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Distribution and Characteristics of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Unlike the long portal vessels that lie on the surface of the stalk, the short portal vessels bridging the neural and anterior lobes are extremely minute and technically inaccessible for cannulation. Therefore, a direct determination of DA levels in these vessels is virtually impossible, and indirect methods must be employed. One such method is posterior pituitary lobectomy (LOBEX). The rationale for this approach is that the removal of the PP should result in a rise in plasma PRL level which is proportional to the DA output from the gland. Indeed, acute LOBEX in rats induces a 2- to 3-fold elevation of plasma PRL levels, without having an effect on plasma LH levels [53]. Furthermore, intracarotid injections of DA immediately reverse the LOBEX-induced rise in PRL.
Neuropeptides: Evidence for Central Pathways and Role in Cardiovascular Regulation
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Giora Feuerstein, Anna Leena Siren, Stefan Vonhof, Robert Willette
A II also has been shown to modulate the release of several hormones from the anterior and posterior pituitary, and among those vasopressin (AVP) is of particular interest because of its participation in central cardiovascular control and interference in baroreflex mechanisms. Both IV and central administration (ICV) of A II lead to a release of AVP (Bonjour and Malvin, 1970), contributing to the pressor effect of A II (Severs et al., 1970). While A II ICV elicits AVP release from the posterior pituitary presumably by a direct action on the magnocellular neurons in the PVN, supraoptic nucleus (SON), and suprachiasmatic nucleus (SCN), which were shown to contain high A II receptor densities (Speth et al., 1985), this may not be the case for peripherally administered A II because of an existing blood–brain barrier in these areas. On the other hand, it is conceivable that IV ATII acts through the CVO’s that are connected to those nuclei as described above (Phillips, 1987).
Hypothalamic Neuroendocrine Regulation
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
The study of hypothalamic regulation had its beginning with the work of Scharrer, Scharrer, and Bargmann and their descriptions of neurosecretory neurons using the Gomori chrome alum hematoxylin stain methods.3,4 In the 40 years since, the chemical neuroanatomical research of the hypothalamus has established a detailed description of the hypothalamic cell types and their processes. The distribution of peptidergic and monaminergic cells and their processes were studied first.5 Until recently, the investigations concentrated on the posterior pituitary and the anterior hypophysiotropic pituitary hormones.
Treatment of Langerhans cell histiocytosis with subcutaneous cytarabine
Published in Pediatric Hematology and Oncology, 2023
Olive S. Eckstein, M. Brooke Bernhardt, Chelsey G. Hood, Vivekanudeep Karri, Stephen F. Kralik, Kenneth L. McClain
At 3.5 years of age, this patient developed isolated diabetes insipidus with an enlarged pituitary stalk and lack of the posterior pituitary bright spot on brain MRI. She had no other clinical signs of LCH and evaluations by skeletal survey, bone scan, abdominal ultrasound, CBC, and liver enzymes were all normal. She received vasopressin and no LCH-directed treatment initially. Molecular evaluations were not done at this time (2006). At age 12, a brain MRI showed increased thickening of the pituitary stalk and abnormal T2 signal in the dentate and peri-dentate regions of the cerebellum consistent with LCH involvement of the pituitary and cerebellum, concerning for progression of disease in the pituitary gland and LCH-associated cerebellar changes which can be seen years after presentation in patients with biopsy-proven LCH. She had no clinical neurologic deficits. A lumbar puncture showed no pleocytosis or protein elevation. Due to the new MRI findings and an inability to biopsy the pituitary, the patient was treated as probable LCH with cytarabine. The patient declined the intravenous route and elected to have subcutaneous injections of cytarabine. The pituitary stalk thickening and abnormal T2 signals in the cerebellum did not progress and have remained stable for 7 years after completion of therapy. PCR testing of peripheral blood mononuclear cells for the BRAFV600E mutation was negative at baseline.
Pharmacological Treatment of Generalised Anxiety Disorder: Current Practice and Future Directions
Published in Expert Review of Neurotherapeutics, 2023
Harry A. Fagan, David S. Baldwin
The neuropeptide oxytocin (OT) is a hormone secreted by the posterior pituitary gland with physiological (milk ejection, uterine contraction during labor) and behavioral roles (maternal behavior, pair bonding). OT exerts these actions through binding at the oxytocin receptor (OXTR) which is expressed widely throughout the mammalian brain [120]. An anxiolytic effect of oxytocin has been identified in rodent models and several translational human studies have been conducted, with exogenous OT usually administered intranasally [121,122]. While the focus of these human studies has been in SAD, one small pilot study has been conducted in GAD [123]. This cross-over trial randomized 13 patients with GAD to receive 3 weeks of intranasal OT (titrated up to 40 international units [IU] twice daily) and 3 weeks of placebo treatment. A significant decrease in anxiety symptoms (on the HAM-A) was noted for male but not female patients. To our knowledge, there have been no further studies of oxytocin in GAD.
The pharmacotherapeutic options in patients with catecholamine-resistant vasodilatory shock
Published in Expert Review of Clinical Pharmacology, 2022
Timothy E. Albertson, James A. Chenoweth, Justin C. Lewis, Janelle V. Pugashetti, Christian E. Sandrock, Brian M. Morrissey
The endogenous hormone vasopressin circulates in the blood after it is released from the posterior pituitary gland. VP mainly ensures osmoregulation by its effect on the arginine vasopressin receptor 2 (AVPR2) located primarily in the distal convoluted tubules promoting water retention. The antidiuretic hormone effect is normally the major effect of VP, but in shock conditions, even higher circulatory levels of VP are naturally released. These higher levels also stimulate arginine vasopressin receptor 1a (AVPR1a) generating powerful vasoconstriction. Potentially when VP is given exogenously, it maintains better kidney perfusion than exogenous NE because there are more AVPR1a receptors in the glomerular efferent than afferent arterioles [21]. In addition, the stimulation of arginine vasopressin receptor 1b (AVPR1b) by VP generates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary resulting in release of cortisol from the adrenal gland. The higher levels of ACTH generated by VP release generate increased natural levels of endogenous cortical steroids in shock patients.