Effects of nitric oxide system and osmotic stress on Aquaporin-1 in the postnatal heart

Netti, Vanina Alejandra; Iovane, Agustina N.; Vatrella, Mariana C.; Zotta, Elsa; Fellet, Andrea L.; Balaszczuk, Ana M.

doi:10.1016/j.biopha.2016.03.050

Cited by 7 publications

(4 citation statements)

References 37 publications

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“…Thus the possibility exists that NOS3-derived NO acts independent of the classical cAMP/PKA/AQP2 pathway. Such regulation could be through alteration in AQP2 trafficking; one such pathway could conceivably involve Snitrosylation of AQP2 [AQP2 has not been described to our knowledge; however, AQP1 can be S-nitrosylated by NO donors (19)].…”

Section: Discussionmentioning

confidence: 99%

Collecting duct-specific knockout of nitric oxide synthase 3 impairs water excretion in a sex-dependent manner

Gao

Stuart

Pollock

et al. 2016

American Journal of Physiology-Renal Physiology

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Nitric oxide (NO) inhibits collecting duct (CD) Na and water reabsorption. Mice with CD-specific knockout (KO) of NO synthase 1 (NOS1) have salt-sensitive hypertension. In contrast, the role of NOS3 in CD salt and water reabsorption is unknown. Mice with CD NOS3 KO were generated with loxP-flanked exons 9-12 (encodes the calmodulin binding site) of the NOS3 gene and the aquaporin-2 promoter-Cre transgene. There were no differences between control and CD NOS3 KO mice, irrespective of sex, in food intake, water intake, urine volume, urinary Na or K excretion, plasma renin concentration, blood pressure, or pulse during 7 days of normal (0.3%), high (3.17%), or low (0.03%) Na intake. Blood pressure was similar between genotypes during DOCA-high salt. CD NOS3 KO did not alter urine volume or urine osmolality after water deprivation. In contrast, CD NOS3 KO male, but not female, mice had lower urine volume and higher urine osmolality over the course of 7 days of water loading compared with control mice. Male, but not female, CD NOS3 KO mice had reduced urinary nitrite+nitrate excretion compared with controls after 7 days of water loading. Urine AVP and AVP-stimulated cAMP accumulation in isolated inner medullary CD were similar between genotypes. Western analysis did not reveal a significant effect of CD NOS3 KO on renal aquaporin expression. In summary, these data suggest that CD NOS3 may be involved in the diuretic response to a water load in a sex-specific manner; the mechanism of this effect remains to be determined.

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Section: Discussionmentioning

confidence: 99%

Collecting duct-specific knockout of nitric oxide synthase 3 impairs water excretion in a sex-dependent manner

Gao

Stuart

Pollock

et al. 2016

American Journal of Physiology-Renal Physiology

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“…Therefore, when the osmolality of the NP cells decreases, it is possible to regulate the distribution of water inside and outside the cell by reducing the expression of AQP1, thereby maintaining the primary cellular function and activity. Therefore, suppression of AQP1 is a regular regulation of cells to maintain the osmotic pressure balance [26,27]. The previous studies have verified the AQP1 downregulation is identified in the IDD [14], which is an adaptive role for these water channels during the hypo-osmotic condition.…”

Section: Discussionmentioning

confidence: 81%

Hypo-osmolality activates Wnt/β-catenin mediated by AQP1 in nucleus pulposus cells degeneration

Xiao Zhang,

Zheng Lv,

Chengjian Wei

2024

Cell Mol Biol (Noisy-le-grand)

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The goals of this study were to investigate whether Wnt/β-catenin signaling plays a role in hypo-osmolalityrelated degeneration of nucleus pulposus (NP) cells, and if so, to define the mechanism underlying AQP1 in this effect. Human NP cells were cultured under hypo-osmotic (300/350/400 mOsm) and iso-osmotic (450 mOsm) conditions. The cell viability, AQP1, the expression of Wnt/β-catenin signaling, collagen II/I, and MMP3/9 were evaluated. To determine the effects of the Wnt/β-catenin signaling, we used the inhibitor and the activator of Wnt during the hypo-osmotic culture of NP cells. We also examined whether the silencing and overexpressing of the AQP1 gene would affect the Wnt/β-catenin expression in NP cells. Hypo-osmolality caused NP cell degeneration and activated the Wnt/β-catenin signaling but suppressed the AQP1 level. Inhibiting the Wnt/β-catenin signaling alleviated the hypo-osmolality-induced NP cell degeneration. On the contrary, activating Wnt/β-catenin aggravated the NP cell degeneration under hypo-osmotic conditions, which did not affect AQP1 expression. AQP1-overexpressed NP cells exhibited decreased Wnt/β-catenin signaling and alleviated cell degeneration under the hypo-osmotic condition. Besides, AQP1 silencing accelerated NP cell degeneration and activated Wnt/β-catenin expression compared with untreated control. Hypo-osmolality promotes NP cell degeneration via activating Wnt/β-catenin signaling, which is suppressed by AQP1 expression. The upregulation of AQP1 suppressed the Wnt/β-catenin signaling and alleviated the hypo-osmolality induced by the NP cell degeneration.

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“…The cardiac AQP presence and expression depends on various factors such as species, sex, development and aging, with data sometimes being contradictory between species [27]. For example, the presence of AQP1 is high in rat heart at embryonic days 14–16 [26], but the level of expression was substantially reduced after birth [26], and even further decreased postnatally [28]. AQP1 was found in the endocardium of the sheep fetal heart at a very early stage [29], but in contrast to rat, was higher at older developmental stages [30].…”

Section: Aqp Presence In the Heartmentioning

confidence: 99%

“…Dehydration is a severe problem in the pediatric [28] and elderly [161] population, but also in critically ill patients [162], being one of the main causes of mortality. Netti and colleagues [28] demonstrated that rats aged 50 days showed upregulation of cardiac AQP1 expression and appearance of AQP1 in cardiomyocyte plasma membranes in response to water restriction. However, such effects were absent in water-restricted rats of 25 days old.…”

Section: Aqp Modifiers and The Heartmentioning

confidence: 99%

Aquaporin Channels in the Heart—Physiology and Pathophysiology

Verkerk

Lodder

Wilders

2019

IJMS

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Mammalian aquaporins (AQPs) are transmembrane channels expressed in a large variety of cells and tissues throughout the body. They are known as water channels, but they also facilitate the transport of small solutes, gasses, and monovalent cations. To date, 13 different AQPs, encoded by the genes AQP0–AQP12, have been identified in mammals, which regulate various important biological functions in kidney, brain, lung, digestive system, eye, and skin. Consequently, dysfunction of AQPs is involved in a wide variety of disorders. AQPs are also present in the heart, even with a specific distribution pattern in cardiomyocytes, but whether their presence is essential for proper (electro)physiological cardiac function has not intensively been studied. This review summarizes recent findings and highlights the involvement of AQPs in normal and pathological cardiac function. We conclude that AQPs are at least implicated in proper cardiac water homeostasis and energy balance as well as heart failure and arsenic cardiotoxicity. However, this review also demonstrates that many effects of cardiac AQPs, especially on excitation-contraction coupling processes, are virtually unexplored.

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Effects of nitric oxide system and osmotic stress on Aquaporin-1 in the postnatal heart

Cited by 7 publications

References 37 publications

Collecting duct-specific knockout of nitric oxide synthase 3 impairs water excretion in a sex-dependent manner

Collecting duct-specific knockout of nitric oxide synthase 3 impairs water excretion in a sex-dependent manner

Hypo-osmolality activates Wnt/β-catenin mediated by AQP1 in nucleus pulposus cells degeneration

Aquaporin Channels in the Heart—Physiology and Pathophysiology

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