Urinary concentrating ability during dehydration in the absence of vasopressin

Gellai, Miklos; Edwards, B. R.; Valtin, Heinz

doi:10.1152/ajprenal.1979.237.2.f100

Cited by 41 publications

(42 citation statements)

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“…An inverse relationship between glomerular filtration rate and renal blood flow on the one hand and urinary concentration on the other hand has been noted in previous studies (Abbrecht and Malvin, 1961;Gellai et al, 1979;Levinsky et al, 1959a). Although the mechanism of this inverse relationship has not been established, it is possible that an increase in GFR and renal blood flow could decrease desmopressin response either by increasing solute concentration of tubular fluid delivered to the collecting duct or by "washing-out* renal interstitial tonicity (Anslow and Wesson, 1955;Atherton et al, 1971;Chan, 1971;de Wardener and DelGreco, 1955).…”

Section: Discussionmentioning

confidence: 54%

“…These studies were undertaken because of the welldocumented effect of glomerular filtration rate (Berliner and Davidson, 1957;Gellai et al, 1979;Levinsky et al, 1959), renal blood flow (Abbrecht and Malvin, 1961), solute excretion rate (Anslow Wesson, 1955;Atherton et al, 1971;deWardener and DelGreco, 1955), and renal interstitial tonicity (Atherton et al, 1971;Chan, 1973Chan, , 1971 to alter the hydro-osmotic effect of vasopressin. In these studies, glomerular filtration rate was estimated from measurements of endogenous creatinine clearance.…”

Section: Role Of Inrrarenal Factorsmentioning

confidence: 99%

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Mechanisms of escape from desmopressin in the rat.

Groß¹,

Kim²

1983

Circulation Research

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SUMMARY. The mechanism(s) of renal escape from the hydro-osmotic effect of vasopressin is unknown. We therefore studied escape in conscious, unrestrained rats receiving continuous intravascular infusions of l-deamino-8-arginine-vasopressin (desmopressin) and hypotonic fluid over 5 days. Escape from desmopressin started 8 hours after exposure and was characterized by a progressive increase in urine flow and decreases in urine osmolality and free water reabsorption. When positive water balance was prevented by matching the rate of infusion of hypotonic fluid to urine flow while maintaining the dose of desmopressin constant, escape did not occur. This suggested that water retention, rather than chronic exposure to desmopressin, mediated the escape. To elucidate the mechanism whereby water retention induces escape from desmopressin, urinary prostaglandin E 2 excretion was measured and found to be increased concomitant with the onset of escape. Prevention of this increase in urinary prostaglandin E2 excretion with indomethacin resulted in additional water retention and a delay in the onset of escape. During the maintenance of escape, after significant water retention occurred, increases in mean arterial pressure, renal blood flow, and glomerular filtration rate were observed. Renal interstitial solute concentration remained constant through escape. Basal and vasopressin-stimulated collecting tubular and thick ascending limb adenylate cyclase did not differ when control and escape animals were compared. These results suggest that enhanced renal synthesis of prostaglandin E 2 facilitates the early phase of escape; later, water retention results in plasma volume expansion with increases in cardiac index, arterial pressure, renal blood flow, and glomerular filtration rate. These systemic and renal hemodynamic alterations may be important in maintaining escape from desmopressin. (CircRes 53: 794-804, 1983)

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Section: Discussionmentioning

confidence: 54%

Section: Role Of Inrrarenal Factorsmentioning

confidence: 99%

Mechanisms of escape from desmopressin in the rat.

Groß¹,

Kim²

1983

Circulation Research

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“…There is clear evidence that vasopressin does indeed increase AQP2 expression. Brattleboro rats have a defect in the neurophysin gene from whose gene product vasopressin is cleaved (84). Thus these animals lack endogenous vasopressin and are profoundly polyuric.…”

Section: Regulation Of Aqp2 Expression Via Vasopressin-dependent Signmentioning

confidence: 99%

Aquaporins in the Kidney: From Molecules to Medicine

Nielsen

Frøkiær

Marples

et al. 2002

Physiological Reviews

1,132

1,022

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The discovery of aquaporin-1 (AQP1) answered the long-standing biophysical question of how water specifically crosses biological membranes. In the kidney, at least seven aquaporins are expressed at distinct sites. AQP1 is extremely abundant in the proximal tubule and descending thin limb and is essential for urinary concentration. AQP2 is exclusively expressed in the principal cells of the connecting tubule and collecting duct and is the predominant vasopressin-regulated water channel. AQP3 and AQP4 are both present in the basolateral plasma membrane of collecting duct principal cells and represent exit pathways for water reabsorbed apically via AQP2. Studies in patients and transgenic mice have demonstrated that both AQP2 and AQP3 are essential for urinary concentration. Three additional aquaporins are present in the kidney. AQP6 is present in intracellular vesicles in collecting duct intercalated cells, and AQP8 is present intracellularly at low abundance in proximal tubules and collecting duct principal cells, but the physiological function of these two channels remains undefined. AQP7 is abundant in the brush border of proximal tubule cells and is likely to be involved in proximal tubule water reabsorption. Body water balance is tightly regulated by vasopressin, and multiple studies now have underscored the essential roles of AQP2 in this. Vasopressin regulates acutely the water permeability of the kidney collecting duct by trafficking of AQP2 from intracellular vesicles to the apical plasma membrane. The long-term adaptational changes in body water balance are controlled in part by regulated changes in AQP2 and AQP3 expression levels. Lack of functional AQP2 is seen in primary forms of diabetes insipidus, and reduced expression and targeting are seen in several diseases associated with urinary concentrating defects such as acquired nephrogenic diabetes insipidus, postobstructive polyuria, as well as acute and chronic renal failure. In contrast, in conditions with water retention such as severe congestive heart failure, pregnancy, and syndrome of inappropriate antidiuretic hormone secretion, both AQP2 expression levels and apical plasma membrane targetting are increased, suggesting a role for AQP2 in the development of water retention. Continued analysis of the aquaporins is providing detailed molecular insight into the fundamental physiology and pathophysiology of water balance and water balance disorders.

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“…The marked reduction of urine volume and the profound increase in urine osmolality to exogenously applied DDAVP in SHRDI and in DI rats demonstrates that the kidney tubules responded normally to vasopressin and that the defect in the ability to concentrate urine in SHRDI was not the result of acquired kidney disease, which confirms that SHRDI respond like DI rats in this respect. 34 " Thus, lack of AVP is responsible for the distinct disturbance of water balance in these rats.…”

Section: Pv Pv So* Somentioning

confidence: 99%

Development of a new strain of spontaneously hypertensive rats homozygous for hypothalamic diabetes insipidus.

Ganten¹,

Rascher²,

Lang³

et al. 1983

Hypertension

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SUMMARY The aim of the present study was to investigate whether the presence of arginine vasopressin (AVP) is necessary for the establishment of high blood pressure in spontaneously hypertensive rats (SHR). For this purpose we crossbred SHR of the stroke-prone substrain (SHRSP) with rats homozygous for hypothalamic diabetes insipidus of the Brattleboro strain (DI) which are unable to synthetize AVP. The successful introduction of the DI gene into the SHRSP strain (SHRDI) was demonstrated by the following observations: In 10-month-old rats, water intake was similarly elevated in SHRDI as in DI rats (137 ± 6.5 vs 125 ± 10.5 ml per 24 hours). AVP was undetectable in the plasma, in the hypothalamus, and in the pituitary of SHRDI and DI rats. Urine osmolality and urinary concentration of sodium and potassium were markedly reduced. SHRDI and DI did not adequately concentrate their urine during an 8-hour period of water deprivation, but both strains of rats responded well with a fall in urine output and a rise in urine osmolality to subcutaneous administration of the non-pressor analog of AVP, DDAVP. Mean arterial blood pressure was markedly increased in SHRDI as well as in SHRSP (184 ± 9.7 vs 197 ± 5.2 mm Hg). Thus, we have developed a new line of spontaneously hypertensive rats homozygous for hypothalamic diabetes insipidus. From this finding it is concluded that AVP is not essential for the development and maintenance of spontaneous hypertension of rats. Authors' Note: The trivial name "Heidelberg Hypertensive Drinkers" (HHD) has been proposed for these rats.AVP-antiserum lowered blood pressure in these rats, it has been concluded that AVP plays a role in the maintenance of high blood pressure in SHRSP. 2In contrast to these results, we have recently found that plasma levels of AVP were below normal in SHRSP at 6, 9, and 12 weeks of age; they were higher than in age-matched Wistar-Kyoto rats (WKY) only in SHRSP older than 24 weeks of age.3 -4 Intravenous administration of specific vasopressor AVP antagonists 3 had no significant influence on mean arterial pressure'-4 and on cardiac output or total peripheral resistance. 4 Furthermore, reduced contents of AVP were found in the hypothalamus, in the brain stem, and in the amygdala of SHRSP.^ From these results we have concluded that circulating AVP does not contribute to the development and maintenance of high blood pressure. The question whether AVP is involved in the pathogenesis of spontaneous hypertension of rats'-2 or not 3 -4 is therefore unresolved.

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Urinary concentrating ability during dehydration in the absence of vasopressin

Cited by 41 publications

References 0 publications

Mechanisms of escape from desmopressin in the rat.

Mechanisms of escape from desmopressin in the rat.

Aquaporins in the Kidney: From Molecules to Medicine

Development of a new strain of spontaneously hypertensive rats homozygous for hypothalamic diabetes insipidus.

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