Browsing by Subject "Vasopressin"

Now showing 1 - 4 of 4
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    Intracellular Ca2+ Pools and Fluxes in Cardiac Muscle-Derived H9c2 Cells
    (2005-08) Lax Pérez, Antonio Manuel; Fernandez Belda, Francisco; Soler Pardo, Fernando; Medicina
    Relevant Ca(2+) pools and fluxes in H9c2 cells have been studied using fluorescent indicators and Ca(2+)-mobilizing agents. Vasopressin produced a cytoplasmic Ca(2+) peak with half-maximal effective concentration of 6 nM, whereas thapsigargin-induced Ca(2+) increase showed half-maximal effect at 3 nM. Depolarization of the mitochondrial inner membrane by protonophore was also associated with an increase in cytoplasmic Ca(2+). Ionomycin induced a small and sustained depolarization, while thapsigargin had a small but transient effect. The thapsigargin-sensitive Ca(2+) pool was also sensitive to ionomycin, whereas the protonophore-sensitive Ca(2+) pool was not. The vasopressin-induced cytoplasmic Ca(2+) signal, which caused a reversible discharge of the sarco-endoplasmic reticulum Ca(2+) pool, was sensed as a mitochondrial Ca(2+) peak but was unaffected by the permeability transition pore inhibitor cyclosporin A. The mitochondrial Ca(2+) peak was affected by cyclosporin A when the Ca(2+) signal was induced by irreversible discharge of the intracellular Ca(2+) pool, i.e., adding thapsigargin. These observations indicate that the mitochondria interpret the cytoplasmic Ca(2+) signals generated in the reticular store.
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    Sex-specific response of the vasopressin-reacting neurons of the paraventricular nucleus of the rat hypothalamus following chronic administration of met-enkephalin
    (Murcia : F. Hernández, 1992) Sánchez, F.; González, R.; Carretero, J.; Rubio, M.; Riesco, J. M.; Blanco, E.; Juanes, J.A.; Vázquez, R.
    Using the peroxidase-antiperoxidase immunocytochernical technique, a morphometric study of the magnocellular neurons of the Paraventricular nucleus of the rat hypothalamus, reactive to specific anti-vasopressin rabbit serum, was made. Following systemic and chronic administration of met-enkephalin the number of immunoreactive neurons was higher, especially in females. Additionally, in the females, it was possible to observe an increase in the immunoreactivity and the presence of well-stained fibres. These findings suggest, especially in females, a blockage in the release of vasopressin, facilitating its immunocytochemical visualization.
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    The effects of chronic administration of captopril on the mouse median eminence
    (Murcia : F. Hernández, 1998) Castañeyra Perdomo, A.; Carmona-Calero, E.; Pérez-Delgado, M. del M.; Pérez-González, H.; Marrero-Gordillo, N.; Ferres Torres, R.
    The effects of Captopril (an angiotensinconverting enzyme inhibitor) on the median eminence (ME) of the male albino mouse have been examined using morphometric and immunohistochemical procedures. We measured the nuclear area of the ependymocytes of the ME and of the glial cells of the reticular external zone of the ME. We also determined the cell/neuropil coefficient (CNC), which expreses the relation between cellular area and neuropil of the ME, and the global volume of the ME in each animal. For the immunohistochemical study we used rabbit antiarginine- vasopressin, and compared the results in the different groups of mice. We detected an increase in the immunoreactive material (arginine-vasopressin, A-V) and an increase in the global volume of the organ and also an increase of the neuropil of the ME after the longest exposure to the drug. These alterations could be related to the inhibition of the brain angiotensin 11 by captopril and the accumulation of vasopressin in the fibrous tract that runs from the paraventricular nucleus (PVN) to the neurohypophysis.
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    Vasopressinergic neurons in periependymal and periventricular areas of the rostral third ventricle
    (Murcia : F. Hernández, 1990) Roy Choudhury, S.; Ray, P.K.
    On the lateral wall of the rostral third ventricle, an area separates the ependyma from the neurosecretory PVN neurons. Since VP from the latter discharges into the vasculature, the above area may be regarded as constituting an interface between the ventncular and vascular compartments of the CNS. As VP release into the two compartments is integrated, the interface region has been explored for possible existence of a neural infrastructure that would allow such an integration. Immunohistochemical staining for VP following colchicine treatment reveals the presence of an elaborate vasopressinergic network in the interface region that is divisible into a media1 periependymal and a lateral periventricular area. A closer examination indicates that the ependymal, periependymal, periventricular and PVN areas (in that order medio-laterally) are al1 interconnected through this network. The media1 area appears to be receptive in nature, while the connectivity of the lateral area points to an effector function. All in all, such a neural network would provide a sound morphological basis for integration of neuroendocrine mechanisms modulating VP release into the ventricular and vascular compartments of the CNS.