The clearance and antidiuretic potency of neurohypophysial hormones in man, and their plasma binding and stability

Fabian, M; Forsling, Mary L.; Jones, Janet; Pryor, J. S.

doi:10.1113/jphysiol.1969.sp008937

Cited by 105 publications

(61 citation statements)

References 26 publications

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“…There have been reports that vasopressin is unstable in blood at ambient temperature. 27 However, we and others 28 have been unable to confirm this.…”

Section: Methodological Considerationscontrasting

confidence: 57%

Plasma and platelet vasopressin in essential hypertension and congestive heart failure.

Preibisz¹,

Sealey²,

Laragh³

et al. 1983

Hypertension

157

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SUMMARY In this study we found that, in 31 normal subjects, close to 90% of circulating arginine vasopressin (AVP), measured by radiolmmunoassay, was associated with platelets. By using routine methods of centrifugation, which do not completely separate platelets, the normal range of plasma vasopressin was higher by twofold than the normal range in platelet-free plasma prepared by differential centrifugation, which was 1.4 ± 1.0 SD pg/ml. Platelet vasopressin was 12.9 ± 5.7 pg/ml. Patients with congestive heart failure had, on average, an elevated platelet-free plasma AVP, as did two patients with thrombocytopenia and one with thrombocytosis. Patients with essential hypertension had slightly high levels of platelet-free plasma AVP and demonstrated an abnormal inverse relationship between platelet-free plasma AVP and serum osmolality. Immunoreactive platelet vasopressin was slightly low in patients with essential hypertension and was subnormal in patients with congestive heart failure. These studies demonstrate that platelets normally present in centrifuged plasma cause an overestimation of the plasma vasopressin levels. Until the physiological meaning of plasma and platelet-bound AVP is understood, studies of circulating vasopressin should probably assess both plasma and platelet AVP levels. 2 Moreover, vasopressin is reported to be involved in various forms.of experimental hypertension, 1 * 9 and lesions of the medulla oblongata have been shown to cause excessive release and acute hypertension. 10 In addition, elevations of urine and plasma vasopressin have been reported in some patients with hypertension"" 13 despite the presence of lower serum sodium. 13On the other hand, the role of vasopressin in the maintenance of hypertension is controversial, 14 " 17 and there is evidence to suggest that vasopressin cannot maintain chronic hypertension because of a compen- Nonetheless, measurements of circulating vasopressin in human hypertension may be of value by providing clues to underlying mechanisms. Vasopressin is released into the circulation in response to either osmotic stimuli or volume-dependent baroreceptor-mediated stimuli. "23 Therefore, assessment of vasopressin levels in relation to serum osmolality should provide evidence of which mechanism is operative in patients who have abnormal levels of vasopressin.In the present study we evaluated arginine vasopressin (AVP) levels in relation to the serum osmolality, in a group of untreated patients with essential hypertension. In the course of this investigation, using a sensitive radioimmunoassay method for vasopressin, 24 we observed abnormally high levels in plasma samples that were contaminated with the buffy coat. We then found that vasopressin levels measured in a platelet fraction were close to tenfold higher than in plateletfree plasma and, that platelet-free plasmas had significantly lower values than in most previous reports. 22 In this paper we report these findings and also the results of vasopressin measurements in platelets and platelet-

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“…There have been reports that vasopressin is unstable in blood at ambient temperature. 27 However, we and others 28 have been unable to confirm this.…”

Section: Methodological Considerationscontrasting

confidence: 57%

Plasma and platelet vasopressin in essential hypertension and congestive heart failure.

Preibisz¹,

Sealey²,

Laragh³

et al. 1983

Hypertension

157

View full text Add to dashboard Cite

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“…5,6 Although AVP was a major contributor to hyponatremia, there was no correlation between sodium and copeptin concentrations in our acute HF population. This observation was noted in previous studies as well.…”

Section: Discussionmentioning

confidence: 98%

“…5 Despite its critical role in free water regulation, AVP is a suboptimal biomarker due its in vitro instability and rapid clearance. 6 Copeptin is synthesized and secreted in equimolar amounts to AVP. Both AVP and copeptin have short halflives in vivo.…”

Section: Clinical Perspective On P 620mentioning

confidence: 99%

Increased 90-Day Mortality in Patients With Acute Heart Failure With Elevated Copeptin

Maisel

Xue

Shah

et al. 2011

Circ: Heart Failure

160

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Background-In patients with heart failure (HF), increased arginine vasopressin concentrations are associated with more severe disease, making arginine vasopressin an attractive target for therapy. However, AVP is difficult to measure due to its in vitro instability and rapid clearance. Copeptin, the C-terminal segment of preprovasopressin, is a stable and reliable surrogate biomarker for serum arginine vasopressin concentrations. Methods and Results-The Biomarkers in Acute Heart Failure (BACH) trial was a 15-center, diagnostic and prognostic study of 1641 patients with acute dyspnea; 557 patients with acute HF were included in this analysis. Copeptin and other biomarker measurements were performed by a core laboratory at the University of Maryland. Patients were followed for up to 90 days after initial evaluation for the primary end point of all-cause mortality, HF-related readmissions, and HF-related emergency department visits. Patients with copeptin concentrations in the highest quartile had increased 90-day mortality (PϽ0.001; hazard ratio, 3.85). Mortality was significantly increased in patients with elevated copeptin and hyponatremia (PϽ0.001; hazard ratio, 7.36). Combined end points of mortality, readmissions, and emergency department visits were significantly increased in patients with elevated copeptin. There was no correlation between copeptin and sodium (rϭ0.047). Conclusions-This study showed significantly increased 90-day mortality, readmissions, and emergency department visits in patients with elevated copeptin, especially in those with hyponatremia. Copeptin was highly prognostic for 90-day adverse events in patients with acute HF, adding prognostic value to clinical predictors, ser um sodium, and natriuretic peptides. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT00537628.(Circ Heart Fail. 2011;4:613-620.)

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“…Estimates of the half-life of either oxytocin or vasopressin range from 3 to 6 min (e.g. Fabian et al, 1969). The half-life is not significantly reduced during pregnancy (Gibbens & Chard, unpublished observations), despite the presence of high circulating levels of a placental enzyme, oxytocinase, which is capable of splitting the molecule of either oxytocin or vasopressin between the N-terminal hemicystine residue and the tyrosine residue (Tuppy & Nesvadba, 1957).…”

mentioning

confidence: 99%

The Posterior Pituitary Gland

Chard

1975

Clinical Endocrinology

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The clearance and antidiuretic potency of neurohypophysial hormones in man, and their plasma binding and stability

Cited by 105 publications

References 26 publications

Plasma and platelet vasopressin in essential hypertension and congestive heart failure.

Plasma and platelet vasopressin in essential hypertension and congestive heart failure.

Increased 90-Day Mortality in Patients With Acute Heart Failure With Elevated Copeptin

The Posterior Pituitary Gland

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