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)

In an in vitro trial on 80 pregnant and nonpregnant mice, the sensitivity of the uterus myometrium to the vasoconstrictors vasopressin, ornipressin, epinephrine, and norepinephrine was examined in comparison with oxytocin as a standardized stimulative drug. The pregnant uterus showed a significantly increased sensitivity to ornipressin, vasopressin, and norepinephrine. Epinephrine showed no uterus-stimulating effect, and an increase of sensitivity caused by pregnancy was not detected.
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PMID:Vasoconstrictors during pregnancy--in vitro trial on pregnant and nonpregnant mouse uterus. 789 Sep 95

Platelets respond through discrete receptors to a number of physiological agonists and foreign surfaces with a sequence of measurable responses: shape change, aggregation, secretion and arachidonate liberation. Three secretory responses are distinguished: exocytosis of substances from (1) dense granules, (2) alpha-granules and (3) lysosomes. Free arachidonate, liberated from phospholipids by phospholipase A2, is rapidly converted (by oxygenation) to prostaglandins and thromboxanes which, together with secreted ADP and close cell contact, will cause further platelet activation through 'positive feedback' (autocrine stimulation). Some agonists are classified as 'weak' (ADP, vasopressin, platelet-activating factor [PAF], serotonin) because they depend on autocrine stimulation to promote the full sequence of responses, while others are 'strong' agonists (thrombin, collagen) and activate all responses directly without autocrine stimulation. Adrenaline, long thought to be a platelet agonist per se, most probably acts by amplifying the activation brought about by other, proper, agonists. Such synergistic interaction among agonists is very typical for platelet activation and most likely takes place in vivo. Shape change, aggregation and secretion(s) may be tested by flow cytometry or electron microscopy in vitro under conditions that probably reflect the in vivo situation. However, the aggregation response to weak agonists in vitro is dependent on the extracellular [Ca2+], with biphasic aggregation at the low [Ca2+] present when citrate is used as anticoagulant (or in suspension of washed platelets) but not at the physiological [Ca2+] present in platelet-rich plasma from heparinized blood.
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PMID:Significance of testing platelet functions in vitro. 801 28

Effect of various doses of oxytocin, vasopressin or adrenalin on the thyroid gland activity was studied in hypophysectomized and nonoperated rats 20 minutes after a single injection of the neurohormones. The minimal applied dose of the neurohormones stimulated increasing of their concentration in blood up to level typical for stress reaction. Injection of oxytocin led to no effect at any dose. In nonoperated rats vasopressin stimulated the thyroid gland but did not influence on TSH level in blood. In hypophysectomized rats thyrostimulating effect of vasopressin was also detected need. Adrenalin injection inhibited the thyroid gland function in both nonoperated and hypophysectomized rats. Effect of adrenalin in combination with vasopressin was like the action of adrenalin alone. Thus, it is possible to assume that under stress conditions a high blood level of adrenalin attenuates thyrostimulating effect of vasopressin.
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PMID:[The blocking effect of adrenaline on the thyroid-stimulating effect of vasopressin in rats]. 804 87

Adrenal-postpituitary imbalances express pathological evolutions of the nonlinear biological oscillator due to hormonal coupling between adrenocortical hormones and vasopressin. This system, based on agonistic-antagonistic equilibration, can be represented by a nonlinear model to be controlled in the pathological case, in order to reach a physiological state. The modeling introduced by E. Bernard-Weil has already led to efficient therapeutics and can thus be considered realistic. We can therefore use the simulated data given by Bernard-Weil, and although our results on control are obtained by simulation, they are meaningful. The therapy is based on the idea of moving the pathological controlled system from the pathological state to the physiological one. However, it is proved that with a periodic control one is not able to achieve the precise objective. This leads us to introduce the locking concept, which allows system parameters to change and provides the basis for an adaptive and iterative control, here given by a sequence of polynomial correctors. In a few iterations we are now able to find the physiological behavior again. Moreover, as we have to identify the parameters of the considered models and control laws, we have to study their structural identifiability. We can prove, thanks to the work of Vajda and his colleagues, the global identifiability of the uncontrolled 12-parameter model. We also prove the local identifiability of the eight-parameter controllers.
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PMID:Nonlinear adaptive control of adrenal-postpituitary imbalances and identifiability analysis. 893 58

Prolonged use of glucocorticoids (GCs) can cause prolonged suppression of the hypothalamus-pituitary-adrenal (HPA) axis. This study examined the possibility that corticotropin or its secretagogues such as vasopressin, corticotropin-releasing hormone (CRH), or insulin accelerate recovery of the HPA axis after prolonged treatment with dexamethasone (DEX). Suppression of the HPA axis was induced in rats by DEX at a dosage of 250 micrograms/100 g body weight (BW)/d for 14 days, after which rats were administered saline, corticotropin (Cortrosyn 0.1 mg), ovine CRH (oCRH 6 micrograms), vasopressin (2 U), or insulin (2 U) each morning. Adrenal weight (AW), BW, plasma corticosterone, and corticotropin, as well as pituitary corticotropin content, decreased significantly after DEX treatment. The plasma corticotropin level was significantly elevated 7 days after discontinuation of DEX treatment (day 8) and remained so until day 11, whereas the pituitary corticotropin content had returned to normal on day 8. Plasma corticosterone was suppressed until day 8, but was not significantly different from normal on day 11. The AW was also decreased until day 4, but was not different from normal on day 8 or day 11. The BW of experimental rats remained subnormal during the study period. Treatment of DEX-suppressed rats with exogenous corticotropin induced adrenal hyperplasia, but suppressed the plasma corticotropin level and delayed the normalization of plasma corticosterone until day 11. The insulin-treated group differed in no respect from the saline-treated group. Treatment with oCRH or vasopressin for 8 days normalized plasma and pituitary corticotropin, as well as plasma corticosterone. Hypothalamic immunoreactive CRH (iCRH) did not differ among any treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Corticotropin secretagogues facilitate recovery of the hypothalamus-pituitary-adrenal axis suppressed by prolonged treatment with dexamethasone. 817 41

Two questions were investigated to elucidate the adrenal function of arginine vasopressin (AVP) in controlling aldosterone secretion: Are vasopressin tissue concentrations in the adrenal modulated by diets that influence aldosterone secretion? Does its direct stimulation of aldosterone secretion from adrenal cells in vitro suggest that vasopressin plays an important role in controlling aldosterone? Diets that modulate aldosterone secretion from rat adrenals did not modulate concentrations of AVP in this tissue: Adrenal AVP concentrations did not differ significantly between rats on low- and high-sodium (22.9 +/- 3.8 and 32.4 +/- 6.4 pg/g) or between low- and high-potassium (25.6 +/- 2.5 and 12.5 +/- 7.3 pg/g) diets. Although the existence of AVP receptors on adrenocortical cells incubated in vitro and the stability of AVP during cell incubation was confirmed, AVP had only a minor direct effect on steroid secretion in short-term incubations alone and in combination with angiotensin II (A II), potassium and atrial natriuretic factor (ANF). The importance of AVP for an indirect control of aldosterone secretion in vivo is discussed.
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PMID:Influence of sodium and potassium diets on adrenal vasopressin content and direct effects of vasopressin on aldosterone synthesis in adrenocortical cells. 822 84

This study was undertaken to investigate in a prospective randomized way the influence of the benzodiazepine antagonist flumazenil on endocrine stress response and haemodynamic parameters after modified neuroleptanaesthesia. A total of 24 patients (ASA scores I or II) aged between 18 and 60 who were scheduled for major gynaecological surgery, were investigated. For modified neuroleptanaesthesia, midazolam, fentanyl and vecuronium were administered in standardized doses. After extubation, patients of the flumazenil group received initial injections of 0.2 mg flumazenil to antagonize the residual effect of midazolam and additional doses of 0.1 mg per minute until the desired level of vigilance was reached (awareness of person, time and place). In the control group no flumazenil was used. Endocrine stress parameters and haemodynamic parameters were measured at 7 different times, from before induction of anaesthesia up to 60 minutes after the operation. In both groups, a marked increase in endocrine stress response was observed. Adrenaline, noradrenaline, antidiuretic hormone, adrenocorticotropic hormone, cortisol, glucose and lactate, however, were not additionally influenced by the antagonism. No influence of flumazenil on mean arterial pressure, heart rate and arterial oxygen saturation was observed. After modified neuroleptanaesthesia, a careful antagonism of midazolam with small doses of flumazenil is not disadvantageous with respect of endocrine stress response and haemodynamic reactions.
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PMID:[The effect of flumazenil on the endocrine stress reaction following modified neuroleptanesthesia]. 824 Jun 40

Bleeding may become a major impediment to accurate and safe dissection by laparoscopy. The traditional maneuvers of pressure, dumping, irrigation, and aspiration frequently applied during open procedures to maintain a clear field of dissection are cumbersome through laparoscopy. Several pharmacologic agents have been used topically or by local injection to stop bleeding or to prevent excessive blood loss during surgical procedures. They include calcium alginate, aluminum salts, silver nitrate, formalin, and coagulating agents like thrombin and collagens, all of which leave a layer of damaged tissue or foreign material on the surface. Epinephrine and vasopressin have been employed mostly by local injections. We report the use of topical epinephrine applied before and during the dissection of the cystic duct and artery area in the course of laparoscopic cholecystectomy. A 3/8-inch gauze sponge, impregnated with a 1:10,000 epinephrine solution, was used to blanch the tissues and to bluntly dissect the cystic duct and artery. It was also used to control minor bleeding in the gallbladder fossa. The prophylactic bleeding control with topical epinephrine proved to be an easy and safe maneuver, and greatly facilitated the dissection of the most critical areas during laparoscopic cholecystectomy. This technique may be applicable to laparoscopic dissection for other procedures.
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PMID:Pharmacologic hemostasis in laparoscopy: topical epinephrine facilitates cholecystectomy. 848 94

Recombinant thrombopoietin has been reported to stimulate megakaryocytopoiesis and thrombopoiesis and it may be quite useful to treat patients with low platelet counts after chemotherapy. As little is known regarding the possible activation of platelets by thrombopoietin, we examined the effects of thrombopoietin on platelet aggregation induced by shear stress and various agonists in native plasma. Using hirudin as an anticoagulant, thrombopoietin (1 to 100 ng/mL) enhanced platelet aggregation induced by 2 micromol/L adenosine-diphosphate (ADP) in a dose dependent fashion. The enhancement was not affected by treatment of platelets with 1 mmol/L aspirin plus SQ-29548 (a thromboxane antagonist, 1 micromol/L) but was inhibited by a soluble form of the thrombopoietin receptor, suggesting that the enhancement was mediated by the specific receptors and does not require thromboxane production. Epinephrine (1 micromol/L), which does not induce platelet aggregation in hirudin platelet rich plasma (PRP), did so in the presence of thrombopoietin (10 ng/mL). Thrombopoietin (10 ng/mL) also enhanced or primed platelet aggregation induced by collagen (0.5 micron.mL),. thrombin, serotonin, and vasopressin. Thrombopoietin does not induce any rise in cytosolic ionized calcium concentration nor activation of protein kinase C, as estimated by phosphorylation of preckstrin, indicating that the priming effects of thrombopoietin does not require those processes. The ADP- or thrombin-induced rise in cytosolic ionized calcium concentration was not enhanced by thrombopoietin (100 ng/mL). Further, shear (ca. 90 dyn/cm2)-induced platelet aggregation was also potentiated by thrombopoietin. The priming effect on epinephrine-induced platelet aggregation in hirudin PRP was unique to thrombopoietin, with no effects seen using interleukin-6 (IL-6), IL-11, IL-3, erythropoietin, granulocyte-colony stimulating factor, granulocyte macrophage-colony stimulating factor, or c-kit ligand. These data indicate that monitoring of platelet functions may be necessary in the clinical trials of thrombopoietin.
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PMID:Thrombopoietin primes human platelet aggregation induced by shear stress and by multiple agonists. 863 35

Stageness in the protein glands development is influenced by the nervous system mediators. Adrenergic mediation was established not to be developed by the period of provisory differentiation and appears to grow weaker by senile age. Acetylcholine stimulates growth and proliferation in the form of layers and bands. Adrenalin exerts its influence on organotypical level, which manifestates in reservation of the specific differentiation and protein type functioning of the gland. Hypothalamic neurohormones (oxytocin, vasopressin) influence the maintainance of the secretory epithelium viability.
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PMID:[The morphofunctional characteristics of the epithelium of the salivary glands and the neuroendocrine regulation of its histogenesis]. 868 39


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