The Role of Vasopressin in Experimental and Clinical Hypertension

Krakoff, Lawrence R.; Elijovich, Fernando; Barry, Cathy

doi:10.1016/s0272-6386(85)80064-0

Cited by 6 publications

(5 citation statements)

References 67 publications

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“…It was higher in the resistant hypertension than in the controlled blood pressure group [geometric mean 5.7 (confidence interval 95% 5.1–6.4) vs. 2.9 (2.3–3.9) fmol/ml, adjusted P < 0.0001) [35]. In fact older studies have already suggested that AVP may have a role in development of hypertension [36, 37]. However, Kawano et al demonstrated that AVP did not play an important role in mild essential hypertension [38–40].…”

Section: Discussionmentioning

confidence: 99%

Pathophysiology of copeptin in kidney disease and hypertension

Afsar

2017

Clin Hypertens

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Copeptin is derived from the cleavage of the precursor of arginine vasopressin (AVP), produced in an equimolar ratio in hypothalamus and processed during axonal transport AVP is an unstable peptide and has a short half-life of 5–20 min. Unlike AVP, copeptin is a stable molecule and can easily be measured. Recent evidence suggest that increased copeptin levels have been associated with worse outcomes in various clinical conditions including chronic kidney disease (CKD) and hypertension. In this review, the data regarding copeptin with kidney function (evaluated as glomerular filtration rate, increased albumin/protein excretion or both) and hypertension with regard to performed studies, prognosis and pathogenesis was summarised.

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Section: Discussionmentioning

confidence: 99%

Pathophysiology of copeptin in kidney disease and hypertension

Afsar

2017

Clin Hypertens

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“…Since this time, there has been a large volume of published studies describing its role in hypertension, however the results have been equivocal. Experimental studies revealed that AVP antagonism may reduce arterial pressure in Goldblatt 1 and 2 kidney hypertension [5]. Plasma arginine vasopressin was reduced in primary aldosteronism, but elevated in malignant hypertension [5].…”

Section: Introductionmentioning

confidence: 99%

“…Experimental studies revealed that AVP antagonism may reduce arterial pressure in Goldblatt 1 and 2 kidney hypertension [5]. Plasma arginine vasopressin was reduced in primary aldosteronism, but elevated in malignant hypertension [5]. In essential hypertension, there was considerable disagreement among various studies in which plasma vasopressin or urine vasopressin excretion were measured as to whether there is evidence for increased secretion of vasopressin.…”

Section: Introductionmentioning

confidence: 99%

“…In essential hypertension, there was considerable disagreement among various studies in which plasma vasopressin or urine vasopressin excretion were measured as to whether there is evidence for increased secretion of vasopressin. Krakoff et al [5] did not find any conclusive evidence that elevated AVP secretion occurs or is necessary for any form of clinical hypertension. Similarly, Kawano et al [6] demonstrated that AVP did not play an important role in mild essential hypertension through its action on the V 1 receptors regardless of dietary sodium intake.…”

Section: Introductionmentioning

confidence: 99%

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Serum copeptin levels in adolescents with primary hypertension

et al. 2013

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BackgroundThe prevalence of hypertension continues to rise in the pediatric population. In recent years, there has been an increasing amount of reports on serum arginine vasopressin and its derivative, copeptin, in blood pressure control, but its role is still unclear. The objective of this study was to assess serum copeptin in adolescents with essential hypertension.MethodsThe study cohort consisted of 84 subjects (30 girls and 54 boys) aged 11–18 years, divided into two groups: hypertension (HT) – 53 subjects with confirmed primary hypertension and R - reference group – 31 subjects in whom hypertension was excluded on the basis of ambulatory blood pressure monitoring (ABPM) (white-coat hypertension). Serum copeptin concentration was measured using a commercially available enzyme-linked immunosorbent assay kit (USCN).ResultsHypertensive patients had higher serum copeptin levels (median, 267 [Q1–Q3: 151.1–499.7 pg/ml]) than controls (median, 107.3 [Q1–Q3: 36.7–203.4 pg/ml]), (p < 0.01). Statistically significant difference was found both in males and females. In both groups, positive correlations between serum copeptin and uric acid levels (r = 0.31, p < 0.01), albuminuria (r = 0.45, p < 0.01), serum triglycerides (r = 0.3, p < 0.05), body mass index (BMI) standard deviation score (SDS) (r = 0.24, p < 0.05) and 24-h systolic blood pressure (SBP) (r = 0.37, p < 0.01) and diastolic blood pressure (DBP) (r = 0.23, p < 0.05) were found.ConclusionsIn summary, higher serum copeptin levels, a surrogate for arginine vasopressin (AVP) release, are associated not only with systolic and diastolic blood pressure but also with several components of metabolic syndrome including obesity, elevated concentration of triglycerides, albuminuria, and serum uric acid level. However, for the time being, more research is needed in order to confirm the role of serum copeptin as a novel marker of elevated blood pressure and predictor of metabolic syndrome.

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“…Similarly, while plasma vasopressin may be elevated in malignant hypertension, there is no conclusive evidence that vasopressin plays a role in clinical hypertension. 67 Finally, renal hypertension as a consequence of hemodynamically significant renal artery stenosis must be considered as a cause of refractory hypertension. Estimates of the prevalence of renovascular hypertension vary widely.…”

Section: Resistant Hypertension/v/a H-81mentioning

confidence: 99%

The patient with resistant hypertension. Cations, volume, and renal factors.

Vidt

1988

Hypertension

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Hypertension that is truly resistant to modern antihypertensive therapy is uncommon. In the majority of cases, apparent resistance is more likely associated with poor patient adherence, interacting drugs, drug interactions, and inappropriate drug dosages. Sodium and fluid volume play a major role in resistant hypertension. There Is considerable evidence to support the role of dietary sodium restriction in successful nonpbarmacological treatment of hypertension. Salt sensitivity in humans appears to represent at least one factor determining individual susceptibility to variable salt intakes. Sodium and water retention may lead to refractoriness to many antihypertensive agents, and there is evidence to suggest that extracellular fluid volume expansion also plays a role in many hypertensive patients. While retention of sodium and water is well established early in patients with renal parenchymal disease, hypertension associated with progression of renal parenchyma! disease is complicated by other factors that include interactions between hemodynamic and humoral factors, functional changes in adrenergic responses, and structural vascular disease. The role of other cations such as potassium, calcium, and magnesium in resistant hypertension has yet to be established. (Hypertension 11 [Suppl II]: U-76-H-83, 1988) KEY WORDS renal failure resistant hypertension • volume • sodium • cations • hypertension in

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The Role of Vasopressin in Experimental and Clinical Hypertension

Cited by 6 publications

References 67 publications

Pathophysiology of copeptin in kidney disease and hypertension

Pathophysiology of copeptin in kidney disease and hypertension

Serum copeptin levels in adolescents with primary hypertension

The patient with resistant hypertension. Cations, volume, and renal factors.

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