Vasopressin regulates the renin-angiotensin-aldosterone system via V1a receptors in macula densa cells

Aoyagi, Toshinori; Yokoyama, Izumi; Hiroyama, Masami; Matsuzaki, Takanobu; Yasuoka, Yukiko; Sanbe, Atsushi; Miyazaki, Hiroyuki; Fujiwara, Yoko; Nakayama, Yushi; Kohda, Yukimasa; Yamauchi, Junji; Inoue, Takeaki; Kawahara, Katsumasa; Saito, Hideyuki; Tomita, Kimio; Nonoguchi, Hiroshi; Tanoue, Akito

doi:10.1152/ajprenal.00088.2008

Cited by 67 publications

(72 citation statements)

References 40 publications

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“…Interestingly, these animals also have a reduction in activation of the reninangiotensin system, whereby release of renin from the kidney is reduced in the absence of V1a-receptor-mediated signalling. 5 This evidence links the increase in metabolic rate back with a reduction in angiotensin that we observed in our study. Moreover, other studies have shown that blockade of angiotensin with AT 1 receptor antagonists also reduces body fat, without increasing water intake.…”

supporting

confidence: 78%

Response to ‘Hydration increases cell metabolism’

Mathai

Weisinger

2009

Int J Obes

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supporting

confidence: 78%

Response to ‘Hydration increases cell metabolism’

Mathai

Weisinger

2009

Int J Obes

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“…Previously, we showed that the stimulation of V1aR in the macula densa is the first step of renin production and the deficient of V1aR in macula densa causes hyporeninemic hypoaldosteronism. 19,20 This study shows that the defect in urinary acid excretion in V1aR Ϫ/Ϫ mice is associated with functional defects in the vasopressin V1aR and subsequent changes in Rhcg, H-K-ATPase, and H-ATPase in the intercalated cells of the collecting ducts. Therefore, V1aR is essential not only for aldosterone production but also for tubular effects of aldosterone.…”

Section: V1armentioning

confidence: 73%

“…18 We have found that the deficient of V1aR causes hyporeninemic hypoaldosteronism. 19,20 Therefore, we investigated acid-base balance in mice lacking V1aR (V1aR Ϫ/Ϫ ). Furthermore, because the target site of aldosterone for acid-base regulation is the intercalated cells of the collecting duct, we established a new cell line of the intercalated cells.…”

mentioning

confidence: 99%

Aldosterone Requires Vasopressin V1a Receptors on Intercalated Cells to Mediate Acid-Base Homeostasis

Yokoyama

Hori

Nakayama

et al. 2011

Journal of the American Society of Nephrology

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Both aldosterone and luminal vasopressin may contribute to the maintenance of acid-base homeostasis, but the functional relationship between these hormones is not well understood. The effects of luminal vasopressin likely result from its interaction with V1a receptors on the luminal membranes of intercalated cells in the collecting duct. Here, we found that mice lacking the V1a receptor exhibit type 4 renal tubular acidosis. The administration of the mineralocorticoid agonist fludrocortisone ameliorated the acidosis by restoring excretion of urinary ammonium via increased expression of Rhcg and H-K-ATPase and decreased expression of H-ATPase. In a cell line of intercalated cells established from transgenic rats expressing the mineralocorticoid and V1a receptors, but not V2 receptors, knockdown of the V1a receptor gene abrogated the effects of aldosterone on H-K-ATPase, Rhcg, and H-ATPase expression. These data suggest that defects in the vasopressin V1a receptor in intercalated cells can cause type 4 renal tubular acidosis and that the tubular effects of aldosterone depend on a functional V1a receptor in the intercalated cells. Aldosterone and vasopressin regulates the acidbase balance by proton secretion through reabsorption of bicarbonate and the excretion of ammonium and titratable acid mainly in the collecting ducts. [1][2][3][4] Principal and intercalated cells are present in the collecting ducts. 1,2 Vasopressin regulates sodium and water transport via the V2 receptor (V2R) in the basolateral membrane of the principal cells and subsequent activation of aquaporin 2 and amiloride-sensitive epithelial sodium channel (ENaC), which is also regulated by aldosterone. 5 Although vasopressin is known to act as an anti-diuretic hormone, findings regarding the effects of luminal (urinary) vasopressin have shown that luminal vasopressin acts as an intrinsic diuretic and regulates the anti-diuretic effects of basolateral vasopressin. 6 The effect of luminal vasopressin has been thought to be caused via V1a receptor (V1aR), probably in the luminal membrane of the intercalated cells, given that V2R is not present in the luminal membrane of the collecting ducts. 6 -9 Al-

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“…We have reported that V1a receptordeficient mice showed decreased renin-angiotensin-aldosterone (RAA) system and V2R-AQP2 system. 25 V1aR in the macula densa cells regulates both the RAA system and the V2R-AQP2 system. Increased V1aR in acidosis may stimulate the RAA system and the V2R-APQ2 system, resulting in the increase in AQP2 expression in the collecting ducts in this study.…”

Section: Discussionmentioning

confidence: 99%

Acute and chronic metabolic acidosis interferes with aquaporin-2 translocation in the rat kidney collecting ducts

et al. 2009

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Renal aquaporin-2 (AQP2) expression plays a key role in urine concentration. However, it is not known whether metabolic acidosis affects urine-concentrating ability through AQP2 expression in the kidney and urine. We examined urinary excretion and renal expression of AQP2 in control and acidosis rats, using RT-competitive PCR, immunoblot and immunocytochemistry. Urinary excretion of AQP2 is decreased by 92% even with the increase in AQP2 mRNA and protein expressions in the collecting ducts by metabolic acidosis in rats. Urine osmolality in control rats was 1670 ± 198 mOsm per kg H 2 O, and immunocytochemistry revealed the presence of AQP2 in the apical plasma membrane of the principal cells in the collecting ducts. Urine osmolality in acidosis rats was lower than that in control (1397±243 mOsm per kg H 2 O), and immunocytochemistry showed the diffuse presence of AQP2 in the cytoplasm of the principal cells. Differential centrifugationcoupled immunoblot showed a significant decrease in the ratio of AQP2 in plasma membrane-enriched fraction to that in intracellular vesicle-enriched fraction by metabolic acidosis. In summary, AQP2 translocation is largely decreased by metabolic acidosis even with increased expression in the collecting ducts. A disorder of AQP2 translocation in the collecting ducts with acidosis may be responsible for the diuresis in patients with chronic renal failure.

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Vasopressin regulates the renin-angiotensin-aldosterone system via V1a receptors in macula densa cells

Abstract: A. Vasopressin regulates the renin-angiotensin-aldosterone system via V1a receptors in macula densa cells.

Cited by 67 publications

References 40 publications

Response to ‘Hydration increases cell metabolism’

Response to ‘Hydration increases cell metabolism’

Aldosterone Requires Vasopressin V1a Receptors on Intercalated Cells to Mediate Acid-Base Homeostasis

Acute and chronic metabolic acidosis interferes with aquaporin-2 translocation in the rat kidney collecting ducts

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