Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously proposed the ovarian ERAANPS (endothelin-rein- angiotensin-atrial natriuretic peptide system). The present study was undertaken to examine in vivo the effects of herbal medicines [Tokishakuyakusan (TS), Keishibukuryogan (KB), Shakuyakukanzoto (SK) and Unkeito (UT)] on endothelin-1 (ET), renin and angiotensin II (A II) in the ovaries, of immature rats treated with 10 IU PMS for 48 h. ET and all components of renin-angiotensin system (RAS) were found at high levels in the ovary. Concomitant treatment with PMS plus TS, KB, SK or UT, especially TS and UT, tended to decrease the ET levels in ovary, while components of RAS tended to increase. However, ET, renin and A II levels in plasma were not at all affected after treatment with TS, KB, SK or UT. These results suggest that TS, KB, SK or UT may regulate the ovarian ERAANPS.
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PMID:Effects of tokishakuyakusan, keishibukuryogan, shakuyakukanzoto and unkeito on ovarian endothelin, renin and angiotensin II in pregnant mare's serum gonadotropin-treated immature rats. 151 58

PMS is probably a group of entities which include various symptoms that occur during the 7 to 10 days before menstruation and disappear a few hours after the onset of menstruation. The definition of PMS lacks objective criteria. The most common symptoms are irritability, bloating, aggressiveness, mastodynia, and headaches. The prevalence of PMS is estimated at 30 to 40 per cent. PMS is more prevalent among women working outside the home, alcoholics, women of high parity, and women with toxemic tendency; it probably runs in families. The etiology of PMS is no less obscure to us than when it was first described by Frank in 1931. No single theory has been established to explain the entire diversity of PMS symptomatology. The multitude of possible etiologic factors includes psychosocial bases, progesterone deficiency, prolactin excess, thyroid hypofunction, renin angiotensin alternations, antidiuretic hormone excess, decreased colloidosmotic pressure, endorphin activity alternations, serotonin metabolism alternations, prostaglandin action, vitamin deficiency, and such unconventional theories as the ovarian infection or the "yeast overgrowth" theory. A partial resolution of this divergence of hypotheses comes from the biopsychosocial model developed by Keye and Trunnel. According to this model, a biologic, perhaps genetically determined, predisposition to PMS is realized when past and present life experiences, attitudes, beliefs, coping styles, and social forces interact to stress a woman. The diagnosis of PMS is based on establishing a relationship between the luteal phase of the cycle and the symptoms. The evaluation of PMS patients includes the use of a monthly diary to scale the symptoms, a physical examination, and biochemical studies to rule out other disorders. Management includes education, reassurance, and drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The premenstrual syndrome. 218 58

Estrogens are known to increase the renin-angiotensin-aldosterone system and to produce fluid retention, while atrial natriuretic peptide (ANP) induces an increase of the urinary output and tends to return the fluid balance to normal. The aim of this study was to test whether the levels of ANP were decreased during chronic estrogen and progestin administration, thereby possibly decreasing the amount of fluid excreted. The authors also studied women with premenstrual syndrome (PMS), because of the associated fluid retention often described with this syndrome. Levels of ANP, plasma renin activity (PRA), and aldosterone were determined in premenopausal women in the early follicular phase (EFP) and on low-dose oral contraceptives (OC), in postmenopausal patients with and without estrogen replacement therapy (ERT), and in women with PMS associated with fluid retention. The concentrations of ANP and PRA were enhanced in the women on OC, but those of aldosterone were unchanged. No differences were observed in the women on ERT or with PMS. It is concluded that the levels of PRA and ANP are affected by estrogen or progesterone therapy or the combination of the two and this response is dose dependent or additive. Furthermore, ANP and PRA do not seem to play a direct role in PMS.
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PMID:Atrial natriuretic peptide, plasma renin activity, and aldosterone in women on estrogen therapy and with premenstrual syndrome. 297 66

Premenstrual syndrome (PMS) is a diagnostic enigma that causes significant morbidity in many woman. Numerous theories have been proposed in an attempt to explain the varied symptoms that occur cyclically in women with PMS. Suggested etiologic theories of PMS include psychological abnormalities, nutritional deficiencies, aberrations in the renin-angiotensin-aldosterone axis, altered prostaglandin activity, hormonal imbalances, and changes in endogenous opioid peptide activity. Because of the lack of standardized diagnostic criteria, clinical drug trials for PMS have been severely compromised. For every proposed cause of PMS, there exists a drug or drug class that has been investigated for treatment of the associated symptoms. Many clinical studies are uncontrolled, a significant deficiency in study design for a disorder that is associated with a high placebo response rate. At the present time, no definitive treatment for PMS exists and therapy must be individualized according to clinical response. This review article defines PMS, describes one of the current approaches to the diagnostic work-up, discusses the proposed etiologies of PMS, and reviews the various proposed treatment modalities.
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PMID:Review of the etiology and treatment of premenstrual syndrome. 390 31

Phasic oral contraceptives (OCs) provide a physiological approach to contraception and most closely approximate the ideals of a combined OC with the lowest possible doses to avoid the metabolic risks of estrogens and progestins, maximal contraceptive protection, and satisfactory cycle control. Earlier studies have demostrated the decline in myocaridal infarct and thromboembolic disease with reduction of ethinyl estradiol (EE) from 50 to 30 mcg, the correlation between progestin dose and cardiovascular and cerebrovascular deaths, and the effects of progestins derived from 19 nortestosterone in reducing the beneficial high density lipoprotein (HDL) cholesterol. The preparation SH B 264 AB for example provides a 1st phase daily dose of 30 mcg EE and 50 mcg levonorgestrel, a sufficient dosage because of the low probability of ovulation but 1 which attempts to mimic the follicular secretion needed for endometrial growth. Daily doses in the 2nd phase increase to 40 mcg EE and 75 levonorgestrel, each of which is capable alone of inhibiting ovulation. The progestin causes a supplementary hypothalamic inhibition and renders the cervical mucus too viscous for sperm penetration, while the EE augments the hypothalamic inhibitory effect of the progestin, prevents release of luteinizing hormone releasing hormone, and suppresses the luteinizing hormone peak by increasing the pituitary threshold to hypothalamic stimulation. The total dose of SH B 264 AB is at least 30% less than that of other OCs. The Pearl index is 0.0-0.6, not quite as good as that of normal dosed OCs. The duration of menstrual bleeding appears unchanged even after prolonged use, while the amount of bleeding is slightly decreased. Amenorrhea and intermenstrual bleeding are rare. The good cycle control occurs because the steroid levels administered in the triphasic pill mimic those of ovarian secretion, leading to better endometrial development. The effects of triphasic pills on glycemia and insulin levels are very weak and are not statistically significant, while their slight estrogen dominance means that they have very slight effects on the level of HDL cholesterol. They cause a slight increase in triglyceride levels, minimal variation in coagulation parameters, a weak variation in factors VII, VIII, X, and plasminogen, and a slight decrease of antithrombin III. Triphasic OCs induce minimal augmentation in activity of the renin-angiotensin system, and in most cases do not affect blood pressure. Because of their estrogenic dominance, triphasic pills improve acne but may be associated with breast problems, water retention, dysmenorrhea, and premenstrual syndrome with irritability, nervousness, and headache. Triphasic pills are indicated for women beginning OCs, women with poor cycle control under other OCs, women at high cardiovascular risk, women with acne, and women whose current OCs cause oily skin, hirsutism, reduced libido or other symptoms. Contraindications for the triphasic pill in addition to the usual factors include benign breast disease, premenstural syndrome, dysmenorrhea, or polycystic ovarian syndrome.
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PMID:[Pros and cons of triphasic oral contraception]. 1226 12

Premenstrual syndrome (PMS) presents with emotional and physical symptoms. Although the emotional symptoms have been extensively studied, the pathophysiology of the fluid-retention symptoms is not currently known. We tested the hypothesis that the fluid regulatory mechanisms are disturbed in PMS. Nine regularly menstruating women with PMS were compared with 9 healthy age-matched women. Hemodynamic parameters and upright plasma volume shift (extrapolated from changes in hematocrit), plasma renin activity (PRA), and plasma aldosterone and sex hormones were measured at different times during the menstrual cycle. During the early follicular and the midluteal phases, the plasma volume shift, supine and upright PRA, and plasma aldosterone were similar in both groups, and none of the participants had edema. However, during the late luteal phase, ankle edema was present only in women with PMS, and their maximal plasma volume shift was lower compared with controls (11.7+/-1.3 versus 15.6+/-0.6; P=0.004). The area under the curve (estimates the amount of the total plasma shift during 30 minutes standing) was 300+/-28 and 406+/-16 in PMS and controls, respectively (P=0.01). PRA and aldosterone levels were higher during the late luteal phase in women with PMS compared with controls (supine PRA: 1.4+/-0.3 [PMS] versus 1.1+/-0.4 [control; P value not significant], upright PRA: 3.9+/-0.08 versus 1.6+/-0.3 ng/mL per hour [P=0.015], supine plasma aldosterone: 131+/-30 versus 68+/-17 pg/mL [P=0.09], and upright plasma aldosterone: 208+/-40 versus 102+/-16 pg/mL [P=0.03]). We, therefore, conclude that women with PMS have increased plasma fluid-regulatory hormones and disturbed fluid distribution only during their late luteal menstrual phase.
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PMID:Hormonal and volume dysregulation in women with premenstrual syndrome. 1825 15

Premenstrual syndrome is defined as recurrent moderate psychological and physical symptoms that occur during the luteal phase of menses and resolve with menstruation. It affects 20 to 32 percent of premenopausal women. Women with premenstrual dysphoric disorder experience affective or somatic symptoms that cause severe dysfunction in social or occupational realms. The disorder affects 3 to 8 percent of premenopausal women. Proposed etiologies include increased sensitivity to normal cycling levels of estrogen and progesterone, increased aldosterone and plasma renin activity, and neurotransmitter abnormalities, particularly serotonin. The Daily Record of Severity of Problems is one tool with which women may self-report the presence and severity of premenstrual symptoms that correlate with the criteria for premenstrual dysphoric disorder in the Diagnostic and Statistical Manual of Mental Disorders, 4th ed., text revision. Symptom relief is the goal for treatment of premenstrual syndrome and premenstrual dysphoric disorder. There is limited evidence to support the use of calcium, vitamin D, and vitamin B6 supplementation, and insufficient evidence to support cognitive behavior therapy. Serotonergic antidepressants (citalopram, escitalopram, fluoxetine, sertraline, venlafaxine) are first-line pharmacologic therapy.
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PMID:Premenstrual syndrome and premenstrual dysphoric disorder. 2201 Jul 72