PLASMA AND PITUITARY PROLACTIN AND BLOOD PRESSURE IN BROMOCRIPTINE-TREATED SPONTANEOUSLY HYPERTENSIVE AND WISTAR-KYOTO RATS

1. The effects on blood pressure (BP) and plasma and pituitary prolactin (PRL) of a 13 day intraperitoneal infusion of bromocriptine delivered by osmotic minipump were investigated in spontaneously hypertensive rats (SHR) and their normotensive controls, the Wistar-Kyoto rats (WKY). 2. In the SHR, a fall in BP which was steepest over the initial few days and sustained up to day 12 was observed in the bromocriptine-treated group compared with the lack of a change in BP observed in the vehicle-treated group. The plasma PRL level taken on day 13 was found to be significantly lower in the bromocriptine-treated group than in the vehicle-treated group. 3. In the WKY, bromocriptine had no significant effect on either BP or plasma PRL. 4. Pituitary PRL content was significantly lower in the SHR than in the WKY. The suppression by bromocriptine treatment was greater in the SHR than in the WKY. 5. These results provide further evidence for a central dopaminergic insufficiency in the SHR and raise the possibility that PRL may, either directly or indirectly by interacting with other factors in the SHR, influence BP.     

CHANGES IN SALINE AND WATER INTAKES IN BROMOCRIPTINE-TREATED GENETICALLY HYPERTENSIVE AND NORMOTENSIVE RATS

1. We have previously reported on the effects of a 13-day intraperitoneal infusion of bromocriptine delivered by osmotic pump on blood pressure, plasma and pituitary PRL levels in genetically hypertensive (GH) rats and their normotensive (NT) controls. This paper reports further on that study in describing the changes in saline and water intakes in rats as a result of bromocriptine (BRC) treatment. 2. In the GH rats, bromocriptine did not have any significant effect on saline or water intake. 3. In the NT rats, bromocriptine significantly decreased saline intake and increased water intake. 4. The saline intake in the vehicle-treated GH rats was significantly lower than that in the vehicle-treated NT rats while the water intake was not significantly different. 5. These results indicate that differences exist between the GH and NT rats with regard to their saline and water intakes and their responses to chronic bromocriptine treatment. The changes in saline and water intakes in the GH rats seem to be different from those seen in the spontaneously hypertensive rat in another study.     

PLASMA AND PITUITARY THYROID-STIMULATING HORMONE LEVELS IN BROMOCRIPTINE-TREATED NEW ZEALAND GENETICALLY HYPERTENSIVE AND NORMOTENSIVE RATS

1. The effects of a 13-day intraperitoneal (i.p.) infusion of bromocriptine, delivered by osmotic pump, on plasma and pituitary thyroid-stimulating hormone (TSH) levels were investigated in New Zealand genetically hypertensive (GH) rats and their normotensive (NT) controls. 2. In both the GH and NT rats, bromocriptine significantly reduced plasma TSH level but did not have any significant effect on pituitary TSH content. 3. No significant difference was found in the plasma TSH level and pituitary TSH content between the vehicle-treated GH and NT rats. 4. These results suggest that there are no differences between the GH and NT rats with regard to the activity of the central dopaminergic system influencing TSH release and also that TSH does not play a role in the hypertension of the GH rats.     

RELATIONSHIP BETWEEN NIFEDIPINE SENSITIVITY OF AORTAE AND BLOOD PRESSURE OF STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS

1. We have previously described an increased sensitivity to inhibition by nifedipine of noradrenaline-induced contractures of blood vessels in hypertension. In this study we have investigated whether changes in blood pressure (BP) change the sensitivity to nifedipine and K⁺ of aortic rings from normotensive (Wistar-Kyoto rats, WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). 2. SHRSP were treated with: hydralazine plus hydrochloro-thiazide; captopril plus hydrochlorothiazide; hydralazine plus guanethidine; or captopril alone. WKY rats were treated with deoxycorticosterone acetate (DOCA) and NaCl. Treatment commenced from 5 weeks of age and continued until 13–15 weeks. 3. The SHRSP treatments produced similar reductions in BP, and the BP of all the treated groups were significantly lower than the mean BP of untreated SHRSP (201.0 ± 7.7 mmHg). The mean BP of the treated WKY rats (134.2 ± 7.6 mmHg) was significantly higher than the mean BP of the untreated WKY rats (86.8 ± 7.4 mmHg). 4. An area-under-curve (AUC) analysis of the inhibitory effects of nifedipine on responses of aortae to noradrenaline showed no differences between treated and untreated SHRSP groups (overall mean 40.6 ± 1.9% and 43.4 ± 3.4% inhibition of control AUC, respectively), or between DOCA-salt treated WKY and untreated WKY groups (58.8 ± 5.9 and 64.8 ± 2.3, respectively). Noradrenaline-induced contractures of aortae from all SHRSP groups were significantly more sensitive to inhibition by nifedipine than aortae from both WKY groups. 5. The molar concentration of agonist required to evoke 50% of the maximum response (EC₅₀) values for potassium chloride (KCI) were significantly increased in the aortae of all treated SHRSP groups in comparison to those from untreated SHRSP (treated SHRSP groups, 15.53 ± 0.68 mmol/L vs untreated SHRSP group, 11.36 ± 1.10 mmol/L). The EC₅₀ values for KC1 for the aortae from the DOCA-treated WKY rats were significantly less than those from aortae of the untreated WKY (11.80 ± 0.80 and 17.08 ± 1.50 mmol/L, respectively). 6. We conclude that reduction (in SHRSP) or increase (in WKY) of the BP has no effect on the sensitivity of aortic smooth muscle to the inhibitory effects of nifedipine on responses to noradrenaline, suggesting that alterations in voltage-dependent Ca²⁺ mechanisms may be a primary phenomenon in the SHRSP. In contrast, the fact that sensitivity to KC1 changes in the treated SHRSP and WKY aortae suggests such sensitivity is secondary to the BP and thus a separate phenomenon from voltage-dependent Ca²⁺ mechanisms.     

Delayed hypotensive effect of the thromboxane A2/prostaglandin H2 receptor antagonist S-1452 in spontaneously hypertensive rats

1. Several lines of evidence indicate that thromboxane (Tx) A2 may contribute to the development and maintenance of hypertension. The present study was undertaken to evaluate the role of TxA2 in the development of hypertension in spontaneously hypertensive rats (SHR) by using an orally active, highly specific TxA2/prostaglandin H2 receptor antagonist S-1452. 2. Vehicle (1% arabic gum solution) alone was given orally to Wistar-Kyoto (WKY) rats (n = 15) and SHR (n = 14), while S-1452 (10 mg/kg per day, twice daily) was administered orally to SHR (n = 16) for 18 weeks (from 5 to 23 weeks of age). 3. No significant difference was observed in tail-cuff blood pressure (BP) between vehicle- and S-1452-treated SHR before and at 5 and 11 weeks after treatment. Thereafter, BP was further elevated in vehicle-treated SHR, but was significantly blunted in SHR treated with S-1452 at 15 (224+/-8 vs 211+/-13 mmHg; P < 0.01) and 18 weeks (227+/-9 vs 206+/-10 mmHg; P < 0.001); this was associated with reduced proteinuria. 4. Urinary TxB2 in vehicle-treated SHR, especially during the early period, was significantly greater than that in WKY rats, while no significant difference was observed in urinary 6-ketoprostaglandin F1alpha (6-keto-PGF1alpha) between the two groups. Treatment with S-1452 reduced urinary excretion of TxB2 at 18 weeks. 5. The present study shows that S-1452, at the dose used, does not reduce BP during the early period of the development of hypertension. These results suggest that the role of enhanced TxA2 production in the development of hypertension is small, if any, in SHR. Delayed response of BP may be independent of the direct pharmacological effects of S-1452.     

HYPOTENSIVE ACTIVITY OF AQUEOUS EXTRACT OF ANDROGRAPHIS PANICULATA IN RATS

1. The hypotensive activity of an aqueous extract of Andrographis paniculata was studied using chronic intraperitoneal (i.p) infusions by osmotic pumps. The extract exhibited a dose-dependent hypotensive effect on the systolic blood presure (SBP) of spontaneously hypertensive rats (SHR). 2. The optimum hypotensive dose determined was repeated in a study in SHR and their normotensive controls, Wistar Kyoto (WKY) rats, to demonstrate its comparative effects on the SBP, plasma and lung angiotensin-converting enzyme (ACE) activities, as well as on lipid peroxidation in the kidneys, as measured by thiobarbituric acid (TBA) assay. 3. The extract significantly lowered the SBP of both SHR and WKY rats. 4. Plasma, but not lung, ACE activity and kidney TBA level were significantly lower in extract-treated SHR when compared with vehicle-treated SHR controls. 5. Plasma and lung ACE activities as well as kidney TBA levels were not significantly different between extract-and vehicle-treated WKY rats. 6. This study indicates that the aqueous extract of A. paniculata lowers SBP in the SHR possibly by reducing circulating ACE in the plasma as well as by reducing free radical levels in the kidneys. The mechanism(s) of hypotensive action seems to be different in WKY rats.     

CARDIOVASCULAR RESPONSE TO EMOTIONAL STRESS AND SPONTANEOUS BLOOD PRESSURE VARIABILITY IN GENETICALLY HYPERTENSIVE RATS OF THE LYON STRAIN

1. Intra-aortic blood pressure (BP) was continuously recorded in freely moving genetically hypertensive (LH), normotensive (LN) and low BP (LL) rats of the Lyon strains under basal conditions and during aversive stimulation (a jet of air for 20 min). Rats were studied when 5 and 14 weeks old. 2. The 24 h standard deviation (i.e., variability) of diastolic BP was significantly greater in LH rats of both ages than in LN and LL control rats. 3. In response to the stressor, LH rats showed larger increases in BP than age-matched controls. 4. The BP variability was related to the BP responses to stress in the whole series of rats. 5. It is concluded that the spontaneous BP variability and the BP responses to an experimental stressor rely upon a common regulatory mechanism in rats and that an increased lability of diastolic BP is a primary characteristic of Lyon hypertensive rats.     

EFFECT OF CAPTOPRIL ON BRAIN CONVERTING ENZYME IN THE SPONTANEOUSLY HYPERTENSIVE RAT

The effect of oral captopril (30 mg/kg per day) on the blood pressure, plasma aldosterone concentration, urinary electrolytes and brain angiotensin-converting enzyme activity of spontaneously hypertensive rats of the Okamoto strain was examined. Over a seven day period, captopril caused a progressive fall in blood pressure with increased sodium excretion and urine volume and a significant fall in plasma aldosterone concentration. Following captopril, angiotensin converting enzyme activity increased significantly in the midbrain and medulla oblongata; the pituitary level of angiotensin converting enzyme activity was significantly decreased. The hypotensive action of captopril in the spontaneously hypertensive rat is associated with changes in body sodium, water and plasma aldosterone concentration. The alterations in brain angiotensin-converting enzyme activity following captopril treatment suggest that, with chronic administration, captopril can alter the activity of the brain renin-angiotensin system.     

INVOLVEMENT OF SYMPATHETIC NERVOUS SYSTEM INHIBITION IN THE HYPOTENSIVE EFFECT OF BROMOCRIPTINE IN SPONTANEOUSLY HYPERTENSIVE RATS

The hypotensive effect of bromocriptine in young (6 week old) spontaneously hypertensive rats (SHR) was studied. Blood pressure and plasma norepinephrine level in bromocriptine-treated SHR were significantly lower than those in vehicle-treated SHR after 3 weeks of treatment (5 mg/kg per day, i.p.), while no significant decrease of blood pressure or plasma norepinephrine level was observed after 2 weeks of treatment. These results suggest the involvement of sympathetic nervous system inhibition in the hypotensive effect of bromocriptine in SHR.     

疏肝饮对肝郁脾虚大鼠CRH和NT的调节作用

目的观察疏肝饮煎剂对脾虚应激大鼠相关胃肠道激素的影响,探讨疏肝饮发挥疏肝健脾作用治疗肠易激综合征（IBS）的可能途径。方法通过番泻叶灌胃加避水应激（WAS）法建立肝郁脾虚型腹泻型IBS大鼠模型,观察疏肝饮对模型大鼠大便粒数、下丘脑及血浆中促肾上腺皮质激素释放激素（CRH）含量的影响以及对下丘脑、血浆、小肠、结肠组织中神经降压素（NT）含量的影响。结果单纯应激组、脾虚应激组大鼠下丘脑、血浆中CRH含量较空白对照组明显升高（P〈0.05）,中药治疗组与脾虚应激组相比下丘脑及血浆中CRH含量降低（P〈0.05）。脾虚应激组大鼠下丘脑、血浆、结肠中NT的含量较空白对照组明显升高（P〈0.05）,中药治疗组与脾虚应激组比较,其值相应降低,而单纯应激组组织和血浆中NT的含量均未见明显变化（P〉0.05）。结论疏肝饮对单纯避水应激和脾虚应激所引起的下丘脑和血浆中CRH分泌和释放的抑制作用;疏肝饮有降低脾虚应激大鼠下丘脑、血浆及结肠组织中NT含量的作用,这可能是疏肝饮发挥疏肝健脾作用治疗IBS的机制之一。     

L-精氨酸对应激性大鼠血压的影响

目的 :研究L 精氨酸 (L ARG)对应激性大鼠血压 (BP)的影响。方法 :给SD大鼠的饮水中添加L ARG ,并给予间断性足底电刺激 15d ,隔日监测尾动脉BP 1次 ,观察其尾动脉BP的变化情况和血浆一氧化氮 (NO)浓度变化。并与单纯应激组和正常对照组比较。结果 :单纯应激组在d 9、d 11、d 13、d15 ,BP升高 ,与正常对照组相比 ,差异有显著的统计学意义 (P <0 .0 5或P <0 .0 1) ;血中NO的浓度低于正常对照组 (P <0 .0 5 )。L ARG +应激组隔日测得BP与对照组相比 ,其差异无统计学意义 ,d 15BP低于正常对照组 (P <0 .0 5 ) ,BP呈下降趋势 ,NO明显升高 (P <0 .0 1)。结论 :L ARG有阻抑应激性大鼠BP升高的作用     

神经肽y与垂体腺瘤发病机制的关系

目的：探讨雌激素诱发大鼠垂体腺瘤及神经肽y（NPy）与垂体腺瘤发病机制的关系。方法：将实验动物分为2组各30只。给药组雌性Wistar-Furth大鼠腹腔注射苯甲酸雌二醇，诱发垂体泌乳素细胞腺瘤；对照组大鼠腹腔注射等量生理盐水。而后观察2组大鼠脑组织和血浆中的神经肽y含量。结果：给药组Wistar-Furth大鼠产生垂体腺瘤，且血浆泌乳素浓度、NPy浓度和垂体及下丘脑NPy含量均明显升高。结论：NPy可能在垂体肿瘤的发生、发展过程中发挥着重要的作用。     

HYPOTENSIVE EFFECT OF CHRONICALLY INFUSED ADRENOMEDULLIN IN CONSCIOUS WISTAR-KYOTO AND SPONTANEOUSLY HYPERTENSIVE RATS

1. The hypotensive effect of chronically infused human adrenomedullin (hAM), a potent vasodilator peptide that has been reported to have a natriuretic action, was examined in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). 2. Conscious WKY rats and SHR were infused with 200 ng/h synthetic hAM for 14 days by means of osmotic minipumps. Control groups were infused at the same schedule with 0.9% saline. Systolic blood pressure (SBP) and daily urinary excretion of Na⁺ and K⁺ were measured before and during the infusion period. In addition, plasma renin activity (PRA), aldosterone and hAM concentrations were measured on day 14 of infusion. 3. A significant reduction in SBP was observed in hAM-treated SHR at day 2 and SBP remained significantly lower throughout the experiment compared with control SHR. Similarly, SBP in the hAM-treated WKY rats was found to be significantly lower than in control WKY rats during infusion. However, the hypotensive effect was not accompanied by any significant increase in urinary volume or Na⁺ excretion in hAM-treated rats of either strain. Chronic infusion with hAM significantly suppressed PRA and lowered the concentration of plasma aldosterone in WKY rats but not in SHR. The plasma hAM levels in treated WKY rats and SHR were 0.0 ± 9.4 and 0.6 ± 0.2 fmol/mL, respectively. 4. These findings demonstrate that chronically infused hAM has a hypotensive effect in both WKY rats and SHR without an increase in urinary volume or Na⁺ excretion at a plasma AM concentration within the physiological limit.     

Effect of the adenosine antagonist 8-phenyltheophylline on glycerol-induced acute renal failure in the rat.

8-Phenyltheophylline (8-PT)(10 mg kg-1) or its vehicle(1 ml kg-1) were administered intravenously or intraperitoneally twice daily over 48 h to rats with acute renal failure (ARF) induced by intramuscular (i.m.) injection of glycerol. Rats treated with 8-PT i.v. had significantly lower plasma urea and creatinine levels at 24 and 48 h compared to untreated animals. The vehicle also reduced plasma urea and creatinine when compared to untreated controls. However, plasma urea levels in 8-PT-treated rats were significantly lower than in vehicle-treated animals at 24 and 48 h after both i.v. and i.p. administration. Plasma creatinine concentrations also tended to be lower in the 8-PT-treated group. [3H]-inulin clearance at 48 h after i.m. glycerol was significantly greater in rats dosed i.p. with 8-PT compared to either untreated or vehicle treated rats. Examination of kidneys taken from rats 48 h after i.m. glycerol showed that 8-PT treatment significantly reduced renal damage and kidney weight compared to the untreated or vehicle-treated groups. In a 7 day study all the rats which received 8-PT i.p. survived whilst in the vehicle and untreated groups the mortality rates were 12 and 21% respectively. In a separate series of experiments 8-PT (10 mg kg-1, i.v. or i.p.) was found to antagonize adenosine-induced bradycardia in conscious rats for up to 5 h. There is no clear explanation for the partial protection afforded by the vehicle but it may be related to either its alkalinity or an osmotic effect produced by the polyethylene glycol component.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of neurotensin microinjected into ventral tegmental area on spontaneous motor activity in neonatal 6-hydroxydopamine-treated rats]

Intracerebroventricular treatment of the catecholamine neurotoxin, 6-hydroxydopamine (6-OHDA) after desmethylimipramine pretreatment results in semipermanent brain dopamine (DA) depletion. It has been shown that rats neonatally treated with 6-OHDA show hyperactivity in an open-field test. The purpose of this study was to investigate the spontaneous motor activity in neonatal 6-OHDA-treated rats following bilateral saline (SAL; 0.25 microliter) or neurotensin (NT; 1.25, 2.50, 5.00 micrograms/0.25 microliter/side) microinjection into the ventral tegmental area. Each dose of NT significantly augmented locomotor activity in 6-OHDA-treated rats. On the other hand, controls did not show significant increase in lower dose of NT. Effect of NT microinjection on number of rearings in the 6-OHDA-treated group was not significantly altered compared to the vehicle-treated group. These results suggest that the responses in locomotor activity to NT the ventral tegmental area increase in neonatal 6-OHDA-treated rats, and imply that residual activity in mesolimbic DA neurons which is mediated by NT receptors contributes to a part of the hyperactivity seen after neonatal 6-OHDA lesion.     

Chronic lead treatment affects dopaminergic control of prolactin secretion in rat pituitary

The effect of lead exposure on dopaminergic mechanisms regulating prolactin (PRL) secretion was studied in rats by measuring dopamine (DA) and dihydroxyphenylacetic acid hypothalamic concentrations and DA receptor density in the hypothalamus and pituitary of lead-exposed animals. [³H]sulpiride was used as dopamine receptor ligand. A decrease of dihydroxyphenylacetic acid (DOPAC) hypothalamic concentrations and a decrease of DA receptor density in the pituitary are shown. The decreased [³H]Sulpiride binding in the pituitary is consistent with the elevated serum PRL concentrations previously described in lead-exposed rats.     

COSEGREGATION OF THE NEW REGION ON CHROMOSOME 3 WITH SALT-INDUCED HYPERTENSION IN FEMALE F2 PROGENY FROM STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE AND WISTAR-KYOTO RATS

1. We investigated candidate loci for salt-sensitive high blood pressure (BP) in F2 progeny from crossing Wistar-Kyoto and stroke-prone spontaneously hypertensive rats. 2. In female F2 progeny, systolic and diastolic BP on the 12th day and the seventh month after salt loading was strongly liked with the D3Mgh12 and D3Mgh6 loci on chromosome 3, respectively. 3. These loci were linked with BP only in female F2 progeny, not in males. 4. These results indicate that hormonal factors may influence salt sensitivity, particularly with respect to gender differences.     

NITRIC OXIDE SYNTHASE INHIBITION WITH Nω-NITRO-L- ARGININE METHYL ESTER AFFECTS BLOOD PRESSURE AND CARDIOVASCULAR STRUCTURE IN THE GENETICALLY HYPERTENSIVE RAT STRAIN

1. Inhibition of nitric oxide (NO) synthesis with the nitric oxide synthase (NOS) inhibitor N^ω-nitro-L-arginine methyl ester (L-NAME) was used as a tool to investigate further a possible endothelial defect in the New Zealand genetically hypertensive (GH) rat strain compared with its normotensive (N) control strain. 2. N^ω-nitro-L-arginine methyl ester was given to GH and N groups in their drinking water from age 7–10 weeks (10 mg/kg per day for weeks 1 and 2 and then 5 mg/kg per day for week 3). Tail-cuff blood pressure (BP) was measured weekly and at the end of the experiment the mesentery was fixed by perfusion, second order branches of the mesenteric artery were embedded in Technovit and stained sections were used to quantify the structure of the mesenteric resistance arteries (MRA). The heart was removed and weighed for determination of left ventricular (LV) mass. 3. In GH rats, BP and LV mass were significantly raised by L-NAME, while in N rats L-NAME treatment significantly elevated BP, but had no effect on LV mass. 4. In GH rats, the media width was significantly increased by L-NAME treatment (P < 0.01) lumen diameter remained unchanged. Thus, the ratio of media width/lumen diameter (M/L) was significantly increased by exacerbation of the hypertrophic outward remodelling characteristic of the GH strain. There were no significant changes in the M/L ratio in L -NAME-treated N rats. 5. Thus, in the GH strain, cardiovascular structure is more sensitive to NOS inhibition than either its N control strain or (on evidence from the literature) the spontaneously hypertensive rat strain.     

Synergistic decrease in blood pressure by captopril combined with losartan in spontaneous hypertensive rats

This study was designed to examine the anti-hypertensive effect of the combination therapy of captopril with losartan by oral administration using both independent and cross-over experimental protocols. In independent experimental protocols, four different groups of spontaneous hypertensive rats (SHR) were treated for 1 or 2 weeks: control, captopril (20 mg/kg/day), losartan (20 mg/kg/day), and combination captopril (10 mg/kg/day) with losartan (10 mg/kg/day). In cross-over protocols, each SHR received all four treatments for 1 or 3 days with an interval of several days between each injection for washing-out and return to high blood pressure (BP) levels. BP and heart rate (HR) were measured in conscious telemetered SHR. According to the results from the independent protocol, regardless of a 1- or 2-week administration period, combination therapy with low doses of captopril and losartan had a greater anti-hypertensive effect than individual high-dose monotherapy. Similarly, results from the cross-over protocol showed that regardless of 1-day or 3-day administration, the decrease in BP in the 11^th and 12^th hour after administration was greatest with the combination of low-dose captopril and losartan. Therefore, combination therapy with low doses of captopril with losartan lowered BP to a greater extent than a high dose of either individual monotherapy.     

桂枝茯苓胶囊对实验大鼠血浆内雌二醇、黄体酮、催乳素的影响

目的 :探讨桂枝茯苓胶囊对实验性高雌、孕激素大鼠血浆内雌二醇、黄体酮、催乳素的影响。方法 :取雌性SD大鼠 10 0只给大鼠腹腔注射 ,苯甲酸雌二醇及黄体酮制作高雌二醇、黄体酮大鼠模型 ,将大鼠随机分成 5组 ,空白对照组、模型组 ,他莫昔芬对照组及桂枝茯苓胶囊 2 0 0 ,4 0 0mg·kg- 1组 ,每组2 0只 ,空白对照组和模型组给等体积蒸馏水 ,其余组分别给桂枝茯苓胶囊混悬液 2 0 0 ,4 0 0mg·kg- 1和他莫昔芬 3mg·kg- 1,每日灌胃 ,共 30d。用放射免疫方法测定各组实验性大鼠模型血浆内雌二醇、黄体酮、催乳素的含量。结果 :桂枝茯苓胶囊 2 0 0与4 0 0mg·kg- 1组可明显降低高雌、孕激素大鼠模型血浆雌二醇和黄体酮 ,2组雌二醇分别为 (12 7±s5 2 )ng·L- 1和 (15 3± 4 9)ng·L- 1,黄体酮分别为 (12± 8) μg·L- 1和 (13± 7) μg·L- 1,与模型组雌二醇(2 71± 10 3)ng·L- 1和黄体酮为 (2 1± 15 ) μg·L- 1比较 ,差异均有显著意义 ,P <0 .0 5 ,但对血浆催乳素影响不大。结论 :桂枝茯苓胶囊能够显著降低异常升高的实验性高雌、孕激素大鼠模型的雌二醇、黄体酮的血浓度。