Levels of Atrial Natriuretic Peptide Are Not Always Consistent With Atrial Pressure: Is There Alternative Regulation as Evidenced in Gordon's and Bartter's Syndromes?

Klemm, Shelley A.; Gordon, Richard D.; Tunny, Terry J.; Hawkins, Peter G.; Finn, Wendy L.; Hamlet, Stephen; Kewal, N; Purton, Karen J.

doi:10.1111/j.1440-1681.1989.tb01556.x

Cited by 2 publications

(2 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Could the high, unregulated plasma level of ANP represent an epiphenomenon and not be the direct cause of the renal sodium loss? Blood levels of ANP are inappropriately high in Bartter's syndrome [16], probably resulting from a direct stimulatory effect of prostaglandins on its synthesis [17]. However, this explanation does not appear to be valid in the present patient because plasma levels of ANP were not influenced by indomethacin administration.…”

Section: Discussionmentioning

confidence: 51%

Salt-losing nephropathy associated with inappropriate secretion of atrial natriuretic peptide - a new clinical syndrome

Rodríguez‐Soriano

Vallo

1997

Pediatric Nephrology

View full text Add to dashboard Cite

A state of normokalemic renal sodium wasting associated with an apparently inappropriate secretion of atrial natriuretic peptide (ANP) has not been previously recognized. We here report an 11-year-old boy who presented with a chronic "salt-losing" nephropathy manifested by normonatremic or mildly hyponatremic extracellular fluid volume depletion, hypodipsia, absence of salt appetite, normokalemic metabolic alkalosis, hyper-reninemic hyperaldosteronism, hypertrophy of the juxtaglomerular apparatus, and highly conserved capacities for concentrating diluting the urine. Plasma ANP values were paradoxically elevated (between 10 and 47 fmol/ml), despite the coexistence of intravascular volume depletion and increased plasma levels of renin and aldosterone. Although the patient had some clinical similarities to Bartter's syndrome, fractional sodium chloride (NaCl) reabsorption during hypotonic saline diuresis was normal and no clinical amelioration was observed while on indomethacin therapy. Neither a tumor nor cardiac or cerebral abnormalities, which could be responsible for the increased ANP secretion, were detected. These clinical, biochemical, and histological features have not been previously described together and may represent a new clinical syndrome. The pathophysiology of this entity remains unknown, but an attractive, although unproven, hypothesis is that the renal defect in NaCl reabsorption in this patient could be related to an inappropriate and unregulated secretion of ANP.

show abstract

Section: Discussionmentioning

confidence: 51%

Salt-losing nephropathy associated with inappropriate secretion of atrial natriuretic peptide - a new clinical syndrome

Rodríguez‐Soriano

Vallo

1997

Pediatric Nephrology

View full text Add to dashboard Cite

show abstract

“…In Bartter's syndrome, a condition of chronic volume contraction, prostaglandin (PG) inhibitors reduce inappropriately raised levels of ANP despite volume expansion, suggesting a role for PG in ANP secretion (Gordon et al 1986;Klemm et al 1989). A11 infusion raises PG levels in man in plasma (Usberti et al 1985) and urine (Frdlich et al 1975;Usberti et al 1985).…”

Section: Introductionmentioning

confidence: 99%

Prostaglandins and Systolic Blood Pressure, but Not Angiotensin Ii, Independently Affect Atrial Natriuretic Peptide Levels in Man

Klemm

Gordon

Tunny

et al. 1992

Clin Exp Pharma Physio

Self Cite

View full text Add to dashboard Cite

1. Two hours after a single dose of indomethacin (INDO), plasma renin activity (PRA) and atrial natriuretic peptide (ANP) levels decreased, which is consistent with an effect of lowering prostaglandins (PG). 2. After 48 h of INDO, PRA remained low but ANP had increased, which is consistent with the known effect of prostaglandin inhibitors to cause sodium retention, with a resulting volume expansion. 3. Infusions of angiotension II (AII), which raises diastolic blood pressure (BP) 20 mmHg or more, consistently raised ANP levels. The ANP response to AII infusion was reduced 48 h after INDO, which is consistent with an important role for PG in AII-stimulated ANP release. 4. After PG were blocked with INDO, the stimulating effect of AII on ANP at doses that increased diastolic BP less than 20 mmHg was insignificant, whereas before INDO it was significant. 5. In dose-response studies, INDO increased the systolic BP response but decreased the ANP response to AII, which is consistent with a direct effect of PG on ANP that is independent of systolic BP. 6. Prostaglandins and BP are important in the ANP response to AII infusion in normal subjects, but AII itself appears to have little direct effect on ANP.

show abstract

Levels of Atrial Natriuretic Peptide Are Not Always Consistent With Atrial Pressure: Is There Alternative Regulation as Evidenced in Gordon's and Bartter's Syndromes?

Cited by 2 publications

References 27 publications

Salt-losing nephropathy associated with inappropriate secretion of atrial natriuretic peptide - a new clinical syndrome

Salt-losing nephropathy associated with inappropriate secretion of atrial natriuretic peptide - a new clinical syndrome

Prostaglandins and Systolic Blood Pressure, but Not Angiotensin Ii, Independently Affect Atrial Natriuretic Peptide Levels in Man

Contact Info

Product

Resources

About