Abstract
th position. Oxytocin is also produced in the hypothalamic nuclei, with a structure similar to ADH, but with leucine in the 8 th position. Both ADH and oxytocin are produced in the magnocellular neurosecretory cells (MNC) of the hypothalamus, mainly in the supraoptic (SON) and paraventricular (PVN) nuclei. While each MNC was initially thought to produce either ADH or oxytocin alone, more recent evidence indicates that there can be some overlap of production [5]. ADH is created as a composite precursor molecule composed of ADH, neurophysin-II (NPII), which is ADH’s carrier protein, and copeptin- a glycopeptides [5,6]. Both NPII and ADH are produced from the same precursor mRNA. After passage through the golgi apparatus the prepropeptide complex is packaged into large dense core vesicles (LDCV) which exit from the trans golgi network. Inside the LDCV enzymatic processing of the precursor molecules takes place. This is facilitated by the LDCV’s mildly acidic (pH 5-6) internal environment. Additionally the acidic environment keeps the fully processed ADH nonapeptide bound to the NPII. After their production, the LDCVs are transported in an anterograde fashion, down the neuronal axon along microtubules at a rate near 140 mm/day. LDCV’s containing ADH is stored in the nerve terminals of the posterior pituitary, awaiting neurosecretion. When an action potential causes an influx of Ca 2+
Highlights
Inappropriate secretion or action of serum antidiuretic hormone (ADH) is termed Diabetes Insipidus (DI), characterized by polyuria and polydipsia [1]
nephrogenic diabetes insipidus (NDI) may present with residual sensitivity to ADH, or with secretion of ADH occurring at higher levels of plasma osmolality in patients with partial Central Diabetes Insipidus (CDI)
DI is a disease of polydipsia and hypotonic polyuria caused by one of 4 etiologies: 1) Inadequate ADH secretion such as in CDI 2) Lack of response to ADH, as seen in NDI 3) Increased metabolism of ADH as occurs in Gestational Diabetes Insipidus (GDI) 4) Massive fluid ingestion as in psychogenic or dipsogenic polydipsia
Summary
Inappropriate secretion or action of serum antidiuretic hormone (ADH) is termed Diabetes Insipidus (DI), characterized by polyuria (defined as 24 hour urine output in excess of 40 ml/kg) and polydipsia [1]. This response to mechanical stretch is mediated via channels called transient receptor potential vanilloid 1 (TRPV1) channels These TRPV1 channels, in response to MNC shrinkage due to hyperosmolality, allow activation of a cation current (Ca2+ and nonspecific monovalent cations), leading to increased action potential firing, resulting in ADH release [8,9,10]. Recent studies done in Madin-Darby canine kidney cells show that AQP-2 phosphorylation and apical insertion are increased by prostaglandin EP2 and EP4 receptors activation [23]. It has been shown in rats that butaprost, a EP2 agonist can increase urinary concentration in rats with the V2R blocked. Further research is required to determine the exact nature of the role of prostaglandins in water balance
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