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)

Mechanisms for the therapeutic effect of oral contraceptives in dysmenorrhea were studied by recording intrauterine pressure on the first day of menstrual bleeding in women with moderate to severe symptoms and after three weeks of oral contraceptive therapy (150 micrograms levonorgestrel + 30 micrograms ethinyl estradiol, daily). Spontaneous uterine activity and reactivity to intravenous injections of vasopressin (6 pmol/kg body weight; n = 8) or prostaglandin F2 alpha (12 nmol/kg body weight; n = 9) at the two sessions were compared. During the first recording when all women had dysmenorrhea, the uterine activity and reactivity to both agonists were pronounced. After therapy, when the women felt essentially no pain, a statistically significant decrease in spontaneous uterine activity in terms of total pressure area, frequency and amplitude of contractions was observed. The agonist injections induced less pain at the second recording, although the magnitude of responses, superimposed on the much smaller uterine activity at this time, were not significantly different from those at the first recording during dysmenorrhea. The mechanism of pain relief by oral contraception in dysmenorrhea could be a lesser impact of the decreased contractile activity on uterine blood flow, abolishing the local ischemia. A reduced uterine reactivity to agonists might also to some extent contribute to the therapeutic effect.
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PMID:Effect of an oral contraceptive in primary dysmenorrhea--changes in uterine activity and reactivity to agonists. 250 70

The mechanisms underlying the therapeutic effect of an oral contraceptive (150 micrograms levonorgestrel and 30 micrograms ethinyl estradiol daily for 21 days) in primary dysmenorrhea were studied by recordings of uterine activity and reactivity to lysine (L) vasopressin (VP) and prostaglandin (PG) F2 alpha on the first day of menstruation in 14 women before and after one period of oral contraceptive treatment. During the first session, when all women had moderate to severe dysmenorrhea, intra-uterine pressure recording showed an intensive uterine activity, and bolus injections of LVP (6 pmol/kg body weight; 6 subjects) or PGF2 alpha (6 or 12 nmol/kg body weight; 4 subjects in each group) increased contractile activity and discomfort. After oral contraceptive treatment, spontaneous uterine activity, measured as total pressure area, decreased significantly (p = 0.02 and p = 0.03 in the VP and PG groups, respectively). The mean uterine responses to LVP and PGF2 alpha were on average smaller after oral contraceptive treatment and the women experienced minimal discomfort after this injection. It is suggested that inhibition of uterine activity could be an important mechanism for the therapeutic effect of gestagen-dominated oral contraceptives in primary dysmenorrhea and that reduced uterine reactivity to agonists might contribute to this effect.
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PMID:The influence of a combined oral contraceptive on uterine activity and reactivity to agonists in primary dysmenorrhea. 280 Oct 28

To learn more about the beneficial effect of combined oral contraceptives (OCs) on symptoms in primary dysmenorrhea, plasma levels of vasopressin and a prostaglandin F2-alpha metabolite in dysmenorrheic women were investigated before and during treatment with a gestagen-dominated OC. The 10 subjects were administered an OC containing 150 mcg of levonorgestrel and 30 mcg of ethinyl estradiol for 21 days. The 7 women with dysmenorrheic symptoms at the time of blood sampling during the 1st menstruation graded their pain as averaging 2.1 (moderate to severe) + or - 0.3; during the 2nd menstruation, the average value was 2.9 (severe) + or - 0.1, indicating a significant increase in pain at the start of the withdrawal bleeding. Vasopressin concentrations in samples obtained on days 1-3 of the control cycle were significantly higher than those on days 6-8, 20-22, and 24-26 of the control cycle and days 1-2 of the next menstruation. Thus, the highest concentrations were obtained at the beginning of the 2 painful menstruations and at ovulation in the control cycle. During treatment, vasopressin concentrations were consistently low, except on the 1st day of withdrawal bleeding. The concentrations of the prostaglandin F2-alpha metabolite showed less variation, again, values at withdrawal bleeding were not different from those obtained during painful menstruation. Plasma concentrations of ovarian and adenohypophysial hormones, as well as osmolality, were normal throughout. Thus, the present study provided no evidence that there is a reduced release of vasopressin and/or prostaglandin F2-alpha capable of accounting for the beneficial effect of OCs on dysmenorrhea. It is possible, however, that a difference in ovarian hormone concentrations is more pronounced in uterine tissue than in plasma.
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PMID:Plasma concentrations of vasopressin and a prostaglandin F2 alpha metabolite in women with primary dysmenorrhoea before and during treatment with a combined oral contraceptive. 312 2

The effect of oral contraceptives on the neurohypophysis was demonstrated by changes in the plasma level of a posterior pituitary protein. neurophysin. Neurophysins are intraneuronal proteins associated with oxytocin and vasopressin. They have been shown to be released into the bloodstream. The resting plasma level of neurophysin in normal nonpregnant women is 0.69 ng/ml+/-0.7 SD. In women on oral contraceptives, the plasma level is 6.4 ng/ml+/-4.2 SD (P<0.001). Estrogen rather than progesterone causes the elevated neurophysin. The effect is observed within 12-24 h of estrogen administration and disappears 3-11 days after estrogen is discontinued. The results indicate that oral contraceptives act on the neurohypophysis and that estrogen is a potent pharmacologic stimulus useful in studying synthesis and release of neurophysin.
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PMID:Elevation of plasma neurophysin in women on oral contraceptives. 483 90

The concentrations of arginine vasopressin, oxytocin, and their related neurophysins were compared in many areas of postmortem human brain and spinal cord using specific radioimmunoassays. In the hypothalamus the ratio of vasopressin to oxytocin was approximately 3:1, and in the extrahypothalamic areas of the brain the greatest amount of both peptides was present in the locus coeruleus, and to a lesser extent the periaqueductal grey. Vasopressin only was found in the substantia nigra, and globus pallidus. In the medulla, including the nucleus of the solitary tract, the dorsal nucleus of the vagus, and the nucleus of the spinal tract of the trigeminal nerve, the amount of oxytocin was greater than that of vasopressin. In the spinal cord oxytocin predominated over vasopressin to an even greater extent, and reached particularly high values in certain segments of the intermediolateral grey column and dorsal horn. Estrogen-stimulated and nicotine-stimulated neurophysins (ESN and NSN) were both found in large amounts in those areas of the brain and spinal cord where the concentrations of the nonapeptides were greatest, but when the molar ratios of ESN to oxytocin and NSN to vasopressin were compared there was an excess of ESN.
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PMID:Vasopressin, oxytocin and neurophysins in the human brain and spinal cord. 669 76

RIA for the measurement of oxytocin in human plasma is described. Extraction of oxytocin from larger peptides in plasma used acetone precipitation with a 75% +or- 2 SEM recovery of oxytocin. Nonspecific binding of the assay was less than 4% and the minimum level of detection was 0.2 mcU/tube. No cross-reactivity was noted with neurophysins, arginine, or lysine vasopressin. The mean basal level (+or- SEM) of oxytocin in men was 1.80 +or- 0.07 mcU/ml and was not different in normal women (1.71 +or- 0.07 mcU/ml). Changes in posture had no effect on the levels of oxytocin. Samples obtained every 15 minutes over 4 hours showed no pulsatile secretion of oxytocin. In women chronically receiving estrogen as an oral contraceptive, oxytocin was greater than normal (4.59 +or- 0.51 mcU/ml; P0.01). Estrogen-stimulated neurophysin was also elevated *8.45 +or- 1.99 ng/ml; P0.005). Acute ingestion of estrogen caused an increase in the level of oxytocin in plasma by 12 hours and a concomitant elevation of estrogen-stimulated neurophysin. When the neurophysin was isolated from plasma obtained from a subject after ingestion of estrogen, the neurophysin from plasma comigrated on a polyacrylamide gel with a human pituitary standard of estrogen-stimulated neurophsin. In the studies in which neurophysin was elevated, the correlation between the level of oxytocin and the level of estrogen-stimulated neurophysin in plasma was significant (P0.01). The observation that estrogen administration stimulates the release of oxytocin and estrogen-stimulated neurophysin provides additional evidence that this neurophysin is the oxytocin-neurophysin of man.
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PMID:Oxytocin in human plasma: correlation with neurophysin and stimulation with estrogen. 722 98

In three experiments, the initial body weight losses after estrogenization were maintained or lagged the weight gains of the controls by the same amount over 61, 138, and 336 days, respectively. The mean serum corticosterone level of the controls was 56% that of the estrogenized rats 341 days after estrogenization. Water consumption (mg/kg b.w.) approximated 150% that of the controls several weeks following estrogenization, remaining elevated until the end of the experiment. Estrogen treatment produced a higher level of water intake in a few rats similar to that previously observed for mice. During the experimental period for water measurement, food consumption (g/kg b.w.) approximated 115% that of the controls. Gnawing and food-spilling behavior was observed in some of the estrogenized rats. Following vasopressin administration, food intake was lowered the first and second days in one estrogenized group; water intake was lowered the first day in the three control and estrogenized groups. In contrast to studies with Marsh mice, estrogenization did not produce bladder damage in Evans rats, but two showed tubular calcification in the kidneys.
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PMID:Long-term estrogenization in mammals. IV. Body, adrenal, and testes weights; polydipsia; food intake; vasopressin administration; and serum corticosterone levels in estrogenized male Evans rats. 724 68

Using in situ hybridization methods that discriminate mRNAs encoding rat vasopressin V1a, V1b, V2 and oxytocin receptors in hepatic, brain and renal tissues, experiments were done to determine whether estrogen and/or progesterone influence renal vasopressin receptor (VR) or oxytocin receptor (OTR) transcripts. Estrogen induced OTR gene expression in the outer stripe of the outer medulla and increased expression of OTRs in macula densa cells. Outer stripe OTR mRNA peaked with 4 days of estrogen treatment, and decreased to undetectable levels with 31 days of treatment of ovariectomized females. Estradiol's induction of outer stripe OTR mRNA expression was blocked by the antiestrogen, tamoxifen, but was not affected by high levels of circulating oxytocin. A role for OTRs in regulating renal function independently of adrenal steroids was suggested by findings that adrenalectomized males showed high levels of OTR transcripts in outer stripe proximal tubule and cortical macula densa cells after 5 and 10 micrograms/100g of estradiol. Consistent with specialized roles for OTRs during female reproduction, OTR transcripts could not be detected in renal tissues of peri-parturient females, at times when OTR mRNA levels were very high in uterus. OTR gene expression in macula densa cells reappeared 4-8 days into lactation and attained control levels by day 20. Physiological experiments showed that estrogen + oxytocin decreased plasma [Na+] levels in ovariectomized rats at a time when proximal tubule OTR expression is maximal. These data are consistent with 1) cell-specific regulation by estrogen of renal OTR gene expression and 2) the possibility that OTRs may be important mediators of steroid-induced alterations in renal fluid and/or solute reabsorption.
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PMID:Oxytocin receptor gene expression in female rat kidney. The effect of estrogen. 871 83

Estrogen administration has a number of favorable cardiovascular effects, and recent evidence suggests that these include an increase in arterial distensibility. Whether this is also the case for the physiological changes in estrogen production during the menstrual cycle has never been determined, however. In 21 premenopausal healthy women, we continuously measured radial artery diameter and blood pressure by an echo-tracking device and a beat-to-beat finger device, respectively. Arterial distensibility was calculated as distensibility/blood pressure curve. The measurements were made during the follicular, ovulatory, and luteal phases of the menstrual cycle. As expected, compared with the follicular phase, plasma estradiol, follicle-stimulating hormone, luteinizing hormone, and prolactin were increased in the ovulatory phase, whereas progesterone was increased in the luteal phase, together with antidiuretic hormone. Radial artery distensibility was increased in the ovulatory and reduced in the luteal phase, the changes being independent of the small, concomitant blood pressure changes. The arterial wall stiffening seen in the luteal phase was associated with a reduction in the flow-dependent endothelial dilatation of the radial artery as assessed by the hyperemia after short-term ischemia of the hand. Thus, the natural menstrual cycle is characterized by alterations in radial artery distensibility. The mechanisms responsible for this phenomenon remain to be clarified. It is possible, however, that the greater arterial distensibility of the ovulatory phase is due to an estrogen-dependent reduction in vascular smooth muscle tone, whereas the arterial stiffening of the luteal phase depends on vascular smooth muscle contraction due to more complex hormonal phenomena, ie, an endothelial impairment due to estrogen reduction but also to an increase in progesterone and antidiuretic hormone levels.
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PMID:Fluctuations of radial artery distensibility throughout the menstrual cycle. 1044 72

This review of the physiology of ovarian contractility cites the functions of FSH and LH and the contribution of chorionic gonadotropin (HCG) to follicular swelling and rupture. Endogenous estrogen priming seems to be needed for this response. Luteninizing hormone releasing hormone (LHRH) administered during the ovulatory phase also causes changes to occur in ovaries treated with smooth muscle stimulants. A contractile response may be induced by alpha-adrenergic receptors, which confirms the finding of smooth muscle fibers in the ovaries. Spontaneous contractions have also been observed in ovaries removed from animals at estrus. Estrogen activate, progesterone inhibits ovarian contractility. In rabbits and guinea pigs spontaneous activity of the ovary is increased during early pregnancy. Treatment with nor- epinephrine inhibits this. Quiescent ovaries show marked activation with nor-adrenergic compounds such as nor-epinephrine and phenilephrine. Pretreatment with alpha-adrenergic blocking agents such as progranolol reverses this effect. Prostaglandin F-2-alpha is a more powerful stimulant on ovarian motility than vasopressin or oxytocin. The role of ovarian contractions in the reproductive function is still unknown. Further studies may provide ways of interfering with reproduction at the ovarian level.
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PMID:Ovarian contractility and ovulation. 1225 6


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