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)

Ovarian hyperstimulation syndrome occurred after induction of ovulation with menotropins (follicle-stimulating hormone and luteinizing hormone) and implantation of an intrauterine pregnancy. Serial determinations of aldosterone, deoxycorticosterone, 17 beta-estradiol, progesterone, human chorionic gonadotropin, urinary and plasma electrolytes, and fluid balance were obtained. Plasma renin activity, aldosterone, deoxycorticosterone, and antidiuretic hormone rose markedly. Hydration for four days improved urinary output but also accelerated sodium and fluid retention. Subsequent restriction of salt and water stabilized the patient. Spontaneous abortion was followed by prompt diuresis without a change in therapy. Regression analysis of the authors' data, the clinical observations, and other data in the literature suggest that the ovarian hyperstimulation syndrome is produced by excessive secretion of an unknown hormone that regulates peritoneal fluid during the normal menstrual cycle, and that elevations of plasma renin, aldosterone, and antidiuretic hormone are secondary.
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PMID:Pathophysiology of the ovarian hyperstimulation syndrome. 392 8

Patients with diabetes insipidus (DI) are at high risk for dehydration, hypernatremia and hemodynamic instability. Ovarian hyperstimulation syndrome (OHSS) likewise has negative effects on electrolyte balance. If ovulation induction is required in a patient with DI, there is thus a strong argument for avoiding techniques that increase the risk of OHSS. This paper reports the results of ovulation induction in a patient with anovulation of hypothalamic origin and central (vasopressin deficit) DI. Ovulation was induced with pulsatile gonadotropin-releasing hormone (GnRH), which induces single-ovule cycles and which does not increase the risk of OHSS. The patient successfully achieved pregnancy after seven ovulatory cycles.
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PMID:Ovulation induction with pulsatile GnRH in a patient with anovulation of hypothalamic origin and central diabetes insipidus. 967 68

Ovarian hyperstimulation syndrome is a complication of the ovulation stimulation, most commonly by gonadotrophins. It frequently occurs in patients included in in vitro fertilization program. The exact mechanism of development of this syndrome has not been elucidated yet. The basic pathogenic mechanism of development of this syndrome is vasodilation of the ovarian blood vessels. Dilated ovarian blood vessels become permeable. Permeability of dilated ovarian blood vessels is more increased by released ovarian mediators. Due to increased permeability of the blood vessels, there is leakage of the intravascular fluid into the extravascular areas resulting in hypovolemia, edema and ascites. Hypovolemia leads to renal perfusion decrease. Increased salt and water reabsorption occurs in the renal tubules so oliguria develops. Decreased arterial blood volume results in stimulation of the renin-angiotensin-aldosterone system, the sympathetic nervous system as well as the antidiuretic hormone. The activation of the sympathetic nervous system via beta adrenergic receptors stimulates renin release and aldosterone secretion. Renin stimulates release of angiotensin I which transforms into angiotensin II. Angiotensin II increases the pressure and stimulates aldosterone secretion. In patients with this syndrome, there is an elevated plasma endothelin and natriuretic peptide level. Endothelin is an important vasoconstrictor. It increases secretion of renin, aldosterone, catecholamines, antidiuretic hormone, and atrial natriuretic peptide, and enhances the vasoconstrictive effect of norepinephrine and angiotensin II. The platelet number increase together with the elevated factor of blood coagulation and hyperviscosity in a severe form of this syndrome may result in development of intravascular thrombosis. The treatment consists of maintenance of circulatory function, i.e. the increase of effective arterial blood volume by applying the plasma volume expanders.
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PMID:[The significance of the ovarian arteriolar vasodilatation in pathogenesis of the ovarian hyperstimulation syndrome]. 1700 17