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Chronic kidney disease with hyperphosphatemia is associated with accelerated atherosclerosis and endothelial dysfunction. However, the contribution of high serum phosphate levels to endothelial injury is incompletely understood. The aim of this work was to evaluate the responses of endothelial cells to elevated levels of extracellular phosphate in vitro. High phosphate in concentrations similar to those observed in uremia-associated hyperphosphatemia (>2.5 mM) induced apoptosis in two endothelial cell lines (EAhy926 cells and GM-7373 cells). This effect was enhanced when cells were incubated for 24 h in the presence of 2.8 mM calcium instead of 1.8 mM. By treating cells with 0.5 or 1.0 mM phosphonoformic acid, an inhibitor of the phosphate transporter, death was completely prevented. The process of phosphate-induced apoptosis was further characterized by increased oxidative stress, as detected by increased ROS generation and disruption of the mitochondrial membrane potential at approximately 2 h after treatment, followed by caspase activation. These findings show that hyperphosphatemia causes endothelial cell apoptosis, a process that impairs endothelial integrity. Endothelial cell injury induced by high phosphate concentrations may be an initial event leading to vascular complications in patients with chronic kidney disease.

The hypothalamo‐hypophyseal system is supplied with two types of specialized glial cells that interact in neuroendocrine functional dynamics: the tanycytes and the pituicytes. Tanycytes are the dominating glial cells within the median eminence. Similar to radial glia, they extend from the floor of the third ventricle to the neurohemal surface of the median eminence. Pituicytes, as specialized astrocytes, are the main glial cells of the neural lobe. They are in intimate contact with the perivascular space of the sinusoidal vessels. Morphological similarities between the two cell types focus on their interaction with terminal branches of hypothalamic neurons in both regions of the neurohypophysis, the median eminence and the neural lobe. Release of hypothalamic hormones is apparently influenced by pituicytes and tanycytes. For instance, both types of cells are capable of closing or opening the access to the vessels. Thereby, in contrast to the “blood–brain‐barrier” function of astrocytes, pituicytes and tanycytes display “brain–blood‐barrier” functions. Pituicytes are characterized by the expression of specific membrane‐bound receptors for opioids, vasopressin, and β‐adrenoceptors, indicating that they receive input by numerous neuroactive substances. Integration of these incoming signals may result in a regulation of neurosecretion, especially by morphological changes and by modulation of extracellular ion concentrations. Comparable modulatory mechanisms of tanycytes have not yet been elucidated in a convincing manner. Besides possible regulatory functions, tanycytes are considered to possess guiding functions for hypothalamic axons and to be involved in transport mechanisms between ventricle and blood vessels of the portal system. Microsc. Res. Tech. 41:29–42, 1998 © 1998 Wiley‐Liss, Inc.

Certain secretory cells in the hypophysial pars tuberalis of the Djungarian hamster display marked circannual structural alterations. The present investigation deals with the immunohistochemical properties of this cell group. A distinct TSH-like immunoreactivity was found in secretory cells of this type in the pars tuberalis of animals exposed to long photoperiods, whereas under short photoperiods the TSH-like immunoreactivity was nearly absent. In the pars distalis, the number and distribution of TSH-positive cells did not differ significantly between animals maintained under long and under short photoperiods. LH- and FSH-positive cells could not be detected in the pars tuberalis, but they are clearly present in the pars distalis of both groups of hamsters. Our immunocytochemical results suggest that photoperiodic stimuli influence the secretory activity of TSH-like immunoreactive cells in the pars tuberalis. A connection with the neuroendrocrine-thyroid axis is discussed.

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