Vasopressin Regulates Adrenal Functions by Acting through Different Vasopressin Receptor Subtypes

Author(s):  
E. Grazzini ◽  
G. Boccara ◽  
D. Joubert ◽  
M. Trueba ◽  
T. Durroux ◽  
...  
2005 ◽  
Vol 5 (5) ◽  
pp. 562-567 ◽  
Author(s):  
Wilson Abrao Saad . ◽  
Luiz Antonio de Arru . ◽  
Jose Antunes-Rodrigu . ◽  
William Abrao Saad . ◽  
Ismael Franscisco Mo . ◽  
...  

2000 ◽  
Vol 129 (8) ◽  
pp. 1700-1706 ◽  
Author(s):  
Shigeki Nakamura ◽  
Yoshitaka Yamamura ◽  
Shuji Itoh ◽  
Takahiro Hirano ◽  
Kenji Tsujimae ◽  
...  

1993 ◽  
Vol 136 (2) ◽  
pp. 283-288 ◽  
Author(s):  
C. P. Smith ◽  
R. J. Balment

ABSTRACT The present study was undertaken to determine the involvement of the two established vasopressin receptor subtypes (V1 and V2) in arginine vasopressin (AVP)-induced natriuresis and also to determine whether changes in mean arterial pressure (MAP) and/or the renally active hormones atrial natriuretic peptide (ANP), angiotensin II (AII) and aldosterone are a prerequisite for the expression of AVP-induced natriuresis. In Sprague–Dawley rats which were anaesthetized with Inactin (5-ethyl-5-(1′-methylpropyl)-2-thiobarbiturate) and infused with 0·077 mol NaCl/l, infusion of 63 fmol AVP/min was found to be natriuretic whereas an approximately equipotent dose of the specific V2 agonist [deamino-cis1, d-Arg8]-vasopressin (dDAVP) did not induce natriuresis. The specific V1 antagonist [β-mercapto-β,β-cyclopenta-methylene-propionyl1, O-Me-Tyr2, Arg8]-vasopressin when administered prior to infusion of 63 fmol AVP/min did not inhibit AVP-induced natriuresis. AVP-induced natriuresis was not accompanied by changes in MAP or in the plasma concentrations of the renally active hormones ANP, AII or aldosterone. These results suggest that neither the V1 nor the V2 receptor subtypes are involved in AVP-induced natriuresis. In addition, it was found that changes in MAP, plasma ANP, All or aldosterone concentrations were not a prerequisite for AVP-induced natriuresis. Journal of Endocrinology (1993) 136, 283–288


Endocrinology ◽  
2015 ◽  
Vol 156 (3) ◽  
pp. 777-788 ◽  
Author(s):  
Grazia Tamma ◽  
Nandu Goswami ◽  
Johannes Reichmuth ◽  
Natale G. De Santo ◽  
Giovanna Valenti

Abstract Functioning of the hypothalamic-neurohypophyseal-vasopressin axis is altered in aging, and the pathway may represent a plausible target to slow the process of aging. Arginine vasopressin, a nine-amino acid peptide that is secreted from the posterior pituitary in response to high plasma osmolality and hypotension, is central in this pathway. Vasopressin has important roles in circulatory and water homoeostasis mediated by vasopressin receptor subtypes V1a (vascular), V1b (pituitary), and V2 (vascular, renal). A dysfunction in this pathway as a result of aging can result in multiple abnormalities in several physiological systems. In addition, vasopressin plasma concentration is significantly higher in males than in females and vasopressin-mediated effects on renal and vascular targets are more pronounced in males than in females. These findings may be caused by sex differences in vasopressin secretion and action, making men more susceptible than females to diseases like hypertension, cardiovascular and chronic kidney diseases, and urolithiasis. Recently the availability of new, potent, orally active vasopressin receptor antagonists, the vaptans, has strongly increased the interest on vasopressin and its receptors as a new target for prevention of age-related diseases associated with its receptor-altered signaling. This review summarizes the recent literature in the field of vasopressin signaling in age-dependent abnormalities in kidney, cardiovascular function, and bone function.


1998 ◽  
Vol 125 (7) ◽  
pp. 1463-1470 ◽  
Author(s):  
Atsuo Tahara ◽  
Masayuki Saito ◽  
Toru Sugimoto ◽  
Yuichi Tomura ◽  
Koh-ichi Wada ◽  
...  

2000 ◽  
Vol 400 (1) ◽  
pp. 121-125 ◽  
Author(s):  
Shigeru Ishiguro ◽  
Takashi Iwasaki ◽  
Atsushi Miyamoto ◽  
Toyoki Mori ◽  
Akira Nishio

Author(s):  
Piotr Lipiec ◽  
Marco Metra

Arginine vasopressin (a peptide neuroendocrine hormone) levels are elevated in patients with HF. Acting through 3 receptor subtypes, it can cause vasoconstriction and cardiac remodelling (receptors V1a), adrenocorticotropic hormone release (receptors V1b) and water reabsorption (receptors V2), thereby increasing preload and afterload. Vasopressin-receptor antagonists (vaptans), induce hypotonic diuresis and have been proposed as a treatment option for hyponatraemia, a known complication of HF. Three vaptans have been so tested; tolvaptan, conivaptan and lixivaptan, and  two (tolvaptan and conivaptan) have been approved for clinical use in hyponatraemia (in the USA). The EVEREST trial studied tolvaptan in over 4100 patients hospitalized with an exacerbation of chronic HF with reduced LVEF. No effect was seen on long-term mortality or HF-related morbidity, but there was greater weight loss and better dyspnoea and oedema relief over the short-term.  Similar results were seen in the AQUAMARINE study. The 2016 European HF guidelines, therefore gave the limited recommendation: “Tolvaptan may be used to treat patients with volume overload and resistant hyponatraemia”. Despite targeting  an attractive  therapeutic target,  vasopressin receptor antagonists (vaptans) have to date played only a minor role in our management of HF.


2018 ◽  
Vol 235 (4) ◽  
pp. 1015-1027 ◽  
Author(s):  
Oscar René Hernández-Pérez ◽  
Minerva Crespo-Ramírez ◽  
Yordanka Cuza-Ferrer ◽  
José Anias-Calderón ◽  
Limei Zhang ◽  
...  

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