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)

The effect of vasopressin on neurons of the rat dorso-lateral septum (DLS) was studied in brain slices with intracellular microelectrodes. Two out of 13 neurons showed a small depolarization, spontaneous activity, and increased input resistances following a 15 min exposure to 10(-6) to 10(-8) M vasopressin (VP). These membrane effects disappeared completely within 3-5 min after the application. The remaining DLS neurons treated with these vasopressin concentrations showed an increase in glutamate-mediated excitatory postsynaptic potentials (EPSPs), evoked by stimulation of the fimbria fibers. As little as 10(-12) MVP increased these EPSPs markedly in nearly 80% of the cells studied. This increase in most of the cells disappeared within 15 min after the application period, whereas the increase in EPSPs induced by 10(-10) M VP outlasted the peptide application period for more than 30 min. Neither the blockade of GABA-ergic synaptic inhibition nor the pre-treatment of the neurons with d(CH2)5-Tyr(Me)-arginine vasopressin or 2-amino-5-phosphonovaleric acid (2-APV), antagonists for the V1 type of vasopressin receptor and NMDA receptors, respectively, interfered with the EPSPs potentiating effect of the peptide. It is concluded that a type of vasopressin receptor other then the V1 type is involved in the long-lasting potentiation of the primarily non-NMDA receptor mediated transmission in DLS neurons.
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PMID:Vasopressin facilitates excitatory transmission in slices of the rat dorso-lateral septum. 197 60

Marfan's syndrome is a dominantly inherited connective tissue disorder characterized by skeletal, ocular, and cardiovascular abnormalities, such as arachnodactyly, dolichostenomelia, kyphosis, scoliosis, pectus excavatum, ectopia lentis, aortic aneurysm and dissection, aortic valve incompetence, and mitral valve prolapse. This report describes the systemic management during dental treatment of a 26-year-old man with Marfan's syndrome. Blood pressure, electrocardiogram, echocardiography, systolic time intervals, and aortic pulse wave velocity were monitored. Nitrous oxide inhalational sedation was employed. In contrast to the vasopressin, felypressin (contained in prilocaine), epinephrine (contained in lidocaine) caused an acceleration of cardiac function--increased heart rate, cardiac output, 1/pre-ejection period (PEP), and aortic pulse wave velocity and decreased PEP and left ventricular ejection time. This experience suggests that the use of anesthetics containing epinephrine in dental patients with Marfan's syndrome needs to be carefully managed.
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PMID:Systemic management of Marfan's syndrome during dental treatment: a case report. 814 82