptides and their receptors are discussed.

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“…Chemical preconditioning with either doxorubicin (Ito et al, 2000), atrial natriuretic peptide (Gerbes et al, 1998) or oxidants (Peralta et al, 1999a) decreases hepatic injury in several experimental models of I/R. However, their possible clinical application seems limited owing to difficulties in implementing them in clinical practice, toxicity problems and the side-effects that have been identified (Fried et al, 1990;Olson and Mushlin, 1990;Peralta et al, 1999a).…”

Section: Surgical Strategiesmentioning

confidence: 99%

Past and future approaches to ischemia-reperfusion lesion associated with liver transplantation

et al. 2006

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Renal and Hemodynamic Effects of Atrial Natriuretic Peptide in Patients with Cirrhosis

Cited by 16 publications

References 22 publications

Refractory Ascites: Modulation of Atrial Natriuretic Factor Unresponsiveness by Mannitol

Refractory Ascites: Modulation of Atrial Natriuretic Factor Unresponsiveness by Mannitol

Natriuretic Peptides: Their Structures, Receptors, Physiologic Functions and Therapeutic Applications

Past and future approaches to ischemia-reperfusion lesion associated with liver transplantation

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