Renal escape from vasopressin: role of pressure diuresis

Hall, Jennifer.; Montani, Jean‐Pierre; Woods, L. L.; Mizelle, H. L.

doi:10.1152/ajprenal.1986.250.5.f907

Cited by 24 publications

(30 citation statements)

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“…16,17 Although vasopressin and norepinephrine are powerful peripheral vasoconstrictors, they usually cause only small increases in blood pressure when chronically infused, as long as kidney function is not markedly impaired. 16,17 That these potent vasoconstrictors cause only mild hypertension, even though they initially elicit large increases in vascular resistance and blood pressure during acute infusions, is difficult to explain if one considers that increased peripheral vascular resistance is the primary cause of hypertension. However, the failure of vasopressin or norepinephrine to cause sustained, severe hypertension is understandable if one considers the fact that they also have relatively weak antinatriuretic actions.…”

Section: Servo-control Of Renal Perfusion Pressure In "Vasoconstrictomentioning

confidence: 99%

The Kidney, Hypertension, and Obesity

2003

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Abstract-This paper provides a personal perspective of the role of abnormal renal-pressure natriuresis in the pathogenesis of hypertension. Direct support for a major role of renal-pressure natriuresis in long-term control of arterial pressure and sodium balance comes from studies demonstrating that (1) pressure natriuresis is impaired in all forms of chronic hypertension and (2) prevention of pressure natriuresis from operating, by servo-control of renal perfusion pressure, also prevents the maintenance of sodium balance hypertension. Although the precise mechanisms of impaired pressure natriuresis in essential hypertension have remained elusive, recent evidence suggests that obesity and overweight may play a major role. Obesity increases renal sodium reabsorption and impairs pressure natriuresis by activation of the renin-angiotensin and sympathetic nervous systems and by altered intrarenal physical forces. Chronic obesity also causes marked structural changes in the kidneys that eventually lead to a loss of nephron function, further increases in arterial pressure, and severe renal injury in some cases. Although there are many unanswered questions about the mechanisms of obesity hypertension and renal disease, this is one of the most promising areas for future research, especially in view of the growing, worldwide "epidemic" of obesity.

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Section: Servo-control Of Renal Perfusion Pressure In "Vasoconstrictomentioning

confidence: 99%

The Kidney, Hypertension, and Obesity

2003

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“…5 Recently, Chou et al 17 have shown that AVP-enhanced water permeability in IM- 18 -20 and increased renal perfusion pressure. 21 The escape is also associated with an increase in renal prostaglandins, 19 a decrease in vasopressin receptors, 22 and a decrease in aquaporin water channels. 23 The present study reveals another pathway whereby AVP can affect IMCDs by increasing intracellular Ca 2ϩ and activating NOS and NO production.…”

Section: Second Pathway For Avp Signal Transduction In Imcdsmentioning

confidence: 99%

Vasopressin Increases Intracellular NO Concentration via Ca ²⁺ Signaling in Inner Medullary Collecting Duct

2002

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Abstract-The present study was designed to determine whether arginine vasopressin (AVP) stimulates NO production in the epithelial collecting duct cells of the inner medulla (IMCDs) and if this is mediated through Ca 2ϩ signaling. Thin tissue layers containing IMCDs were dissected from Sprague-Dawley rats. Intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) and NO production were measured in IMCDs by a fluorescence imaging system with the use of fura 2-AM and the cell-permeable form of the NO-sensitive dye 4,5-diaminofluorescein (DAF-2), respectively. AVP (100 nmol/L) produced a rapid peak increase in [Ca 2ϩ ] i of 320Ϯ70 nmol/L within a few seconds and a sustained increase of 120Ϯ62 nmol/L. The peak increase in [Ca 2ϩ ] i was followed by a significant increase of NO production (34Ϯ7 U). This was similar to that produced by 20 mol/L of the NO donor DETA-NONOate (42Ϯ11 U Key Words: vasopressins Ⅲ nitric oxide Ⅲ calcium Ⅲ kidney Ⅲ signal transduction S everal observations in our laboratory have suggested indirectly that arginine vasopressin (AVP) may stimulate the production of NO in the epithelial collecting duct cells of the inner medulla (IMCDs). Using an oxyhemoglobintrapping microdialysis technique, 1 we have found that renal medullary interstitial administration of AVP increases NO in the renal medulla. NO synthase (NOS), measured by L-arginine/L-citrulline conversion, was also observed to be highest in IMCDs, as determined from microdissected tubular and vascular segments. 2 In addition, we have reported that AVP stimulates medullary NO production only through vasopressin V 2 -like receptors 1 and that the mRNA for V 2 receptors was present only in tubules such as medullary thick ascending limbs and collecting ducts 3 but not in the renal vasculature or in the vasa recta. On the basis of these observations, we have proposed that IMCDs may play the largest part in the renal medullary production of NO in response to AVP.The well-recognized classical pathway transducing the effects of AVP on IMCDs is through V 2 receptor activation of adenylyl cyclase, resulting in increased cAMP 4 and an increase in the hydraulic conductivity of IMCDs via the aquaporin shuttle system. 5 AVP has also been shown to increase intracellular Ca 2ϩ in IMCDs possibly via V 2 receptors. 6 However, the effects of this release of Ca 2ϩ have been largely unexplored, and the effect of AVP stimulation on NO production in IMCDs is unknown.Constitutive NOS is known to be modulated by intracellular Ca 2ϩ , 7 and the aim of the present study was to determine whether AVP can stimulate NO production in IMCDs and to clarify whether this is a Ca 2ϩ -dependent pathway. Kojima et al 8 recently established the use of the NO-sensitive dye DAF-2, and the cell-permeable form of this dye (DAF-2DA) has allowed NO detection in individual cells. Therefore, an imaging technique applied to these renal medullary tissue slices that enables the application of the NO-sensitive dye DAF-2DA and the Ca 2ϩ -sensitive dye fura 2-AM has been developed. The present st...

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“…Chief among these is the phenomenon of renal escape from antidiuresis. In animal models of sustained AVP administration and in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH), water loading typically results in free water retention and progressive hyponatremia for several days, which is then followed by escape from the AVP-induced antidiuresis (4,16). With the onset of vasopressin escape, water excretion increases despite sustained administration of AVP, allowing water balance to be reestablished and the serum [Na ϩ ] to be stabilized at a steady, albeit decreased level.…”

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confidence: 99%

Sex differences in vasopressin V₂ receptor expression and vasopressin-induced antidiuresis

Sharma²,

Zheng

et al. 2011

American Journal of Physiology-Renal Physiology

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Because clinical data suggests that females may be more prone to hyponatremia from AVP-mediated antidiuresis, we investigated whether there are sex differences in the expression and function of the renal V 2R. In normal Sprague-Dawley rat kidneys, V 2R mRNA and protein expression was 2.6-and 1.7-fold higher, respectively, in females compared with males. To investigate the potential physiological implications of this sex difference, we studied changes in urine osmolality induced by the AVP V 2R agonist desmopressin. In response to different doses of desmopressin, there was a graded increase in urine osmolality and decrease in urine volume during a 24-h infusion. Females showed greater mean increases in urine osmolality and greater mean decreases in urine volume at 0.5 and 5.0 ng/h infusion rates. We also studied renal escape from antidiuresis produced by water loading in rats infused with desmopressin (5.0 ng/h). After 5 days of water loading, urine osmolality of both female and male rats escaped to the same degree physiologically, but V 2R mRNA and protein in female kidneys was reduced to a greater degree (Ϫ63% and Ϫ73%, respectively) than in males (Ϫ32% and Ϫ48%, respectively). By the end of the 5-day escape period, renal V2R mRNA and protein expression were reduced to the same relative levels in males and females, thereby abolishing the sex differences in V2R expression seen in the basal state. Our results demonstrate that female rats express significantly more V2R mRNA and protein in kidneys than males, and that this results physiologically in a greater sensitivity to V2R agonist administration. The potential pathophysiological implications of these results are that females may be more susceptible to the development of dilutional hyponatremia because of a greater sensitivity to endogenously secreted AVP. renal escape; desmopressin; hyponatremia THE PRIME DETERMINANT OF WATER homeostasis in animals and man is the regulation of urinary free water excretion by circulating plasma levels of the hormone arginine vasopressin (AVP). AVP is a nine-amino acid peptide that is synthesized in magnocellular neural cells located in the hypothalamus. The synthesized peptide is enzymatically cleaved from its prohormone and is transported to the posterior pituitary where it is stored within neurosecretory granules until specific stimuli cause secretion of AVP into the bloodstream (23). Antidiuresis then occurs via interaction of the circulating hormone with AVP V 2 receptors (V 2 Rs) in the kidney, which results in increased water permeability of the collecting duct through the insertion aquaporin-2 (AQP2) water channels into the apical membranes of renal collecting duct principal cells (19). The importance of AVP in water homeostasis is underscored by the pathophysiology that occurs when AVP, or AVP-mediated receptor activation, is either deficient or excessive (27).The most common disorder of AVP dysregulation encountered in clinical medicine is hypoosmolar hyponatremia. Studies of hyponatremia in hospitalized patients have ...

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Renal escape from vasopressin: role of pressure diuresis

Cited by 24 publications

References 0 publications

The Kidney, Hypertension, and Obesity

The Kidney, Hypertension, and Obesity

Vasopressin Increases Intracellular NO Concentration via Ca ²⁺ Signaling in Inner Medullary Collecting Duct

Sex differences in vasopressin V₂ receptor expression and vasopressin-induced antidiuresis

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Renal escape from vasopressin: role of pressure diuresis

Cited by 24 publications

References 0 publications

The Kidney, Hypertension, and Obesity

The Kidney, Hypertension, and Obesity

Vasopressin Increases Intracellular NO Concentration via Ca 2+ Signaling in Inner Medullary Collecting Duct

Sex differences in vasopressin V2 receptor expression and vasopressin-induced antidiuresis

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Vasopressin Increases Intracellular NO Concentration via Ca ²⁺ Signaling in Inner Medullary Collecting Duct

Sex differences in vasopressin V₂ receptor expression and vasopressin-induced antidiuresis