CEFYBO   02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
artículos
Título:
Nitric Oxide at the crossroad of immunoendocrine interactions
Autor/es:
RETTORI, V; FERNANDEZ-SOLARI, J; MOHN, C.; ZORRILLA ZUBILETE, M; DE LA CAL, C; PRESTIFILIPPO, J; DE LAURENTIIS, A
Revista:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Referencias:
Año: 2009 p. 35 - 47
ISSN:
0027-8424
Resumen:
Nitric oxide (NO)was initially described as a mediator of endothelial relaxation, and now
its participation is recognized in numerous physiological and pathological processes.
It was demonstrated that lipopolysaccharide-stimulated corticotropin-releasing factor
release involves NO production. Furthermore, it has been shown that interleukin (IL)-1,
tumor necrosis factor (TNF)-á, IL-6, and IL-2 can stimulate adrenocorticotropic hormone
release from anterior pituitary via NO. Also, we found that NO released from
hypothalamic NOergic neurons in response to norepinephrine diffuses to luteinizing
hormone-releasing hormone (LHRH) neurons that activate cyclooxygenase and guanylate
cyclase. This activation results in an increase in prostaglandin E2 and cyclic guanosine
monophosphate, respectively, which leads to the exocytosis of LHRH granules.
During pathological conditions, such as manganese intoxication, NO production is increased,
leading to an increase in LHRH secretion that can advance puberty. In another
study we demonstrated that NO reduces oxytocin as well as vasopressin secretion from
the posterior pituitary, suggesting it has a modulatory role during dehydration. An increase
in NO synthase (NOS) activity and protein in the hippocampus and cerebellum
was found in offspring of rats that were subjected to prenatal stress, and this was correlated
with behavioral changes in adults. Also NO participates in signal transduction
pathways in peripheral tissue in physiological processes, such as in corticosterone release
from the adrenal gland. Pathological conditions, such as tumors of the head and
neck, that are treated with radiation are followed by xerostomy. In a rat model, radiation
diminished NOS activity in the submandibulary gland, and this was followed by
inhibition in salivary secretion. In summary, this review describes the wide participation
of NO in the cross-talk between neuroendocrine and neuroimmune systems in
physiological and pathological processesá, IL-6, and IL-2 can stimulate adrenocorticotropic hormone
release from anterior pituitary via NO. Also, we found that NO released from
hypothalamic NOergic neurons in response to norepinephrine diffuses to luteinizing
hormone-releasing hormone (LHRH) neurons that activate cyclooxygenase and guanylate
cyclase. This activation results in an increase in prostaglandin E2 and cyclic guanosine
monophosphate, respectively, which leads to the exocytosis of LHRH granules.
During pathological conditions, such as manganese intoxication, NO production is increased,
leading to an increase in LHRH secretion that can advance puberty. In another
study we demonstrated that NO reduces oxytocin as well as vasopressin secretion from
the posterior pituitary, suggesting it has a modulatory role during dehydration. An increase
in NO synthase (NOS) activity and protein in the hippocampus and cerebellum
was found in offspring of rats that were subjected to prenatal stress, and this was correlated
with behavioral changes in adults. Also NO participates in signal transduction
pathways in peripheral tissue in physiological processes, such as in corticosterone release
from the adrenal gland. Pathological conditions, such as tumors of the head and
neck, that are treated with radiation are followed by xerostomy. In a rat model, radiation
diminished NOS activity in the submandibulary gland, and this was followed by
inhibition in salivary secretion. In summary, this review describes the wide participation
of NO in the cross-talk between neuroendocrine and neuroimmune systems in
physiological and pathological processes