How Does the Brain Sense Osmolality?

Verbalis, Joseph G.

doi:10.1681/asn.2007070825

Cited by 58 publications

(42 citation statements)

References 19 publications

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“…A feature that sets AQP2 apart from the other members of the AQP family is that VP largely mediates its expression. VP secretion from the posterior pituitary gland varies in response to plasma osmolality (170). As discussed below, VP participates in both short-term (minutes) and long-term (hours or days) regulation of CD water permeability by binding to the V 2 receptor located in the basolateral membrane of CD principal cells, which in turn leads to activation of the G s ␣/adenylyl cyclase system, increased concentrations of intracellular cAMP and PKA activation (94).…”

Section: The Aqp2 Water Channelmentioning

confidence: 99%

Controlled aquaporin-2 expression in the hypertonic environment

Hasler¹

2009

American Journal of Physiology-Cell Physiology

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The corticomedullary osmolality gradient is the driving force for water reabsorption occurring in the kidney. In the collecting duct, this gradient allows luminal water to move across aquaporin (AQP) water channels, thereby increasing urine concentration. However, this same gradient exposes renal cells to great osmotic challenges. These cells must constantly adapt to fluctuations of environmental osmolality that challenge cell volume and incite functional change. This implies profound alterations of cell phenotype regarding water permeability. AQP2 is an essential component of the urine concentration mechanism whose controlled expression dictates apical water permeability of collecting duct principal cells. This review focuses on changes of AQP2 abundance and trafficking in hypertonicity-challenged cells. Intracellular mechanisms governing these events are discussed and the biological relevance of altered AQP2 expression by hypertonicity is outlined.

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Section: The Aqp2 Water Channelmentioning

confidence: 99%

Controlled aquaporin-2 expression in the hypertonic environment

Hasler¹

2009

American Journal of Physiology-Cell Physiology

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“…In the general circulation, secreted AVP regulates water homeostasis by increasing water permeability of the collecting duct of the kidney, and oxytocin regulates labor and milk let down by causing the respective contraction of the smooth muscle of the uterus and of the myoepithelial cells of breast ducts (for review, see Burbach et al, 2001; Gimpl and Fahrenholz, 2001; Verbalis, 2007). These physiological activities are conserved: in teleost fish, the AVP-like neuropeptide (Avpl) (a.k.a.…”

Section: Introductionmentioning

confidence: 99%

The Hypothalamic Neuropeptide Oxytocin Is Required for Formation of the Neurovascular Interface of the Pituitary

et al. 2011

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SUMMARY The hypothalamo-neurohypophyseal system (HNS) is the neurovascular structure through which the hypothalamic neuropeptides oxytocin and arginine-vasopressin exit the brain into the bloodstream, where they go on to affect peripheral physiology. Here, we investigate the molecular cues that regulate the neurovascular contact between hypothalamic axons and neurohypophyseal capillaries of the zebrafish. We developed a transgenic system in which both hypothalamic axons and neurohypophyseal vasculature can be analyzed in vivo. We identified the cellular organization of the zebrafish HNS as well as the dynamic processes that contribute to formation of the HNS neurovascular interface. We show that formation of this interface is regulated during development by local release of oxytocin, which affects endothelial morphogenesis. This cell communication process is essential for the establishment of a tight axovasal interface between the neurons and blood vessels of the HNS. We present a unique example of axons affecting endothelial morphogenesis through secretion of a neuropeptide.

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“…Release of the antidiuretic hormone arginine vasopressin (AVP) in response to increases in osmolality is controlled by specific and highly sensitive osmoreceptors in the hypothalamus (9,10). Hypoosmolar conditions trigger an adaptation to maintain cell volume by extruding intracellular solutes, including electrolytes and organic osmolytes, in cells of the brain and peripheral tissues.…”

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confidence: 99%

Osteoclast Response to Low Extracellular Sodium and the Mechanism of Hyponatremia-induced Bone Loss

Bársony

Sugimura

Verbalis

2011

Journal of Biological Chemistry

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160

146

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Our recent animal and human studies revealed that chronic hyponatremia is a previously unrecognized cause of osteoporosis that is associated with increased osteoclast numbers in a rat model of the human disease of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). We used cellular and molecular approaches to demonstrate that sustained low extracellular sodium ion concentrations ( Hyponatremia, defined as serum sodium ion concentration ([Na ϩ ]) less than 135 mmol/liter, is a frequently encountered electrolyte abnormality in patients. Chronic hyponatremia is an especially common disorder in elderly people, often due to the dysregulation of hypothalamic osmoregulatory mechanisms, leading to the syndrome of inappropriate antidiuretic hormone secretion (SIADH).2 Hyponatremia may also arise from chronic heart failure or cirrhosis and from treatment with a large number of drugs, including diuretics and selective serotonin reuptake inhibitors. The estimated prevalence of chronic hyponatremia in the United States is in the range of 3.2-6.1 million persons annually, 75-80% of whom are without obvious neurological symptoms. Although chronic hyponatremia is often considered to be "asymptomatic," recent reports have shown its adverse effects, namely impaired gait stability and neurocognitive functions and, therefore, a greater risk of falls and fractures. In one recent case-controlled study of asymptomatic chronic hyponatremic patients, even mild hyponatremia was associated with a 67-fold increased odds ratio for falling compared with normonatremic controls. Even more alarming, a recent study from Belgium found that mild asymptomatic hyponatremia was associated with bone fractures in ambulatory elderly subjects (adjusted odds ratio of 4.16, 95% confidence interval: 2.24 -7.71) (1), and the incidence of hyponatremia in patients aged 65 or older with skeletal fractures was more than double that of patients with no fracture (9.1 and 4.1%, respectively; p ϭ 0.007) (2). Recent studies from our laboratory have indicated that hyponatremia is also associated with osteoporosis due to increased osteoclastic bone resorption in a rat model of SIADH (3). Histomorphometric analysis indicated that osteoclast number was increased 5-10-fold in excised femurs, tibia, and spine from hyponatremic rats, and analysis of blood samples revealed no significant metabolic or hormonal change that could account for the increased osteoclastic bone resorption (3). Early studies of radionucleotide distribution indicated that approximately one-third of the body's sodium is stored in the bone matrix along with calcium and phosphorus and is released during osteoclastic resorption (4). A more recent study has also shown that large amounts of sodium are stored in an osmotically inactive compartment in the bones of dogs and are released from this store during prolonged dietary sodium deprivation (5). The primary components of bone matrix are removed by osteoclasts first by demineralization of the inorganic mineral through acidification of the...

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How Does the Brain Sense Osmolality?

Cited by 58 publications

References 19 publications

Controlled aquaporin-2 expression in the hypertonic environment

Controlled aquaporin-2 expression in the hypertonic environment

The Hypothalamic Neuropeptide Oxytocin Is Required for Formation of the Neurovascular Interface of the Pituitary

Osteoclast Response to Low Extracellular Sodium and the Mechanism of Hyponatremia-induced Bone Loss

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