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)

Sixty-six patients with chronic hypertension were cared for during a total of 72 pregnancies. Patients were treated at home primarily by greater than or equal to 4 hours of bed rest daily in the left recumbent position. Only patients whose diastolic blood pressures remained greater than 110 mmHg were treated with hydralazine (Apresoline, Ciba). With this plan of treatment there were only 3 perinatal deaths for an uncorrected perinatal mortality of 4.1% (1.4% corrected). Twenty-nine percent of the patients had babies that were small for gestational age, 13.8% had positive oxytocin challenge tests, and 36.8% developed superimposed preeclampsia. When compared with the outcome of previous pregnancies, the program of bed rest lowered perinatal mortality from 16.8 to 8.8%. Thus, it is suggested that bed rest together with the avoidance of diuretics and the judicious use of hydralazine results in the most favorable fetal outcome.
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PMID:Evaluation of a program of bed rest in the treatment of chronic hypertension in pregnancy. 42 5

Since 1955, a standardized treatment regimen has been used to manage 245 cases of eclampsia at Parkland Memorial Hospital. Magnesium sulfate alone effectively controlled controlled convulsions in the great majority of cases. The only maternal death among the 245 cases reemphasizes the risk of respiratory arrest that is inherent in the administration of magnesium sulfate when given in large doses intravenously. Hydralazine to lower the diastolic blood pressure somewhat, when it was 110 mm Hg or higher, prevented intracranial hemorrhage. Avoidance of diuretics and hyperosmotic agents and limitation of fluid intake were not associated with severe renal failure. Pulmonary edema was rare. Vaginal delivery was achieved in the majority of cases. Oxytocin often proved effective for initiating and maintaining labor even remote from term. The results obtained with this regimen justify its continued clinical application.
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PMID:The Parkland Memorial Hospital protocol for treatment of eclampsia: evaluation of 245 cases. 671 34

Hemorrhage and nonhypotensive hypovolemia are known to increase plasma levels of oxytocin (OT) and vasopressin (VP) in rats. The present experiments demonstrated that secretion of OT and VP also are stimulated by acute drug-induced hypotension. Injection of hydralazine abruptly decreased arterial blood pressure in conscious rats and induced Fos expression, a marker of neuronal activation, within OT and VP neurons in the hypothalamus. Hydralazine also elicited substantial increases in plasma levels of both OT and VP. Injection of chlorisondamine similarly elicited acute hypotension and increased plasma levels of OT and VP. Furthermore, when the hypotensive effect of chlorisondamine was blunted by coinfusion of phenylephrine, the induced increases in OT and VP were markedly attenuated. Across all treatments, arterial blood pressure was inversely related to plasma levels of OT and VP. Plasma osmolality was not increased by hydralazine, nor was there evidence of gastric malaise, two known stimuli for OT secretion in rats. These results suggest that arterial hypotension increases neurohypophysial release of OT and VP in conscious rats.
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PMID:Decreases in arterial pressure activate oxytocin neurons in conscious rats. 936 14

Tachykinin neurokinin 3 receptor (NK3R) signaling has a broad role in vasopressin (VP) and oxytocin (OT) release. Hydralazine (HDZ)-induced hypotension activates NK3R expressed by magnocellular neurons, increases plasma VP and OT levels, and induces c-Fos expression in VP and OT neurons. Intraventricular pretreatment with the specific NK3R antagonist, SB-222200, eliminates the HDZ-stimulated VP and OT release. NK3R are distributed in the central pathways conveying hypotension information to the magnocellular neurons, and the NK3R antagonist could act anywhere in the pathways. Alternatively, the antagonist could act at the NK3R expressed by the magnocellular neurons. To determine whether blockade of NK3R on magnocellular neurons impairs VP and OT release to HDZ, rats were pretreated with a unilateral PVN injection of 0.15 M NaCl or SB-222200 prior to an intravenous injection of 0.15 M NaCl or HDZ. Blood samples were taken, and brains were processed for VP/c-Fos and OT/c-Fos immunohistochemistry. Intravenous injection of 0.15 M NaCl did not alter plasma hormone levels, and little c-Fos immunoreactivity was present in the PVN. Conversely, intravenous injection of HDZ increased plasma VP and OT levels and c-Fos expression in VP and OT magnocellular neurons. Intra-PVN injection of SB-222200 prior to an intravenous injection of HDZ significantly decreased c-Fos expression in both VP and OT neurons by approximately 70% and attenuated plasma VP and OT levels by 33% and 35%, respectively. Therefore, NK3R signaling in magnocellular neurons has a critical role for the release of VP and OT in response to hypotension.
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PMID:Blockade of NK3R signaling in the PVN decreases vasopressin and oxytocin release and c-Fos expression in the magnocellular neurons in response to hypotension. 1865 Mar 16