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)

A new hypothesis is presented for the first time to explain the etiology of osteoporosis. Prostaglandins (E2 and F2 alpha) at precise concentrations, have been observed to be involved in bone formation. A close association exists between levels of prostaglandins (E2 and F2 alpha) demonstrated in the neonatal mouse leading to bone formation, with estimated prostaglandins (E2 and F2 alpha) concentrations reported in man. Several hormones (vasopressin, oxytocin, luteinizing hormone, follicle-stimulating hormone, cortisol, estradiol, and testosterone) can indirectly affect prostaglandin formation leading to reduced bone formation. The association between these hormones and prostaglandins (E2 and F2 alpha) explains the physiological mechanism whereby estradiol can be effective for the treatment of osteoporosis. This association also explains the etiology of lumbar spondylitis/spondylodynia, reasons for complaints of increased pain in wet cold weather among arthritics and a multitude of other events. Mechanisms related to this interaction between various hormones and the effect of prostaglandins (E2 and F2 alpha) on bone formation are discussed.
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PMID:New clues into the etiology of osteoporosis: the effects of prostaglandins (E2 and F2 alpha) on bone. 132 11

The Asu-AVT (1,6-aminosuberic acid -8-arginine-vasotocin) in an analogue of 8-arginine-vasotocin (AVT) which is one of pineal hormones. The effect of Asu-AVT on the pain threshold and EA analgesia was studied in rats. An increase of 16.2-41.5% in pain threshold was observed within 70 min. after ivc of Asu-AVT (75ng), while the Asu-AVT injection in combination with EA produced a significant increase of 164.6-309.1% in pain threshold, which was much higher than that in the saline-EA group (p < 0.05-0.01). The effect of Atu-AVT is analogous to that of oxytocin and arginine-vasopressin. The data indicate ivc of ASu-AVT not only elevates the pain threshold, but also enhances the EA analgesia. These results suggest that the pineal hormone, AVT may play a role in the EA analgesia.
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PMID:[Effect of Asu-AVT on electroacupuncture (EA) analgesia]. 133 26

In a phase I trial, 12 patients with GD2 antigen-positive metastatic melanoma received the murine anti-GD2 monoclonal antibody 14G2a. The monoclonal antibody was administered in four doses over an 8-day period with total dose ranging from 10 to 120 mg. All patients receiving greater than 10 mg of 14G2a experienced transient abdominal/pelvic pain during the antibody infusion. Five patients had a delayed extremity pain syndrome following the third and fourth antibody infusion. Four of the five patients developed neurological toxicity, including two patients with significant although reversible motor neuropathy. Two of the patients developed hyponatremia secondary to a syndrome of inappropriate antidiuretic hormone. All 12 patients developed high levels of human anti-14G2a antibody. The plasma half-life of 14G2a was 42 +/- 6 (SD) h. One patient each had a partial response, mixed response, and stable disease, respectively. The very modest antitumor activity accompanied by dose-limiting neurological toxicity at total doses greater than 80 mg may restrict the clinical utility of murine 14G2a.
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PMID:Phase I trial of the murine monoclonal anti-GD2 antibody 14G2a in metastatic melanoma. 164 31

The opioid peptide, beta-endorphin, originates from proopiomelanocortin (POMC) under the influence of corticotropin releasing hormone (CHR). It increases the threshold of pain and has a certain influence on the formation of hypophyseal hormones, especially in stress. It is found that beta-endorphin stimulates the secretion of prolactin, a growth hormone, and vasopressin; it inhibates formation of follicle-stimulating and luteinizating hormones, oxytocin and dopamine, and gonadotropin, a releasing hormone. The process of acetylization decreases its activity. The results of experimental trials revealed that acetylisation in the foetal period was absent. The aim of the study was to define beta-endorphin concentration during normal vaginal labor and Cesarean section. Samples of peripheral blood of patients with spontaneous vaginal labor (n = 15) and of those in whom labor was operatively terminated (Cesarean section) (n = 10), were analysed. Values of this opiate were determined in the umbilical cord of newborn infants, in the amniotic fluid and placental compartment. The obtained results were statistically analysed. In intrapartum beta-endorphins were significantly increased reaching the highest level during expulsion (326 pg/ml); in the placental compartment these values were higher (in retroplacental blood 514 pg/ml) reaching the highest value of 917 pg/ml, p less than 0.01 in the placenta. In Cesarean section beta-endorphin values in the peripheral blood showed no significant differences during spontaneous vaginal labor. However, increased values of this natural opiate were observed six hours after surgery. Beta-endorphin concentrations in the placental compartment and the placenta during normal vaginal labor were significantly higher in comparison with labor by Cesarean section (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The opioid peptide, beta-endorphin, in spontaneous vaginal delivery and cesarean section]. 180 97

The purpose of the present study was to measure plasma levels of atrial natriuretic peptide (ANP) in patients with acute myocardial infarction without heart failure, and also to assess the temporal sequence of changes of plasma ANP during the first hours of recovery from myocardial infarction. The study was performed in 22 patients who were admitted to the Intensive Care Unit with the diagnosis of acute myocardial ischaemia that had an evolution of less than 6 h. Blood samples were drawn on admission and at 1, 8, and 24 h, and plasma concentrations of ANP, renin, aldosterone, epinephrine, norepinephrine and vasopressin were measured. Compared with control subjects, on admission patients showed increased plasma levels of ANP, as well as increased plasma renin activity (PRA), aldosterone, norepinephrine, epinephrine, dopamine, and antidiuretic hormone (ADH). ANP, but not renin or aldosterone plasma values, decreased with time, and there was a significant correlation between ANP and time after onset of pain. No increase in plasma creatinine was observed during the hospital stay, and the patients showed a negative fluid balance. No relationship was found between the location or extension of the infarction, or morphine treatment and ANP plasma levels. The high levels of ANP seem to counteract the haemodynamic and fluid-retention effects of the vasoconstrictive factors released after myocardial infarction.
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PMID:Atrial natriuretic peptide in patients with acute myocardial infarction without functional heart failure. 182 81

Recent evidence has indicated that vasopressin (VP) can increase the pain threshold. It is not clear whether the paraventricular nucleus (PVN) of hypothalamus, which is one of the main nuclei that secrete VP in brain, is involved in the acupuncture analgesia (AA). The present study was designed to examine the role of PVN in AA. Experiments were carried out on Wistar rats using tail stimulation vocalization test to measure the pain threshold. The acupoints "Renzhong" and "Chengjiang" were selected for electroacupuncture. Electrical stimulation of PVN could increase significantly the pain threshold and enhance the effect of AA. On the contrary, electrolytical lesion of PVN could decrease the effect of AA obviously, which could be recovered by cerebroventricular injection (ICV) of 300 ng of arginine VP. Pretreatment with AVP-antiserum (ICV) could attenuate the effect of AA. These data indicated that PVN plays an important role in pain modulation and in the effect of AA. This role might be mediated by the VP-containing neurons in PVN.
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PMID:[The role of paraventricular nucleus of hypothalamus in acupuncture analgesia in rats]. 187

The analgesic effect of electrical stimulation of the hypothalamic paraventricular nucleus (PVN) was studied. Additionally, the involvement of vasopressin and opioid peptides in this process was examined by comparing vasopressin-deficient (Brattleboro) and Long-Evans rats and by administering the opiate antagonist naloxone. Rats were chronically implanted with a stimulating electrode in the parvocellular (PVN-Pc) and magnocellular (PVN-Mg) divisions of the PVN. At least 10 days after surgery, the analgesic effects of PVN stimulation were examined in lightly anesthetized rats, using the tail-flick method, and in unanesthetized rats, using the hot-plate test. PVN stimulation produced marked analgesia in both tests. Current threshold for analgesia was lower from PVN-Pc than from PVN-Mg. Threshold did not differ significantly between Brattleboro and Long-Evans rats and was not affected by naloxone administration. The results indicate that the PVN is part of the brain's pain inhibitory system, and show that the analgesia induced by PVN stimulation is not mediated by either vasopressin or opioid peptides.
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PMID:Stimulation of the hypothalamic paraventricular nucleus produces analgesia not mediated by vasopressin or endogenous opioids. 198 39

Patient preparation and a modified operative technique are described for electrocoagulation ablation of the endometrium using a roller-bar electrode. No preoperative or postoperative endometrial suppression was used. Rather, the endometrial cavity was denuded by suction curettage just before ablation, which was performed in the early proliferative phase of the menstrual cycle. Lidocaine paracervical block containing vasopressin was injected at the start of the procedure to control pain and to minimize bleeding and irrigation fluid absorption. Pulsed irrigation of the uterus was used to improve visibility through uterine debris and the bubbles generated by the electrical current. The first 20 patients who had electrocoagulation ablation of the endometrium with these modifications were compared with the first 18 patients who had laser coagulation ablation using standard technique and preoperative endometrial suppression. Compared with the laser method, the modified coagulation method resulted in a comparable rate of satisfactory bleeding decrease at 6 months (90 versus 94%), but involved a clinically significant reduction in total anesthesia time (66.8 versus 117.3 minutes) and volume of irrigation fluid used (5.7 versus 15.9 L).
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PMID:Modified endometrial ablation: electrocoagulation with vasopressin and suction curettage preparation. 203 Aug 76

A review of the clinical features, diagnosis and management of primary and secondary dysmenorrhea updates some old views. Dysmenorrhea is painful menstruation, either cramps with no visible cause, primary dysmenorrhea, or secondary to specific pelvic pathology. Primary dysmenorrhea occurs in as many as 50% of young women, only in ovulatory cycles, and usually limited to the first 48 or 72 hours of menstruation. Secondary dysmenorrhea can be caused by any of a dozen or so disorders such as endometriosis, pelvic inflammatory disease, IUDs, irregular cycles or infertility problems, ovarian cysts, adenomyosis, uterine myomas or polyps, intrauterine adhesions or cervical stenosis. Psychological factors are now known not to cause dysmenorrhea, only to add to the reactive component of the pain. The pain is due to uterine cramps, hypoxia or ischemia, due to overproduction of prostaglandins, leukotrienes or vasopressin. Thus, primary dysmenorrhea can be treated with oral contraceptives if the women wishes to take pills for contraception and they are not contraindicated, or with non-steroidal antiinflammatory agents for the full 72 hours after pain begins. Calcium channel-blockers are also used on a research basis; transcutaneous electrical nerve stimulation is sometimes effective. If these treatments are not effective, investigation for causes of secondary dysmenorrhea is indicated, preferably for laparoscopy.
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PMID:Dysmenorrhea. 217 34

A total of 119 patients with myocardial infarction hospitalized within 24 hrs from the disease onset were examined. He-Ne laser irradiation of the blood (daily 40 min sessions for 3-5 days) was carried out in 45 patients (Group 1). The rest 74 patients (Group 2) were administered common therapy. A number of biologically active substances were radioimmunoassayed in the blood of 12 Group 1 and 11 Group 2 patients on days 1, 3, and 7 of the disease. The pain syndrome was alleviated in Group 1 patients, in contrast to Group 2 patients, and the frequencies of ventricular arrhythmias, of heart failures, and of the condition recurrences were reduced, as was the mortality rate. Laser therapy resulted in reduction of the activities of the hypophyseoadrenocortical and aldosteron-renin-angiotensin systems. Besides blood levels of dilatants and proaggregants (PGF2 alpha, vasopressin, angiotensin II) reduced in these patients, whereas vasodilating and antiaggregation hormones (PGE, PGI2) levels increased and the PGI2/TxB2 ratio improved.
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PMID:[The use of low-intensity laser irradiation of the blood in myocardial infarction]. 236 94


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