Urapidil permeates the intact blood-brain barrier

Castor, G.; Schmidt, U

doi:10.1007/bf01708965

Cited by 6 publications

(2 citation statements)

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“…Unaltered frequency of DP TCR high thymocytes (being intermediary cells between the DP TCR ␣ ␤ low and SP TCR ␣ ␤ high stages), in conjunction with greater Thy-1 thymocyte surface density, suggested a more efficient positive/reduced negative thymocyte selection following urapidil treatment. Given that urapidil crosses the bloodbrain barrier [186,187] and then acting at the central level decreases sympathetic outflow [190] , the greater Thy-1 thymocyte surface density was thought to be, at least partly, related to a decline in central sympathetic flow. Moreover, urapidil favored DP TCR high differentiation towards CD4+CD8-TCR ␣ ␤ high cells, so that in urapidil-administered rats both the relative and absolute numbers of the most mature CD4+CD8-TCR ␣ ␤ high cells were increased, while the frequency of CD4-CD8+TCR ␣ ␤ high cells was diminished although their number remained unaltered [143] .…”

Section: Role Of ␣ -Ar-mediated Mechanisms In T Cell Developmentmentioning

confidence: 99%

“…However, this discrepancy could also be related to the differential ability of these ligands to cross the blood-brain barrier. Namely, differently from urapidil [186,187] , prazosin does not cross the blood-brain barrier [188] . Finally, distinct duration of these two treatments could also contribute to this inconsistency.…”

Section: Role Of ␣ -Ar-mediated Mechanisms In T Cell Developmentmentioning

confidence: 99%

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Age-Associated Remodeling of Neural and Nonneural Thymic Catecholaminergic Network Affects Thymopoietic Productivity

Leposavić

Pilipović

Perišić

2011

Neuroimmunomodulation

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Ageing is associated with a progressive decline in thymic cytoarchitecture followed by a less efficient T cell development and decreased emigration of naïve T cells to the periphery. These thymic changes are linked to increased morbidity and mortality from infectious, malignant and autoimmune diseases in old age. Therefore, it is of paramount importance to understand the thymic homeostatic processes across the life span, as well as to identify factors and elucidate mechanisms driving or contributing to the thymic involution. Catecholamines (CAs) derived from sympathetic nerves and produced locally by thymic cells represent an important component of the thymic microenvironment. In young rats, they provide a subtle tonic suppressive influence on T cell development acting via β₂- and α₁-adrenoceptors (ARs) expressed on thymic nonlymphoid cells and thymocytes. In the face of thymic involution, a progressive increase in the thymic noradrenaline level, reflecting a rise in the density of noradrenergic nerve fibers and CA-synthesizing cells, occurs. In addition, the density of β₂- and α₁-AR-expressing thymic nonlymphoid cells and the α₁-AR thymocyte surface density also exhibit a pronounced increase with age. The data obtained from studies investigating effects of AR blockade on T cell development indicated that age-related changes in CA-mediated thymic communications, certainly those involving α₁-ARs, may contribute to diminished thymopoietic efficiency in the elderly. Having in mind thymic plasticity in the course of ageing, and broadening possibilities for pharmacological modulation of CA signaling, we here present and discuss the progress in research related to a role of CAs in thymic homeostasis and age-related decay in the thymic naïve T cell output.

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