Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrolytic lesion of the paraventricular nucleus (PVN) of the hypothalamus blocks the tachycardia response to stress. The current study examined the effects of chemical lesion of PVN parvocellular neurons on the cardiovascular and endocrine responses to stress and on the content of hypothalamic oxytocin (OT) mRNA levels. Acute footshock stress increased heart rate in both ibotenic acid lesion and control groups of animals; however, the tachycardia was significantly lower in animals with a PVN lesion than the controls. Lesion of the PVN also attenuated the increase in plasma OT induced by stress, 4-fold in the lesion group versus 20-fold for the controls. There was not a generalized decrease in hormonal responsiveness since the OT response to an osmotic challenge was exaggerated in the lesion group. There was no difference between the groups in the arterial pressure and vasopressin responses to acute stress. Neurotoxin lesions of the PVN also resulted in significant depletions of VP and OT in all levels of the spinal cord and decreased OT levels in the dorsal brainstem. Ibotenic acid lesions of the PVN resulted in no significant changes in OT mRNA in the PVN, SON and PP. In addition, the 48-h dehydration resulted in a significant increase in plasma OT and OT mRNA in the PVN. These data indicate that the parvocellular neurons of the PVN play a role in integration of cardiovascular and endocrine responses to both stressful and osmotic stimuli and provide further evidence that parvocellular OT and VP neurons project to the brainstem and spinal cord.
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PMID:Excitotoxin paraventricular nucleus lesions: stress and endocrine reactivity and oxytocin mRNA levels. 147 37

Recent evidence is showing that the paraventricular nucleus (PVN) of the hypothalamus plays a key role in autonomic regulation. Studies by the author of the PVN neurones that project to the spinal cord are reviewed. These neurones are inhibited by arterial baroreceptors and excited or inhibited by pulmonary/cardiac vagal afferents. Volume load or low dose atrionatriuretic peptide can stimulate vagal afferents to excite PVN-spinal neurones. Ibotenic acid-induced lesions of PVN-spinal neurones abolish a reflex increase in renal vascular conductance following volume load. This effect appears to be independent of the PVN-vasopressin or oxytocin-containing neurones which directly excite spinal sympathetic neurones. It is suggested that different chemically coded PVN-spinal neurones produce differential effects on spinal cardiovascular neurones, either monosynaptically or via interneurones.
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PMID:Cardiovascular function of the paraventricular nucleus of the hypothalamus. 875 Sep 40