Vasopressin: Sexual Dimorphism in Secretion, Cardiovascular Actions and Hypertension

Share, Leonard; Crofton, J. T.; Ouchi, Y.

doi:10.1097/00000441-198804000-00017

Cited by 56 publications

(29 citation statements)

References 23 publications

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“…16 -19 These observations may be relevant to patients with AD-PKD. AVP secretion is more sensitive to osmotic stimuli, 22 and plasma and/or urinary AVP levels [23][24][25] and urine osmolality 26 are higher in men than in women. Whether men have a higher or a lower renal sensitivity to AVP than women is not clear, because studies on this issue are not in agreement.…”

Section: Resultsmentioning

confidence: 99%

Vasopressin Directly Regulates Cyst Growth in Polycystic Kidney Disease

Wang

Ward

et al. 2008

Journal of the American Society of Nephrology

244

187

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The polycystic kidney diseases (PKD) are a group of genetic disorders causing renal failure and death from infancy to adulthood. Arginine vasopressin (AVP) V2 receptor antagonists inhibit cystogenesis in animal models of cystic kidney diseases, presumably by downregulating cAMP signaling, cell proliferation, and chloride-driven fluid secretion. For confirmation that the protective effect of these drugs is due to antagonism of AVP, PCK (Pkhd1 ), and adolescent nephronophthisis (pcy mouse) by downregulating cAMP signaling, cell proliferation, and chloride-driven fluid secretion. [3][4][5] Clinical trials with V2 receptor antagonists have been initiated. The mechanism by which these drugs inhibit the development of polycystic kidney disease has not been fully elucidated. In addition to V2 antagonism, these drugs could exert an effect by favoring the action of AVP on V1a receptors or by an AVP unrelated mechanism. RESULTS AND DISCUSSIONTo confirm that inhibition of AVP action on the kidney accounts for the effect of V2 receptor antagonists on the development of PKD, we generated PCK AVP ϩ/ϩ , PCK AVP ϩ/Ϫ , and PCK AVP Ϫ/Ϫ rats, as well as wild-type and Brattleboro controls, by breeding F1 rats resulting from PCK (Pkhd1 Ϫ/Ϫ ) and Brattleboro (AVP Ϫ/Ϫ ) crosses. PCK rats are homozygous for a splicing mutation (IVS35-2A3 T)

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Section: Resultsmentioning

confidence: 99%

Vasopressin Directly Regulates Cyst Growth in Polycystic Kidney Disease

Wang

Ward

et al. 2008

Journal of the American Society of Nephrology

244

187

View full text Add to dashboard Cite

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“…ADH secretion seems to be more sensitive to osmotic stimuli in males than in females (49). A higher sensitivity to ADH in humans is also suggested by the higher urine osmolarity observed in men compared to women who exhibit similar plasma vasopressin levels (59).…”

Section: Changes In Sodium and Water Handlingmentioning

confidence: 95%

Gender-dependent effects of aging on the kidney

Gava

Freitas

Meyrelles

et al. 2011

Braz J Med Biol Res

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“…V1a receptors (V1aR), abundantly expressed in vascular smooth muscle cells, and signaling through calcium and phosphatidylinositol transducer pathways, are responsible for the pressor effects. V2 receptors (V2R), expressed mainly in principal cells of the renal collecting duct (CD), and signaling through cAMP, mediate the antidiuretic actions of the hormone (113).Vasopressin is elevated in some forms of human hypertension (26,92,111) and in animal models of hypertension (see reviews in Refs. 91 and 108).…”

mentioning

confidence: 99%

“…Vasopressin is elevated in some forms of human hypertension (26,92,111) and in animal models of hypertension (see reviews in Refs. 91 and 108).…”

mentioning

confidence: 99%

Vasopressin V2 receptors, ENaC, and sodium reabsorption: a risk factor for hypertension?

Bankir

Bichet

Bouby

2010

American Journal of Physiology-Renal Physiology

106

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Excessive sodium reabsorption by the kidney has long been known to participate in the pathogenesis of some forms of hypertension. In the kidney, the final control of NaCl reabsorption takes place in the distal nephron through the amiloride-sensitive epithelial sodium channel (ENaC). Liddle's syndrome, an inherited form of hypertension due to gain-of-function mutations in the genes coding for ENaC subunits, has demonstrated the key role of this channel in the sodium balance. Although aldosterone is classically thought to be the main hormone regulating ENaC activity, several studies in animal models and in humans highlight the important effect of vasopressin on ENaC regulation and sodium transport. This review summarizes the effect of vasopressin V2 receptor stimulation on ENaC activity and sodium excretion in vivo. Moreover, we report the experimental and clinical data demonstrating the role of renal ENaC in water conservation at the expense of a reduced ability to excrete sodium. Acute administration of the selective V2 receptor agonist dDAVP not only increases urine osmolality and reduces urine flow rate but also reduces sodium excretion in rats and humans. Chronic V2 receptor stimulation increases blood pressure in rats, and a significant correlation was found between blood pressure and urine concentration in healthy humans. This led us to discuss how excessive vasopressin-dependent ENaC stimulation could be a risk factor for sodium retention and resulting increase in blood pressure. water conservation; antidiuresis; sodium excretion; collecting duct VASOPRESSIN WAS FIRST IDENTIFIED as a pressor hormone and later recognized to be also a potent antidiuretic hormone. Today, these early historical discoveries have been explained by the identification of different receptor types. V1a receptors (V1aR), abundantly expressed in vascular smooth muscle cells, and signaling through calcium and phosphatidylinositol transducer pathways, are responsible for the pressor effects. V2 receptors (V2R), expressed mainly in principal cells of the renal collecting duct (CD), and signaling through cAMP, mediate the antidiuretic actions of the hormone (113).Vasopressin is elevated in some forms of human hypertension (26,92,111) and in animal models of hypertension (see reviews in Refs. 91 and 108). This hormone has long been suspected to play a role in blood pressure control because of its vasoconstrictive effects, well demonstrated in vitro. However, the studies trying to evaluate the contribution of V1aR-dependent effects in hypertension are inconclusive [either in favor of (27,35,70) or against (59, 98)].Excessive sodium reabsorption by the kidney is known to participate in the pathogenesis of some forms of hypertension.Among the genes responsible for monogenic forms of blood pressure disorders identified to date, the majority either mediate renal sodium transport in the distal part of the nephron or are involved in its regulation. Loss of function of the corresponding proteins leads to salt-wasting states with hypotension (48), ...

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Vasopressin: Sexual Dimorphism in Secretion, Cardiovascular Actions and Hypertension

Cited by 56 publications

References 23 publications

Vasopressin Directly Regulates Cyst Growth in Polycystic Kidney Disease

Vasopressin Directly Regulates Cyst Growth in Polycystic Kidney Disease

Gender-dependent effects of aging on the kidney

Vasopressin V2 receptors, ENaC, and sodium reabsorption: a risk factor for hypertension?

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