title: Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage.
abstract: BACKGROUND
  Subarachnoid haemorrhage is commonly associated with natriuresis and hyponatraemia. One possible explanation for these features is a defect in the central regulation of renal sodium reabsorption with increased secretion of a natriuretic factor. We investigated whether excess sodium secretion in patients with subarachnoid haemorrhage is related to increased secretion of natriuretic peptides or to the presence of digoxin-like immunoreactive substances.
  
  
  METHODS
  We measured the plasma concentrations of digoxin-like immunoreactive substances (by a fluorescence polarisation immunoassay) and natriuretic peptides, aldosterone, renin, and antidiuretic hormone (by radioimmunoassay) in ten patients with aneurysmal subarachnoid haemorrhage, ten patients undergoing elective craniotomy for cerebral tumours, and 40 healthy controls of similar age and sex distribution. Samples were collected before surgery, 1 h, 4 h, and 12 h after surgery, then daily until 7 days postoperatively in the two groups of patients.
  
  
  RESULTS
  All patients with subarachnoid haemorrhage, but none of the tumour patients, showed increased urine output and urinary excretion of sodium (p = 0.018 for comparison of means of curves to 7 days). The patients with subarachnoid haemorrhage had much higher plasma concentrations of brain natriuretic peptide (BNP) than controls, on admission (mean 15.1 [SE 3.8] vs 1.6 [1.0] pmol/L, p < 0.001) and throughout the study period, accompanied by lower than normal aldosterone concentrations and normal plasma concentrations of atrial and C-type natriuretic peptides (ANP, CNP). The patients with tumours had similar plasma concentrations of ANP, BNP, and CNP to the controls. We did not detect digoxin-like immunoreactive substances in either group of patients.
  
  
  CONCLUSIONS
  Salt-wasting of central origin may induce hyponatraemia in patients with aneurysmal subarachnoid haemorrhage, possibly as a result of increased secretion of BNP with subsequent suppression of aldosterone synthesis.
authors.affiliation: Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Westfälische Wilhelms-Universität Münster, Germany.
authors.forename: E
authors.initials: E
authors.lastname: Berendes
authors.forename: M
authors.initials: M
authors.lastname: Walter
authors.forename: P
authors.initials: P
authors.lastname: Cullen
authors.forename: T
authors.initials: T
authors.lastname: Prien
authors.forename: H
authors.initials: H
authors.lastname: Van Aken
authors.forename: J
authors.initials: J
authors.lastname: Horsthemke
authors.forename: M
authors.initials: M
authors.lastname: Schulte
authors.forename: K
authors.initials: K
authors.lastname: von Wild
authors.forename: R
authors.initials: R
authors.lastname: Scherer
mesh_terms: D001932:Brain Neoplasms / Q000378:metabolism / Q000601:surgery; D002298:Cardenolides; D004077:Digoxin; D004791:Enzyme Inhibitors / Q000097:blood; D005260:Female; D016231:Fluorescence Polarization Immunoassay; D006801:Humans; D007010:Hyponatremia / Q000209:etiology; D002532:Intracranial Aneurysm / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D045283:Natriuretic Agents / Q000097:blood; D020097:Natriuretic Peptide, Brain; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D012503:Saponins / Q000097:blood; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors; D013345:Subarachnoid Hemorrhage / Q000378:metabolism*
chemical_list: D002298:Cardenolides; D004791:Enzyme Inhibitors; D045283:Natriuretic Agents; D009419:Nerve Tissue Proteins; D012503:Saponins; C034504:digoxin-like factors; D020097:Natriuretic Peptide, Brain; D004077:Digoxin; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase