Effects of selected vasoactive substances on adenylate cyclase activity in brain, isolated brain microvessels, and primary cultures of brain microvessel endothelial cells

1992 ◽  
Vol 17 (2) ◽  
pp. 209-214 ◽  
Author(s):  
Anna Baranczyk-Kuzma ◽  
Kenneth L. Audus ◽  
Fran�ois L. Guillot ◽  
Ronald T. Borchardt
Keyword(s):  
Endothelial Cells ◽  
Adenylate Cyclase ◽  
Primary Cultures ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Vasoactive Substances ◽  
Brain Microvessels ◽  
Microvessel Endothelial Cells ◽  
Brain Microvessel

Adenosine and its analogue ( − )-N6-R-phenyl-isopropyladenosine modulate anterior pituitary adenylate cyclase activity and prolactin secretion in the rat

1990 ◽  
Vol 5 (1) ◽  
pp. 69-76 ◽  
Author(s):  
G. Schettini ◽  
E. Landolfi ◽  
O. Meucci ◽  
T. Florio ◽  
M. Grimaldi ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Anterior Pituitary ◽  
Primary Cultures ◽  
Prolactin Secretion ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Low Concentrations ◽  
High Concentrations

ABSTRACT The effect of adenosine and its analogue ( − )-N6-R-phenylisopropyladenosine (PIA) on both anterior pituitary adenylate cyclase activity and prolactin secretion was examined in the rat. Adenosine inhibited basal adenylate cyclase activity in a dose-dependent manner and also reduced the stimulation of the enzyme by vasoactive intestinal peptide (VIP). Likewise, in primary cultures of anterior pituitary cells, adenosine decreased prolactin secretion in both basal and VIP-stimulated conditions. In perifusion experiments, adenosine also inhibited prolactin release in both basal and TRH-stimulated conditions. PIA produced a biphasic pattern of response of basal adenylate cyclase activity, being inhibitory at low and stimulatory at high concentrations. In VIP-stimulated conditions, low concentrations of PIA inhibited both adenylate cyclase activity and prolactin release from primary cultures of pituitary cells, while no additive stimulatory effect was seen at high concentrations. Similarly, low concentrations of PIA reduced both basal and TRH-stimulated prolactin release from perifused pituitaries, while increasing PIA concentrations restored prolactin release. These data show that adenosine affects basal and stimulated prolactin secretion from anterior pituitary cells. Adenosine receptors seem to be coupled to the adenylate cyclase system in the anterior pituitary gland, suggesting a possible relationship between the effect of adenosine on adenylate cyclase activity and prolactin secretion.

scholarly journals Angiotensin Peptide Regulation of Fluid-Phase Endocytosis in Brain Microvessel Endothelial Cell Monolayers

1990 ◽  
Vol 10 (6) ◽  
pp. 827-834 ◽  
Author(s):  
François L. Guillot ◽  
Kenneth L. Audus
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Lucifer Yellow ◽  
Primary Cultures ◽  
Fluid Phase ◽  
Ang Ii ◽  
Microvessel Endothelial Cell ◽  
Fluid Phase Endocytosis ◽  
Microvessel Endothelial Cells ◽  
Brain Microvessel

An in vitro model comprised of primary cultures of brain microvessel endothelial cells was used to investigate angiotensin II (Ang II) effects on blood–brain barrier fluid-phase endocytosis. The effects of Ang II, saralasin, sarathrin, bradykinin (BK), and phorbol myristate acetate (PMA) on brain microvessel endothelial cell fluid-phase endocytosis were determined using the fluorescent marker, Lucifer yellow. Nanomolar concentrations of saralasin (a partial Ang II agonist) stimulated brain microvessel endothelial cell endocytosis by 30% whereas Ang II treatment enhanced Lucifer yellow uptake by 20%. Sarathrin (an Ang II antagonist) had no effect on Lucifer yellow uptake. Nanomolar concentrations of BK and PMA also stimulated Lucifer yellow uptake by the brain microvessel endothelial cell by 40 and 95%, respectively. Stimulatory effects of Ang II and saralasin on Lucifer yellow uptake by brain microvessel endothelial cells could be completely blocked by pretreatment with either sarathrin or indomethacin (an inhibitor of prostaglandin synthesis). In contrast, the effects of neither BK nor PMA on brain microvessel endothelial cell uptake of Lucifer yellow were altered by indomethacin pretreatment. Results indicated that Ang II, saralasin, BK, and PMA produce similar stimulatory effects on brain microvessel endothelial cell fluid-phase endocytosis with only Ang II and saralasin, producing increases in brain microvessel endothelial cell fluid-phase endocytosis that appeared to be mediated by prostaglandins.

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