Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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)-alpha, 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.
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PMID:Nitric oxide at the crossroad of immunoneuroendocrine interactions. 1923 26

The aims of the present study were to determine whether natriuretic peptide receptors coupled to guanylate cyclase are present in the neural lobe (NL) of the pituitary and eventually localized on pituicytes and/or on nerve fibers and whether cyclic GMP may be involved in the regulation of vasopressin secretion. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) enhanced cyclic GMP content of NLs in a dose-related fashion, with ED(50) values of about 5 x 10(-8)M, while CNP failed to significantly elevate guanylate cyclase activity. ANP stimulated cyclic GMP accumulation in NLs lacking functional nerve fibers, while it was without significant effect on isolated nerve terminals. In the brain, ANP-enhanced cyclic GMP production was similarly expressed in glial and not in neuronal cultures, although intracellular guanylate cyclase activity (stimulated by sodium nitroprusside) was present in both cell types. Finally, the cell permeant S-bromoguanosine 3':5'-monophosphate GMP failed to change either basal or isoproterenol-stimulated vasopressin secretion from incubated NLs. We conclude that in the NL, as well as in brain tissue cultures, the guanylate cyclase-NP receptor complex (most probably the ANP-A subtype) is localized on pituicytes/filial cells rather than on nerve fibers/cells and that cyclic GMP may not be directly involved in the regulation of vasopressin output from the NL.
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PMID:Evidence for the presence of guanylate cyclase-coupled receptors for atrial natriuretic peptide on pituicytes of the neurohypophysis. 1991 20

The balance between vasoconstrictor/sodium-retaining and vasodilator/natriuretic systems is essential for maintaining body fluid and electrolyte homeostasis. Natriuretic peptides, such as atrial natriuretic peptide (ANP), belong to the vasodilator/natriuretic system. ANP is produced by the conversion of pro-ANP into ANP, which is achieved by a proteolytical cleavage executed by corin. In the kidney, ANP binds to the natriuretic peptide receptor-A (NPR-A) and enhances its guanylyl cyclase activity, thereby increasing intracellular cyclic guanosine monophosphate production to promote natriuretic and renoprotective responses. In the glomerulus, ANP increases glomerular permeability and filtration rate and antagonizes the deleterious effects of the renin-angiotensin-aldosterone system activation. Along the nephron, natriuretic and diuretic actions of ANP are mediated by inhibiting the basolaterally expressed Na(+)-K(+)-ATPase, reducing apical sodium, potassium, and protein organic cation transporter in the proximal tubule, and decreasing Na(+)-K(+)-2Cl(-) cotransporter activity and renal concentration efficiency in the thick ascending limb. In the medullary collecting duct, ANP reduces sodium reabsorption by inhibiting the cyclic nucleotide-gated cation channels, the epithelial sodium channel, and the heteromeric channel transient receptor potential-vanilloid 4 and -polycystin 2 and diminishes vasopressin-induced water reabsorption. Long-term ANP treatment may lead to NPR-A desensitization and ANP resistance, resulting in augmented sodium and water reabsorption. In mice, corin deficiency impairs sodium excretion and causes salt-sensitive hypertension. Characteristics of ANP resistance and corin deficiency are also encountered in patients with edema-associated diseases, highlighting the importance of ANP signaling in salt-water balance and renal pathophysiology.
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PMID:ANP-induced signaling cascade and its implications in renal pathophysiology. 2565 59


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