Ultrastructural localization of nitric oxide synthase and endothelin in coronary and pulmonary arteries of newborn rats

This is the first report on the ultrastructural distribution of nitric oxide synthase and endothelin immunoreactivities in the coronary and pulmonary arteries of newborn Wistar rats. The distribution of nitric oxide synthase and endothelin was investigated using pre-embedding peroxidase-antiperoxidase immunocytochemistry. In both arteries examined, positive labelling for nitric oxide synthase was localized both in the endothelium and smooth muscle, whereas positive labelling for endothelin was localized in the endothelium exclusively. In the coronary artery, approximately 80% and 55% of the endothelial cells examined were positive for nitric oxide synthase and endothelin, respectively, whereas in the pulmonary artery, 77% and 60% of the endothelial cells were positive for nitric oxide synthase and endothelin, respectively. These findings indicate that nitric oxide synthase and endothelin are colocalized in some of the endothelial cells of the newborn rat. In the endothelium, nitric oxide synthase and endothelin immunoreactivities were distributed throughout the cell cytoplasm and in association with the membranes of intracellular organelles. In smooth muscle, a relationship of nitric oxide synthase immunoreactivity to endoplasmic reticulum was observed in the pulmonary artery. In summary, in the newborn rat, endothelial cells of the coronary and pulmonary artery are rich in nitric oxide synthase (neuronal isoform) and endothelin, and it is suggested therefore that they may be substantially involved in vasomotor control of the cardiac and pulmonary circulation during early stages of postnatal development.     

Mitochondrial abnormalities in human phaeochromocytoma

Summary Mitochondrial abnormalities are reported in four cases of phaeochromocytoma. These abnormalities include swelling and scant cristae, intramitochondrial dense bodies, septate-like junctions, intercristal fusion plus spheroidal bodies, and intramitochondrial rodlets. These structural mitochondrial changes are associated with reduction in activity of the mitochondrial enzymes, monoamine oxidase and succinic dehydrogenase.Supported by a grant-in-aid from the National Health and Medical Research Council     

SUSO PINTOR

Purinergic Signalling -     

Editor’s note

Purinergic Signalling -     

Developmental expression of P2X5 receptors in the mouse prenatal central and peripheral nervous systems

The functions of P2X purinoceptors (P2X1-7) in the nervous system of adults have been widely studied. However, little is known about their roles during embryonic development. Our previous work has reported an extensive expression of P2X5 receptors in the adult mouse central nervous system. In the present study, we have examined the expression pattern of P2X5 receptor mRNA and protein during prenatal development of the mouse nervous system (from embryonic day E8 to E17). P2X5 receptors appeared in the neural tube as early as E8 and were gradually confined to new-born neurons in the cortical plate and ventral horn of the spinal cord. Heavy signals for P2X5 receptors were also found in dorsal root ganglia (DRG), retina, olfactory epithelium, and nerve fibers in skeletal muscles. In conclusion, P2X5 receptors were strongly represented in the developing mouse nervous system. The transient high expression pattern of P2X5 receptors in epithelium-like structures suggests a role during early neurogenesis.     

Block of P2X7 receptors could partly reverse the delayed neuronal death in area CA1 of the hippocampus after transient global cerebral ischemia

Transient global ischemia (which closely resembles clinical situations such as cardiac arrest, near drowning or severe systemic hypotension during surgical procedures), often induces delayed neuronal death in the brain, especially in the hippocampal CA1 region. The mechanism of ischemia/reperfusion (I/R) injury is not fully understood. In this study, we have shown that the P2X7 receptor antagonist, BBG, reduced delayed neuronal death in the hippocampal CA1 region after I/R injury; P2X7 receptor expression levels increased before delayed neuronal death after I/R injury; inhibition of the P2X7 receptor reduced I/R-induced microglial microvesicle-like components, IL-1β expression, P38 phosphorylation, and glial activation in hippocampal CA1 region after I/R injury. These results indicate that antagonism of the P2X7 receptor and signaling pathways of microglial MV shedding, such as src-protein tyrosine kinase, P38 MAP kinase and A-SMase, might be a promising therapeutic strategy for clinical treatment of transient global cerebral I/R injury.