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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of baroreceptors in common carotid and vertebral arteries and arteries in the thoracic cavity in vasopressin secretion was investigated in this study. Effects of bilateral occlusion of common carotid and vertebral arteries on blood ADH level as well as mean arterial pressure were studied in common carotid arterial plexus-denervated dogs, cervically vagotomized dogs and intact dogs. Blood ADH titers were determined by bioassay technic before and 5 minutes after the occlusion of the arteries and were compared with the changes of mean arterial pressure (MAP). The following results were obtained. (1) Blood ADH titers and MAP were elevated by the occlusion of the common carotid arteries in both intact and vagotomized dogs, while they were not significantly affected in denervated dogs. Elevation of blood ADH titers was more pronounced in vagotomized dogs than in intact dogs. (2) Blood ADH titers and MAP were elevated by the occlusion of vertebral arteries in all groups of dogs. However, the elevation of blood ADH titers in denervated dogs was more pronounced than in intact dogs, but less than in vagotomized dogs. (3) The effects of the occlusion of common carotid arteries on blood ADH titers and MPA were more pronounced than those of the occlusion of vertebral arteries. These results may suggest that: a. baroreceptors involved in vasopressin secretion are present in vertebral arteries as well, and that b. the intrathoracic baroreceptors are dominant in controlling vasopressin secretion, while those in common carotid arteries are secondly and those in vertebral arteries thirdly dominant.
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PMID:[Studies on the role of high pressure baroreceptors in vasopressin (ADH) secretion. Effect of occlusion of common carotid and vertebral arteries on blood ADH level (author's transl)]. 91 22

In the present paper the effects of nonapeptide hormones and of some of their chemical analogues were investigated on progesterone and testosterone production in granulosa cells of sow ovaries; the experiments were made in vitro. This objective was given by data on potential regulatory roles of nonapeptides at the level of hypothalamus, pituitary and reproductive organs. The goal of this experiment was to analyze the effects of various doses of oxytocin (OT), arginine-8-vasopressin (AVP), arginine-8-vasotocin and of some of their analogues on progesterone and testosterone production in vitro in granulosa cells of sow ovaries. The production activity of granulosa cells was investigated which were obtained from slaughtered sows without any changes in their reproductive process and abnormalities in their reproductive organs. Follicles of the size 2-5 mm without marked paleness in the early follicular phase were selected for aspiration. Granulosa cells with determined viability (more than 75%) and concentration (2 million/ml) were cultivated in defined culture conditions (37.5 degrees C, 5% CO2) after threefold resuspension and centrifugation of follicle fluid. These hormonal preparations were used in the experiments: pFSH, synthetic OT, synthetic AVP, synthetic AVP with antidiuretic effects and synthetic AVT. Progesterone and testosterone concentrations were analyzed radioimmunoanalytically using commercial kits of the Institute of Radio ecology and Nuclear Technology at Kosice. Statistically significant differences between the groups were evaluated by Student's t-test. The administered preparations were found to influence progesterone and testosterone production in dependence on the doses applied (Figs. 1-6). OT stimulation of progesterone production in granulosa cells indicated its regulatory role in relation to secretion of this hormone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Production of progesterone and testosterone in ovarian granulosa cells in sows after administration of nonapeptide hormones in vitro]. 141 99

1. The actions of angiotensin II, bradykinin, oxytocin, arginine vasopressin, relaxin, serotonin and the prostaglandins E2 and F2 alpha were examined on preparations of costo-uterine muscle from stilboestrol-treated rats. 2. All the agonists, except relaxin, when used in concentrations which contract the rat uterus, also produced contractions of costo-uterine muscles. Concentration-response curves were steep and maximal responses to the agonists were comparable. The negative log molar EC50 values were: serotonin, 6.5; angiotensin II, 8.8; bradykinin, 8.4; PGE2, 8.3; PGF2 alpha, 7.1. The EC50 values (units/L) for oxytocin and vasopressin were 4.4 and 2.7 respectively. 3. Indomethacin (2.8 or 5 mumol/L) did not decrease the contractile effects of the peptides or serotonin. The effects of serotonin were reduced, but not reversed, by methysergide (0.94 mumol/L). 4. Porcine relaxin inhibited field stimulation-induced contractions of costo-uterine muscle and uterine horns from immature rats pretreated with oestradiol cypionate and from stilboestrol-treated mature rats. It was much less potent, and its effects were less clearly concentration-related, on costo-uterine muscle. 5. The inhibitory effects of relaxin on the uterus were unaffected by propranolol (1 mumol/L), confirming that on this tissue relaxin acts independently of the release of catecholamines. Progesterone (30 mumol/L) was also without effect on the action of relaxin on the uterus. 6. These results taken together indicate that the costo-uterine muscle of the rat: (i) contracts in response to serotonin and the peptides angiotensin II, arginine vasopressin, bradykinin and oxytocin independently of the release of the contractile prostaglandins F2 alpha and E2; and (ii) in contrast to the uterus, may lack a significant population of receptors for relaxin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Actions of some autacoids and peptides, including relaxin, on costo-uterine muscle from rats. 257 64

Injection of a synthetic progesterone, medroxyprogesterone acetate (MPA or Depo-ProveraR), a widely used contraceptive, into Chinese hamsters (Cricetulus griseus) induced a profound polyuria with daily output of dilute urine equal to about 50% body weight of the hamster. However, relatively normal ability for renal urine concentration was demonstrated by administration of exogenous vasopressin. Body weight did not increase during onset of MPA-induced polyuria or during interval of vasopressin-induced oliguria, suggesting that primary polydipsia was not etiologic. Administration of this steroid to Chinese hamsters was nontoxic, although these polyuric animals were unusually sensitive to water deprivation. This polyuria was not observed when progesterone alone was injected into Chinese hamsters or when MPA was given to other related hamster species (Armenian, Syrian, Turkish or Djzungarian). The MPA-injected Chinese hamster represents a unique model of vasopressin sensitive diabetes insipidus induced by a steroid in a species-specific fashion.
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PMID:Medroxyprogesterone acetate induces diabetes insipidus in Chinese hamsters. 293 35

Oestrous rats were anaesthetized with pentobarbital, one of the femoral arteries and veins and one of the ovarian veins were cannulated, and a thin polyethylene cannula was fixed in the ovarian bursa. Five-min blood fractions were collected from the ovary for 50 min. Following the control fractions 15 mU of oxytocin, 15 mU of vasopressin or 50 microliter of 0.9% NaCl solution was given into the ovarian bursa over 10 min. Blood pressure and ovarian blood flow were continuously recorded. Progesterone (P) and oestradiol-17 beta (E2) were determined from the blood samples by RIA. Oxytocin did not alter the blood pressure, whereas the ovarian blood flow showed a short increasing tendency. Later, however, it started to decrease in parallel with the decrease in blood pressure owing to blood loss. The secretion of P and E2 remained unchanged. No changes in blood pressure were observed after vasopressin administration, although the ovarian blood flow quickly decreased in parallel with the secretion of P and E2. It is suggested that oxytocin has no direct effect on ovarian blood flow and hormone secretion in the rat. Vasopressin, however, is an effective vasoconstrictor in the rat ovary and may in this way reduce hormone synthesis.
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PMID:Effects of oxytocin and vasopressin on the ovarian blood flow, progesterone and oestradiol-17 beta secretion in oestrous rats. 406 Sep 75

Bovine ovaries were obtained from the abattoir and corpora lutea were classified as: (1) early luteal phase (approximately Days 1-4); (2) mid-luteal phase (Days 5-10); (3) late luteal phase (Days 11-17); (4) regressing (Days 18-20) and (5) pregnant (Days 90-230). In addition, preovulatory follicles and whole ovaries without luteal tissue were collected. Concentrations of oxytocin, vasopressin, bovine neurophysin I and progesterone were measured in each corpus luteum by radioimmunoassay. Progesterone and neurophysin I levels increased from Stage 1 to Stage 2, plateaued during Stage 3 and declined by Stage 4. Oxytocin and vasopressin concentrations increased from Stage 1 to Stage 2 but declined during Stage 3 and were low (oxytocin) or undetectable (vasopressin) in follicles, whole ovaries and pregnancy corpora lutea. Therefore the concentrations of both peptide hormones were maximal during the first half of the cycle and declined before those of progesterone. The high concentration of oxytocin within the corpus luteum coupled with the presence of bovine neurophysin I suggests that oxytocin is synthesized locally.
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PMID:Variations in oxytocin, vasopressin and neurophysin concentrations in the bovine ovary during the oestrous cycle and pregnancy. 674 62

To determine which ovarian hormone is involved in the sexually dimorphic antidiuretic action of vasopressin, the antidiuretic response to vasopressin was examined in sham-operated nonestrous female rats chronically treated with vehicle and in ovariectomized rats treated with vehicle, progesterone, estradiol, or the combination of estradiol and progesterone, respectively. Three-week-old female rats were sham operated or ovariectomized, and a slow-release hormone pellet was implanted at the 6th wk. The experiment was performed at the 10th to 12th wk in conscious, chronically instrumented rats hydrated with tap water (2% body wt). Infusion of vasopressin at rates of 10-1,000 pg.min-1.kg body wt-1 resulted in a dose-dependent antidiuretic response that was significantly enhanced in ovariectomized rats compared with the intact nonestrous females. Progesterone had no effect, whereas estradiol attenuated and restored the antidiuretic response to vasopressin to a level similar to that in intact nonestrous female rats. These results suggest that it is estrogen, but not progesterone, that reduces the antidiuretic response to vasopressin in the female rat.
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PMID:Estradiol attenuates the antidiuretic action of vasopressin in ovariectomized rats. 773 6

We investigated the effects of 17 beta-estradiol (beta E2), alpha-estradiol (alpha E2), and progesterone (P) on baseline and vasopressin (AVP)-induced [Ca2+]i in human platelets obtained from healthy male and female volunteers. Platelets were treated with beta E2, alpha E2, P, or ethanol vehicle for 30 min at 37 degrees C. In males, both beta E2 and P at 10(-5) mol/L reduced the AVP-induced rise in [Ca2+]i, to 72 +/- 3% (mean +/- SEM) and 53 +/- 3%, respectively. However, at 10(-6) mol/L only beta E2 had a significant effect (P < .02). In females, 10(-6) and 10(-5) beta E2 reduced the AVP response to 85.3 +/- 4.6% and 80.8 +/- 5.4% of control values, respectively. Progesterone (10(-6) and 10(-5) mol/L) reduced the AVP response to 83.8 +/- 5.1% and 60.3 +/- 2.0% of control values, respectively. The inactive estrogen alpha E2 had no effect on basal or AVP-induced rise in [Ca2+]i in either subject population, suggesting hormonal specificity. Neither beta E2 nor P affected baseline [Ca2+]i in either population. Thus, by attenuating [Ca2+]i responses in platelets, beta E2 and P may modulate platelet aggregation and atherosclerosis.
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PMID:Effects of estradiol and progesterone on platelet calcium responses. 775 50

We have shown previously that, in rats with deoxycorticosterone (DOC)-salt hypertension, arterial blood pressure rises more rapidly and reaches a higher level in male than in female rats and that the course of the hypertension was ameliorated by gonadectomy in male rats and exacerbated by gonadectomy in female rats. The present investigation was undertaken to examine the role of the gonadal steroid hormones in modulating the course of DOC-salt hypertension in the rat. Our previous findings with respect to the effects of gender and gonadectomy on DOC-salt hypertension were confirmed in this study. Chronic treatment with gonadal steroids was begun 1 week before the start of the DOC-salt protocol. 17 beta-Estradiol attenuated the course of the hypertension in intact male rats and in gonadectomized females. Testosterone exacerbated the development of the hypertension in gonadectomized male rats but was without effect in intact females. Progesterone alone had no effect on the hypertension in ovariectomized rats but when given to ovariectomized rats in combination with estradiol transiently prevented the ameliorating effect of the estradiol. These effects of the gonadal steroid hormones could not be attributed to effects of saline intake. Thus, these findings demonstrate that the gonadal steroid hormones play an important role in modulating the pathogenesis of DOC-salt hypertension in the rat. It is suggested that the effects of the gonadal hormones on the course of the hypertension may be due to modulation of the cardiovascular and renal actions of vasopressin, since vasopressin is required for this model of hypertension.
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PMID:Gonadal hormones modulate deoxycorticosterone-salt hypertension in male and female rats. 903 48

The affinity and specificity of an antagonist of oxytocin, [1-D(CH2)5,Tyr(ME)2,Thr4,Tyr-NH2(9)]ornithine vasotocin (OTA), to oxytocin receptors (OTR) in bovine gestational endometrium was determined in displacement experiments with oxytocin (OT) and vasopressin (AVP) analogues and compared to myometrial OTR. OTA had the highest affinity in both tissues. The effect of OTA on OT-induced increase in plasma concentration of 13,14-dihydro-15-keto-prostaglandin F2alpha metabolite (PGFM) was studied in 24 late-pregnant cows. Treatments consisted of i.v. saline; OT (50 IU); OTA (1200 microg); and OTA (400, 1200, or 4000 microg) injected i.v. 5 min before OT (50 IU) (n = 4 each). Samples were collected from jugular vein at 15-min intervals for 30 min before and 3 h after the injection of OT. Progesterone was measured in once-daily samples taken for 7 days after the experiment. OT caused a twofold increase in plasma PGFM within about 60 min (p < 0.005), with levels returning to baseline at 150-180 min; OTA (1200 microg) caused a gradual lowering of basal plasma PGFM over 180 min (p < 0.05). The 400-microg or 1200-microg dose of OTA did not alter OT-induced PGFM response, whereas the 4000-microg dose inhibited it almost completely (p < 0.005). Plasma progesterone declined after the experiment in all cows, with no differences among groups. Because OTA inhibits OT-induced release of endometrial prostaglandin F2alpha it may be a good tocolytic agent.
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PMID:Oxytocin antagonist [1-D(CH2)5,Tyr(ME)2,Thr4,Tyr-NH2(9)]ornithine vasotocin inhibits oxytocin-induced prostaglandin F2alpha release in late-pregnant cows. 924 Oct 61


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