Vasopressin and its role in critical care

Sharman, Andrew; Low, James A.

doi:10.1093/bjaceaccp/mkn021

Cited by 75 publications

(56 citation statements)

References 10 publications

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“…One example is vasopressin, which contains an L-Arg and has a half-life of 10-35 min in humans (80). The D-Arg analog, desmopressin, has a half-life of 3.7 h in healthy human volunteers (81).…”

Section: And Replacing L-amino Acids With D-amino Acidsmentioning

confidence: 99%

Strategic Approaches to Optimizing Peptide ADME Properties

2014

AAPS J

513

429

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Development of peptide drugs is challenging but also quite rewarding. Five blockbuster peptide drugs are currently on the market, and six new peptides received first marketing approval as new molecular entities in 2012. Although peptides only represent 2% of the drug market, the market is growing twice as quickly and might soon occupy a larger niche. Natural peptides typically have poor absorption, distribution, metabolism, and excretion (ADME) properties with rapid clearance, short half-life, low permeability, and sometimes low solubility. Strategies have been developed to improve peptide drugability through enhancing permeability, reducing proteolysis and renal clearance, and prolonging half-life. In vivo, in vitro, and in silico tools are available to evaluate ADME properties of peptides, and structural modification strategies are in place to improve peptide developability.

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Section: And Replacing L-amino Acids With D-amino Acidsmentioning

confidence: 99%

Strategic Approaches to Optimizing Peptide ADME Properties

2014

AAPS J

513

429

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“…1) [18,19,20]. Under normal physiological conditions, changes in plasma osmolality are the main regulator of AVP release [20,23,24,25,26]. In comparison with a rise in plasma osmolality, decreases in plasma volume and blood pressure are less potent stimuli for AVP release, but the magnitude of the potential AVP response to hypovolemia and hypotension exceeds the potential AVP response elicited by an increase in plasma osmolality [23,26].…”

Section: Physiology Of Avpmentioning

confidence: 99%

“…Importantly, the baroreceptor and osmoreceptor pathways do not function in isolation since a reduction in plasma volume increases the sensitivity of the osmoreceptors [26]. AVP release is also stimulated by nausea and pain via central nervous input [19,26].…”

Section: Physiology Of Avpmentioning

confidence: 99%

Dialysis Hypotension: A Role for Inadequate Increase in Arginine Vasopressin Levels? A Systematic Literature Review and Meta-Analysis

Ettema¹,

Zittema²,

Kuipers

et al. 2014

Am J Nephrol

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Background: Intradialytic hypotension is a common complication of hemodialysis (HD). Some studies have suggested that inadequate arginine vasopressin (AVP) increase could play a role in the pathogenesis of intradialytic hypotension. However, AVP levels during HD and its relation to hypotension has never been systematically studied. Summary: PubMed and Embase were searched (1970-2013, search terms ‘vasopressin' and ‘hemodialysis') for studies reporting on AVP levels during standard HD or other dialysis techniques. Observational studies reporting on AVP levels pre- and postdialysis were additionally included in a meta-analysis. Thirty-seven studies were included in the systematic literature review, of which 26 studies were eligible for meta-analysis. The main findings were that pretreatment AVP levels were higher in dialysis patients compared with healthy controls (6.4 ± 3.5 vs. 2.5 ± 1.3 pg/ml, p = 0.003) and that plasma AVP levels showed little or no increase during HD (from 7.0 ± 4.9 to 8.8 ± 9.3, p = 0.433). Significant heterogeneity was found between studies. Meta-regression analysis revealed no significant associations between AVP and patient or study characteristics. Studies on other dialysis techniques showed mixed results regarding the AVP course. The eight studies that addressed the relation between intradialytic hypotension and AVP also showed inconsistent results. Key Messages: Plasma AVP levels are higher in dialysis patients compared with healthy controls, but show little or no increase during HD. The lack of a rise in AVP levels during HD may be pathophysiologically involved in the onset of intradialytic hypotension, but firm conclusions are not possible from our review of the literature.

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“…Vasopressin is metabolized by vasopressinases in the kidney and liver; the hormone's half-life in plasma is 10 -35 minutes (15). The release of vasopressin is promoted by high plasma osmolality, reduced plasma volume, nausea, vomiting, stress, hypoxia, and exercise, as well as dopamine, acetylcholine, angiotensin II, and histamine (16). Vasopressin secretion is inhibited by reduced plasma osmolality, increased plasma volume, alcohol consumption, opioids, and gamma-aminobutyric acid (12,16).…”

mentioning

confidence: 99%

Diabetes Insipidus: Celebrating a Century of Vasopressin Therapy

et al. 2014

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Diabetes mellitus, widely known to the ancients for polyuria and glycosuria, budded off diabetes insipidus (DI) about 200 years ago, based on the glucose-free polyuria that characterized a subset of patients. In the late 19th century, clinicians identified the posterior pituitary as the site of pathology, and pharmacologists found multiple bioactivities there. Early in the 20th century, the amelioration of the polyuria with extracts of the posterior pituitary inaugurated a new era in therapy and advanced the hypothesis that DI was due to a hormone deficiency. Decades later, a subset of patients with polyuria unresponsive to therapy were recognized, leading to the distinction between central DI and nephrogenic DI, an early example of a hormone-resistant condition. Recognition that the posterior pituitary had 2 hormones was followed by du Vigneaud's Nobel Prize winning isolation, sequencing, and chemical synthesis of oxytocin and vasopressin. The pure hormones accelerated the development of bioassays and immunoassays that confirmed the hormone deficiency in vasopressin-sensitive DI and abundant levels of hormone in patients with the nephrogenic disorder. With both forms of the disease, acquired and inborn defects were recognized. Emerging concepts of receptors and of genetic analysis led to the recognition of patients with mutations in the genes for 1) arginine vasopressin (AVP), 2) the AVP receptor 2 (AVPR2), and 3) the aquaporin 2 water channel (AQP2). We recount here the multiple skeins of clinical and laboratory research that intersected frequently over the centuries since the first recognition of DI.

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Vasopressin and its role in critical care

Cited by 75 publications

References 10 publications

Strategic Approaches to Optimizing Peptide ADME Properties

Strategic Approaches to Optimizing Peptide ADME Properties

Dialysis Hypotension: A Role for Inadequate Increase in Arginine Vasopressin Levels? A Systematic Literature Review and Meta-Analysis

Diabetes Insipidus: Celebrating a Century of Vasopressin Therapy

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