Plasma vasopressin response to osmotic and hemodynamic stimuli in heart failure

Uretsky, Barry F.; Verbalis, Joseph G.; Generalovich, Thomas; Valdes, Anita M.; Reddy, P S

doi:10.1152/ajpheart.1985.248.3.h396

Cited by 47 publications

(54 citation statements)

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“…These levels of vasopressin, although much higher than physiological levels of peripherally measured vasopressin, are within the range of what has been measured in monkey portal blood (26).…”

Section: Resultssupporting

confidence: 70%

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Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Salata¹,

Jarrett²,

Verbalis³

et al. 1988

J. Clin. Invest.

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The diurnal response of ACTH release to intravenously administered arginine vasopressin was tested in normal volunteers given consecutively moderate doses of vasopressin every 15 min (0.1, 03, 1.0, and 3.0 IU) at 2200 h and again at 0700 h (PM/AM). This protocol was repeated 4 wk later with the times reversed (AM/PM). A dose-related increase in ACIH secretion was observed in all subjects. When the AM response of the AM/PM protocol was compared with the PM response of the PM/AM protocol, the release of ACTH was greater in the morning (P < 0.05) as evaluated by the following criteria: peak value of ACTH (129.9±30.4 pg/ml in the AM vs. 57.1±20.2 in the PM), area under the curve (689 in the AM vs.259 in the PM); and, sensitivity of the ACTH dose-response curve (first significant increase in ACTH with 1 IU of vasopressin in the AM but not significant even after 3 IU in the PM). In addition, when the AM vasopressin testing followed a previous evening stimulation (PM/AM protocol), there was a blunted ACTH response compared with the AM/PM protocol.Corticotropin-releasing factor (CRF) is probably the major ACTH secretagogue, but since vasopressin acts synergistically with CRF to produce an augmented release of ACTH, we suggest that the ACTH response to administered vasopressin depends upon the ambient endogenous level of CRF. We interpret our data and published data that CRF produces a lesser release of ACTH in the AM as follows: in the morning endogenous CRF is high and administered CRF produces little further release of ACTH, but administered vasopressin acting synergistically with high endogenous CRF causes a greater release of ACTH; conversely, in the evening endogenous CRF is low and administered CRF causes a greater release of ACHI, but vasopressin (a weak secretagogue by itself) gives a low ACTH response. We conclude that vasopressin stimulation of ACTH secretion can be used as an in vivo bioassay of endogenous CRF, and that there is a diurnal rhythm of CRF in hypophyseal portal blood.

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Section: Resultssupporting

confidence: 70%

“…Plasma AVP was assayed as described previously (26). For statistical analysis, pretest values for ACTH and cortisol were defined as the mean of the -15 min and 0 time values.…”

Section: Methodsmentioning

confidence: 99%

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Salata¹,

Jarrett²,

Verbalis³

et al. 1988

J. Clin. Invest.

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“…However, in edematous states, there appears to be a shift in regulation toward relatively greater influence of the nonosmotic mechanisms. 11 The response to osmotic changes appears to occur at lower plasma osmolality levels in edematous states and is more pronounced, as demonstrated by a greater increment of vasopressin levels in patients with HF compared with non-HF subjects after an osmotic load of mannitol. 11 Several studies have shown a significant elevation in mean values of plasma vasopressin in populations of patients with HF and/or LV dysfunction.…”

Section: Evidence For Elevated Vasopressin Levels In Hf And/or LV Dysmentioning

confidence: 99%

Arginine Vasopressin Antagonists for the Treatment of Heart Failure and Hyponatremia

2008

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A rginine vasopressin has attracted attention as a potentially important neurohormonal mediator of the heart failure (HF) syndrome and hyponatremic states in humans 1 because vasopressin influences renal handling of free water, vasoconstriction, and myocyte biology. 2,3 Several vasopressin antagonists are under development, 4 and one of these agents, conivaptan, recently received US Food and Drug Administration approval for short-term intravenous treatment in patients with euvolemic or hypervolemic hyponatremia. The Role of Vasopressin in HF and HyponatremiaA neurohypophysial hormone, vasopressin (also called antidiuretic hormone [ADH]), affects free water reabsorption by the kidney, body fluid osmolality, blood volume, vasoconstriction, and myocardial contractile function. 2,3 Vasopressin is synthesized by neurosecretory cells located predominantly in the supraoptic and paraventricular hypothalamic nuclei. These neurons have axons terminating in the neural lobe of the posterior pituitary (neurohypophysis) that release vasopressin and oxytocin. 5

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“…Other studies have documented dysregulation of vasopressin levels in the heart failure state. Lack of suppression of vasopressin levels with a water load, 17 as well as exaggerated release in response to an osmotic load, 15 have been reported.…”

Section: Discussionmentioning

confidence: 99%

Acute Hemodynamic Effects of Conivaptan, a Dual V _1A and V ₂ Vasopressin Receptor Antagonist, in Patients With Advanced Heart Failure

et al. 2001

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Background-Arginine vasopressin may contribute to abnormalities in hemodynamics and fluid balance in heart failure through its actions on V 1A (vascular and myocardial effects) and V 2 receptors (renal effects). Inhibiting the action of vasopressin may be beneficial in patients with heart failure. Methods and Results-A total of 142 patients with symptomatic heart failure (New York Heart Association class III and IV) were randomized to double-blind, short-term treatment with conivaptan, a dual V 1a /V 2 vasopressin receptor antagonist, at a single intravenous dose (10, 20, or 40 mg) or placebo. Compared with placebo, conivaptan at 20 and 40 mg significantly reduced pulmonary capillary wedge pressure (Ϫ2.6Ϯ0.7, Ϫ5.4Ϯ0.7, and Ϫ4.6Ϯ0.7 mm Hg for placebo and 20 and 40 mg groups, respectively; PϽ0.05) and right atrial pressure (Ϫ2.0Ϯ0.4, Ϫ3.7Ϯ0.4, and Ϫ3.5Ϯ0.4 mm Hg for placebo and 20 and 40 mg groups, respectively; PϽ0.05) during the 3-to 6-hour interval after intravenous administration. Conivaptan significantly increased urine output in a dose-dependent manner (Ϫ11Ϯ17, 68Ϯ17, 152Ϯ19, and 176Ϯ18 mL/hour for placebo and 10, 20, and 40 mg groups, respectively; PϽ0.001) during the first 4 hours after the dose. Changes in cardiac index, systemic and pulmonary vascular resistance, blood pressure, and heart rate did not significantly differ from placebo. Conclusions-In patients with advanced heart failure, vasopressin receptor antagonism with conivaptan resulted in favorable changes in hemodynamics and urine output without affecting blood pressure or heart rate. These data suggest that vasopressin is functionally significant in advanced heart failure and that further investigations are warranted to examine the effects of conivaptan on symptom relief and natural history in such patients. Key Words: heart failure Ⅲ hemodynamics Ⅲ hormones A rginine vasopressin is a peptide hormone with significant cardiovascular and renal effects. 1-3 These effects are mediated through at least 2 receptor subtypes: the V 1A receptor, which is found on vascular smooth muscle cells and in the myocardium, and V 2 receptors, which are found in the distal tubule of the kidney. 2,3 Stimulation of the V 1A receptor results in vasoconstriction in the peripheral and coronary circulations and has other effects, including increasing intracellular calcium levels in cardiac myocytes. [2][3][4] Recent studies have also demonstrated that arginine vasopressin increases the rate of protein synthesis in the myocardium, leading to myocyte hypertrophy, a direct effect mediated by the V 1A receptor. [5][6][7] The V 2 receptor mediates renal water retention and is predominantly responsible for the antidiuretic effect of this hormone. 2,3 Under normal circumstances, vasopressin release is predominantly influenced by small changes in plasma osmolality, resulting in tight regulation of serum osmolality and serum sodium levels. 3 In heart failure and left ventricular (LV) dysfunction, however, numerous nonosmotic mechanisms assume a more prominent role in the contro...

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Plasma vasopressin response to osmotic and hemodynamic stimuli in heart failure

Cited by 47 publications

References 0 publications

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Arginine Vasopressin Antagonists for the Treatment of Heart Failure and Hyponatremia

Acute Hemodynamic Effects of Conivaptan, a Dual V _1A and V ₂ Vasopressin Receptor Antagonist, in Patients With Advanced Heart Failure

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Plasma vasopressin response to osmotic and hemodynamic stimuli in heart failure

Cited by 47 publications

References 0 publications

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

Arginine Vasopressin Antagonists for the Treatment of Heart Failure and Hyponatremia

Acute Hemodynamic Effects of Conivaptan, a Dual V 1A and V 2 Vasopressin Receptor Antagonist, in Patients With Advanced Heart Failure

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Acute Hemodynamic Effects of Conivaptan, a Dual V _1A and V ₂ Vasopressin Receptor Antagonist, in Patients With Advanced Heart Failure