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1.
In the present study, the effects of chronic lithium pre-treatment (30 days) on penile erection (PE) induced by bromocriptine were investigated in rats. Intraperitoneal administration of the dopamine receptor agonist, bromocriptine (4-32 mg/kg) induced PE in a biphasic manner. The maximum response was obtained with 8 mg/kg of bromocriptine and the effect was decreased with increasing doses of the drug from 8 to 32 mg/kg. When animals were pre-treated with different doses of the D-1 dopamine receptor antagonist, SCH 23390, or the D-2 dopamine receptor antagonist, sulpiride, the PE response was decreased. The response induced by bromocriptine (4-32mg/kg) was reduced in animals pre-treated with chronic lithium. SCH 23390 did not produce a larger inhibitory effect on the bromocriptine response in animals pre-treated with chronic lithium, but the inhibitory effect of sulpiride was increased in this condition. It is concluded that chronic lithium treatment may alter the D-1/D-2 receptor activity and inhibit bromocriptine-induced PE.  相似文献   

2.
NEUROLEPTICS INDUCE PENILE ERECTION IN THE RABBIT   总被引:1,自引:0,他引:1  
1. Intramuscular (i.m.) administration of the neuroleptics chlorpromazine, haloperidol and spiperone at doses ranging from 0.1 to 0.4 mg/kg in male rabbits induced a dose-dependent penile erection. 2. The i.m. administration of the α1-adrenoceptor antagonists prazosin and bunazosin (0.1–0.4 mg/kg), induced a dose-dependent penile erection. However, that of the peripheral dopamine receptor antagonist domperidone (0.4–4.0 mg/kg) and the dopamine receptor agonist apomorphine (0.1–1.0 mg/kg) did not. Penile erection was not induced by i.m. injection of chlorpromazine in combination with intrapenile administration of the α1-adrenoceptor agonist methoxamine. 3. Penile erection was induced by the administration of chlorpromazine (0.25–1.00 mg/body) into the lateral cerebral ventricle. At a low dose, however, the administration of chlorpromazine into the lateral ventricle induced a less notable penile erection than that induced intramuscularly. 4. Penile erection was induced by i.m. injection of the ganglionic blocker hexamethonium (5–20 mg/ kg). When chlorpromazine was given after pretreatment with hexamethonium, penile erection was more notable than that induced by either drug given alone. 5. These results suggest that neuroleptics could act locally in the penile structure to cause penile erection by α1-adrenoceptor-blocking actions.  相似文献   

3.
1. Mixed D-1/D-2 dopamine agonist apomorphine induced a penile erection (PE) in rats in a biphasic manner. 2. The response was decreased with increasing doses of the drug. 3. The maximum effect was obtained by 0.1 mg/kg of apomorphine. 4. In animals pretreated with D-1 antagonist SCH 23390, high doses of apomorphine showed higher PE response, while D-2 antagonist sulpiride pretreatment decreased the response of the low doses of the drug. 5. The inhibitory effect of sulpiride was dose-dependent. 6. The D-2 agonists bromocriptine or quinpirole induced a dose-dependent PE. 7. The effects of both drugs were decreased by sulpiride or SKF 38393 pretreatment. 8. Cholinergic drugs physostigmine and neostigmine did not induce PE, but antimuscarinic agent atropine decreased the effects of apomorphine, bromocriptine or quinpirole. 9. It is concluded that D-2 dopamine receptor stimulation may induce PE, while D-1 activation elicit an opposite effect. 10. However, cholinergic stimulation is not able to induce PE, cholinergic inhibition may decrease the PE induced by dopaminergic agents.  相似文献   

4.
The aim of this study was to elucidate whether penile erection induced by electrical stimulation of the cavernous nerve was affected in male rats with nitrate tolerance. Nitrate tolerance to nitroglycerin was induced by oral administration of isosorbide dinitrate (ISDN) at 1000 mg/kg to rats, once or twice a day for 5 or 6 days. The rats were anesthetized with sodium pentobarbital 18-24 h after the last dosing with ISDN or its vehicle. Penile erection induced by electrical stimulation was monitored by measuring the penile diameter sonomicrometrically. After measurement of the penile erectile response, nitroglycerin (3-300 microg/kg) was intravenously (i.v.) injected into eight rats treated with the vehicle or ISDN to examine its hypotensive effect. In the vehicle-treated rats, the maximal developed penile diameter (D-max) and the duration of penile erection (T50%, period of time from the maximum erection to its 50% decline) produced by electrical stimulation were 509+/-47 microm and 14.2+/-1.7 s, respectively. On the other hand, neither D-max nor T50% in ISDN-treated rats (509+/-36 microm and 13.1+/-1.3 s, respectively) was different from those in the vehicle-treated rats. However, the hypotensive effects of i.v. injected nitroglycerin were significantly attenuated in the ISDN-treated group as compared with the vehicle-treated group. It is concluded that nitrate tolerance fails to influence penile erection induced by cavernous nerve electrical stimulation in rats.  相似文献   

5.
Abstract: In the present study, effects of lead exposure on licking and yawning behaviour have been studied. The dopaminergic receptor agonist, apomorphine (0.15, 0.25 and 0.5 mg/kg), induced dose-dependent licking in rats. The maximum response was obtained with 0.5 mg/kg of the apomorphine. Lead acetate (0.05%) exposure significantly increased apomorphine-induced licking. Yawning induced by the D2 dopaminergic agonist, bromocriptine (2, 3, 4, 8 mg/kg), and the cholinergic drug, physostigmine (0.1 or 0.3 mg/kg), was significantly decreased by lead acetate (0.05%) exposure. It may be concluded that the behaviour induced by dopaminergic or cholinergic agents can be affected by lead subchronic exposure.  相似文献   

6.
The effects of bromocriptine, sulpiride or their combination on free amino acids in the kidneys and the heart after acute and chronic treatment of rats were investigated, using an automatic LKB Amino Acid Analyzer. Bromocriptine at a single dose of 4 or 10 mg/kg (i.p.) did not affect the level of any amino acid; however, at a dose of 20 mg/kg it significantly elevated the content of taurine in the kidney from 7.00 +/- 0.30 to 9.70 +/- 0.1 and in the heart from 22.9 +/- 1.7 to 30 +/- 1.2 mumol/g wet tissue (P less than 0.05, N = 7). It also increased glutamic acid in the heart from 3 +/- 0.1 to 4.5 +/- 0.25 mumol/g wet tissue (P less than 0.05, N = 7). Chronic oral treatment of rats with bromocriptine (20 mg.kg-1.day-1) for 5 weeks significantly elevated the level of taurine in the kidney from 7.2 +/- 0.3 (control) to 11.1 +/- 0.90 and in the heart from 23.1 +/- 1.7 to 38.8 +/- 1.8 mumol/l g wet tissue. It also increased cardiac glutamic acid content from 3 +/- 0.1 to 4.8 +/- 0.24 mumol/g wet tissue (P less than 0.01, N = 7). Concurrent administration of sulpiride (20 mg/kg) significantly suppressed bromocriptine-induced increases in taurine and glutamic acid in both organs, suggesting an activation of D2 receptors by bromocriptine. Due to the similarities between bromocriptine and the affected amino acids in renal and cardiac actions, it is suggested that mobilization of taurine and glutamic acid may at least in part contribute towards bromocriptine-induced renal and cardiac actions.  相似文献   

7.
Mice pretreated with reserpine 5 mg/kg (4 h prior to the start of motor activity recording) showed locomotor activation after the administration of the D-2 agonist bromocriptine (5 mg/kg). This bromocriptine-induced locomotor activity was dose dependently inhibited by the co-administration of a D-2 antagonist (sulpiride) and dose dependently potentiated by a D-1 agonist (CY 208-243). The potentiating effect of the D-1 agonist could be inhibited by either a D-1 or a D-2 antagonist (SCH 23390 1 mg/kg or sulpiride 100 mg/kg, respectively). The bromocriptine-induced locomotor activity was not altered by either blockade of D-1 dopaminergic receptors (SCH 23390 1 mg/kg) or by co-administration of a greater dose of reserpine (10 mg/kg) plus the dopamine synthesis inhibitor, alpha-methyl-p-tyrosine (200 mg/kg). The adenosine agonists, L-PIA (a preferentially A-1 adenosine agonist) and NECA (an A-1 and A-2 adenosine agonist with above 10-fold greater affinity for A-2 than L-PIA) inhibited in a dose-dependent manner the effect of bromocriptine, NECA being above ten times more potent than L-PIA. The findings show that bromocriptine stimulates postsynaptic D-2 receptors in dopamine-depleted mice and that this effect can be inhibited by adenosine stimulation. The existence of a postsynaptic D-2/A-2 interaction is suggested, the stimulation of A-2 receptors causing an inhibition of responses elicited by postsynaptic D-2 stimulation.  相似文献   

8.
The effect of excitatory amino acid receptor antagonists, (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclo-hepten-5, 10-imine hydrogen maleate ((+)-MK-801), (+/-)-3-(2-carboxy-piperazin-4-yl)-propyl-1-phosphonic acid (CPP), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and (+/-)-2-amino-4-phosphonobutanoic acid (AP-4), on penile erection and yawning induced by subcutaneous apomorphine (80 micrograms/kg), intracerebroventricular (i.c.v.) oxytocin (30 ng) and adrenocorticotropin (ACTH)-(1-24) (10 micrograms) was studied in male rats. Intraperitoneal (0.1-0.4 mg/kg) and i.c.v. (10-50 micrograms) (+)-MK-801 prevented dose dependently the penile erection and yawning induced by the three drugs. The (+)-MK-801 effect coincided with the appearance of head weaving, body rolling, hyperlocomotion and ataxia. Haloperidol (0.5 mg/kg i.p.) antagonized the prevention by (+)-MK-801 of oxytocin responses. Penile erection but not yawning was also prevented by high, but not low doses of CPP and CNQX, which impaired motor performance, AP-4 was ineffective at all doses tested. The above compounds were ineffective when injected into the paraventricular nucleus of the hypothalamus, the brain area where apomorphine and oxytocin act to induce penile erection and yawning. The results suggest that excitatory amino acid transmission is not involved in the expression of penile erection and yawning induced by the above compounds.  相似文献   

9.
Caffeine and its first-stage metabolites (paraxanthine, theophylline and theobromine) caused a significant potentiation of the locomotor activity induced by bromocriptine, 5 mg/kg, in mice pretreated with reserpine, 5 mg/kg (4h prior to the start of motor activity recordings). None of these substances significantly enhanced locomotor activity in reserpinized mice when administered alone. The rank order of potency was caffeine greater than paraxanthine greater than theophylline greater than theobromine. A high dose of a D-2 antagonist (sulpiride 100 mg/kg) caused a marked inhibition of the locomotor activity induced by bromocriptine, 5 mg/kg, plus 25 mg/kg of caffeine, paraxanthine or theophylline. However, a high dose of a D-1 antagonist (SCH-23390 1 mg/kg) caused a significant decrease of the locomotor activity induced by bromocriptine 5 mg/kg, plus 25 mg/kg of caffeine or paraxanthine, but did not change the locomotor activity caused by bromocriptine, 5 mg/kg, plus theophylline 25 mg/kg. The inhibitory effect of 5'-(N-ethyl)carboxamido-adenosine (NECA), 0.025 mg/kg, on bromocriptine-induced locomotor activation in reserpinized mice was reversed by the simultaneous administration of 10, 25 and 50 mg/kg of caffeine, paraxanthine or theophylline. The rank order of potency for reversal was theophylline greater than paraxanthine = caffeine. We suggest that methylxanthines act postsynaptically by potentiating the effects of D-2 stimulation and that this potentiation can be produced by D-1 agonism (paraxanthine or caffeine) and by adenosine antagonism (theophylline, paraxanthine or caffeine), most probably involving A-2 receptors.  相似文献   

10.
1. In the present study, we investigated the effects of hyperprolactinaemia, induced by transplantation of anterior pituitary glands under the kidney capsule in female rats, on the relationship between serum and pituitary concentrations of the gonadotropins and on the oestrous cycle. 2. Rats with pituitary transplants showed increased serum prolactin concentrations and decreased serum concentrations of gonadotropins and increased pituitary concentrations of gonadotropins. Moreover, these rats showed persistent dioestrous and anovulation from 3 to 6 days after transplantation. 3. A single oral administration of cabergoline (at doses between 0.001 and 0.1 mg/kg) dose-dependently inhibited the elevated serum prolactin concentrations in hyperprolactinaemic rats. At 0.1 mg/kg, cabergoline induced a continuous reduction in serum prolactin concentrations for 5 days after administration. Terguride (0.1 mg/kg) and bromocriptine (10 mg/kg) also reduced serum prolactin concentrations at 1 and 3 days after administration. All three dopamine D2 receptor agonists increased serum gonadotropin concentrations and ovarian weight at 3 days after administration. 4. In rats exhibiting anovulation, a single oral administration of any one of the three dopamine D2 receptor agonists dose-dependently restored ovulation and a normal oestrous cycle appeared. Oral administration of cabergoline (0.03 mg/kg) or terguride (0.1 mg/kg) restored ovarian function and abolished the anovulation following a reduction in serum prolactin concentrations. However, bromocriptine (10 mg/kg) did not completely abolish anovulation. Following administration of terguride (0.3 mg/kg) or bromocriptine (30 mg/kg), only one normal oestrous cycle appeared; however, following cabergoline (0.1 mg/kg), two normal oestrous cycles appeared. 5. These results suggest that cabergoline has a potent and long-lasting action as a dopamine D2 receptor agonist and, thus, should be a useful drug for the treatment of galactorrhoea and hyperprolactinaemic amenorrhoea and/or anovulation in humans.  相似文献   

11.
1. Administration of bromocriptine (0.1-2.5 mg/kg, i.p.) to mice produced hypothermia. 2. Pretreatment with the alpha 1-adrenoceptor blocker, prazosin (2.0 mg/kg, i.p.) or the alpha 2-adrenoceptor antagonist yohimbine (2.5 mg/kg, i.p.) had no effect on this response. 3. The inhibitor of catecholamine synthesis, alpha-methyl-p-tyrosine, and the muscarinic antagonist, atropine (10 mg/kg, i.p.) failed to alter the hypothermia. 4. Pretreatment with the dopamine (DA) receptor antagonists haloperidol (0.02 mg/kg, i.p.) or cis-flupenthixol (0.01 mg/kg, i.p.) completely blocked this response while trans-flupenthixol (0.05 mg/kg, i.p.) was inactive. 5. Depletion of 5-HT in the brain by p-chlorophenylalanine reduced the hypothermic response. 6. Similarly, pretreatment with the serotonergic (5-HT) receptor blocker ketanserin (1 mg/kg, i.p.) attenuated the hypothermia and at a dose of 2 mg/kg (i.p.) it completely blocked the hypothermic response. 7. Methysergide (5 mg/kg, i.p.) was also effective in antagonizing the hypothermia. 8. It was concluded that both DA and 5-HT mechanisms are involved in bromocriptine-induced hypothermia in mice.  相似文献   

12.
The effect of morphine administered systemically or into the paraventricular nucleus of the hypothalamus (PVN) on penile erection and yawning induced either by oxytocin or by the dopaminergic agonist apomorphine was studied in male rats. Systemic morphine (0.5 to 5 mg/kg intraperitoneally [IP]) prevented in a dose-dependent manner penile erection and yawning induced by the intracerebroventricular injection (ICV) of oxytocin (30 ng) or by the subcutaneous (SC) administration of apomorphine (80 micrograms/kg). Morphine (0.1 to 5 micrograms), but not U-69,593 (5 micrograms), injected into the PVN 10 minutes before oxytocin or apomorphine, was found to be able to prevent penile erection and yawning induced by the unilateral PVN microinjection of oxytocin (10 ng) or apomorphine (50 ng). The morphine-induced prevention of these behavioral responses was abolished by pretreatment with naloxone (3 mg/kg IP) 15 minutes before morphine. The present results suggest that morphine prevents apomorphine- and oxytocin-induced penile erection and yawning by inhibiting the activity of oxytocinergic neurons through mu-type receptors in this hypothalamic nucleus.  相似文献   

13.
A small dose of apomorphine (25 or 50 micrograms/kg, SC) induced repeated episodes of yawning, penile erection, genital grooming and a decrease in locomotor activity in rats. Hypophysectomy almost completely abolished yawning, penile erection and genital abolished yawning, penile erection and genital grooming but failed to modify the hypomotility induced by apomorphine. These results suggest that pituitary hormones are directly or indirectly involved in the apomorphine-induced yawning, penile erection and genital grooming but not in the sedative response to this drug.  相似文献   

14.
The effect of verapamil, flunarizine, nimodipine, nicardipine, and nifedipine, calcium channel inhibitors, and of indomethacin and aspirin, inhibitors of prostaglandin synthesis, on penile erection and yawning induced by oxytocin was studied in male rats. All calcium channel inhibitors given intraperitoneally (IP) 60 min before the intracerebroventricular (ICV) injection of oxytocin (30 ng) prevented in a dose-dependent manner oxytocin effect. Nimodipine and nicardipine were the most effective being active at doses between 5 and 20 mg/kg, while the others were active at doses higher than 15 mg/kg. Prevention of oxytocin effect was also seen after ICV injection of the above compounds. Unlike calcium channel inhibitors, indomethacin given either IP (10 and 50 mg/kg) or ICV (50 micrograms), or aspirin (100 mg/kg IP) were ineffective. Microinjection of calcium, but not of prostaglandin E2 and prostaglandin F2 alpha in the paraventricular nucleus of the hypothalamus, the brain area most sensitive for the induction of the above behavioral responses by oxytocin, induced a symptomatology similar to that induced by oxytocin. The present results suggest that calcium might be the second messenger which mediates the expression of penile erection and yawning induced by oxytocin.  相似文献   

15.
《General pharmacology》1995,26(5):1015-1020
  • 1.1. The effects of chronic lithium pretreatment (600 mg/l in drinking rats, 30 days) on penile erection (PE) induced by apomorphine were investigated in rats. This treatment resulted in a serum Li concentration after 30 days of 0.31 ± 0.01 mmol/l.
  • 2.2. Subcutaneous (s.c.) administration of mixed Dl/D2 dopamine receptor agonist apomorphine (0.05–0.5 mg/kg) induced PE in a biphasic manner. The maximum effect was obtained with 0.1 mg/kg of the drug while the response decreased with increasing doses of apomorphine from 0.1 to 0.5 mg/kg.
  • 3.3. Pretreatment of animals with 0.0125-0.1 mg/kg of D1 dopamine receptor antagonist SCH 23390 or D2 dopamine receptor antagonist sulpiride (12.5–100 mg/kg) decreased apomorphine-induced PE. Combination of SCH 23390 (0.025 mg/kg) with sulpiride (12.5 mg/kg) caused a stronger inhibitory effect on apomorphine response. This indicates that both D1 and D2 dopamine receptors may be involved in PE induced by apomorphine.
  • 4.4. The response induced by apomorphine (0.05-0.5 mg/kg) was decreased in animals pretreated with chronic lithium. The inhibitory effect of sulpiride on apomorphine response, increased in animals pretreated with lithium, in contrast the inhibitory effect of SCH 23390 did not change in this condition. However, a combination of SCH 23390 with sulpiride increased inhibitory effect on apomorphine response in lithium pretreated rats.
  • 5.5. It is concluded that chronic lithium inhibits PE induced by dopaminergic mechanism(s).
  相似文献   

16.
A small dose of apomorphine (25 or 50 μg/kg, SC) induced repeated episodes of yawning, penile erection, genital grooming and a decrease in locomotor activity in rats. Hypophysectomy almost completely abolished yawning, penile erection and genital grooming but failed to modify the hypomotility induced by apomorphine. These results suggest that pituitary hormones are directly or indirectly involved in the apomorphine-induced yawning, penile erection and genital grooming but not in the sedative response to this drug.  相似文献   

17.
The present study was performed to determine whether measurement of penile diameter in an in vivo rat model is useful for pharmacologic and physiologic investigations on penile erection. Penile erection induced by electrical stimulation of the cavernous nerve was monitored by measuring the penile diameter sonomicrometrically with a pair of 10-MHz piezoelectric crystals glued to the opposite surfaces of the adventitia of the penile erectile chamber in anesthetized rats. Using this method, we examined the effects of a nitric oxide (NO) synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), and a well-known phosphodiesterase 5 (PDE5) inhibitor, zaprinast, on the maximal developed penile diameter (D-max) and the time from the maximum response to 50% recovery (T50%) of the maximum response as an index of the duration of penile erection. An intravenous injection of L-NAME at a dose of 10 mg/kg significantly inhibited D-max produced by cavernous electrical stimulation at 5 to 50 V, without affecting T50%. Sequential intravenous infusions of 10, 30, 100, and 300 microg/kg/min of zaprinast at 30-min intervals did not show any effect on D-max, heart rate, and systolic arterial pressure, although doses of 100 and 300 microg/kg/min significantly prolonged T50% and the maximum dose decreased diastolic arterial pressure. Moreover, zaprinast produced a more prominent increase in cyclic guanosine monophosphate (cGMP) levels than cyclic adenosine monophosphate levels in the plasma taken at the end of the maximum dose infusion. Measurement of murine penile diameter with a sonomicrometrical device, indicating that a NO-cGMP-PDE5 pathway plays a pivotal role in the penile diameter increase and its maintenance, would be useful for pharmacologic and physiologic investigations on penile erection.  相似文献   

18.
RATIONALE: Developmental lead exposure may alter responsiveness to cocaine well into adulthood, and ultimately influence drug-use patterns. OBJECTIVES: The present study examined the effect of perinatal lead exposure on the discriminative stimulus properties of cocaine. METHODS: Female rats were treated with 0, 8, or 16 mg lead daily for 30 days before breeding with untreated males. This exposure regimen continued through gestation and until postnatal day (PND) 21, i.e., weaning. At PND 60 male pups were trained to discriminate between saline and cocaine (5 mg/kg) injections. After acquisition, a series of generalization/substitution tests were performed using a cumulative dosing procedure. RESULTS: Developmental lead exposure produced subsensitivity to SKF-82958 (D1-like dopamine receptor agonist), quinpirole (D2-like dopamine receptor agonist), and apomorphine (mixed D1-like/D2-like dopamine receptor agonist); but no differences were evident among lead-treatment groups on generalization/substitution tests with cocaine, d-amphetamine, or GBR-12909. Furthermore, when the kappa-opioid receptor agonist U69,593 was administered prior to cocaine (5 mg/kg), generalization to the cocaine stimulus decreased in control rats, but generalization in lead-exposed rats was not altered. Group differences were not evident in tolerance or recovery of tolerance to cocaine following repeated cocaine administration (60 mg/kg per day for 14 days). Furthermore, no differences were found across groups in concentrations of lead in brain, although pups exposed to 16 mg lead had slightly elevated blood lead concentrations (<7 microg/dl). CONCLUSIONS: These results further a growing research literature that suggests developmental lead exposure can produce long-lasting changes in drug responsiveness, even after exposure to the toxicant has been discontinued.  相似文献   

19.
Rats were treated for 21 days with the selective D-1 blocker SCH 23390 (0.1 mg/kg SC). Threshold doses of apomorphine for hypermotility (0.15 mg/kg SC) and for stereotyped response (0.25 mg/kg SC) were given 7, 21, 35, and 77 days after discontinuation of the chronic treatment. The rats always showed enhanced stereotyped response to the higher dose of apomorphine but never any change in their motility response to the lower dose of dopamine agonist. This finding may represent a behavioral correlate of the reported supersensitivity of D-1 receptors induced by SCH 23390.  相似文献   

20.
1 The dopamine agonist, bromocriptine, produced a hypotensive response following oral administration to conscious normotensive and spontaneously hypertensive (SH)-rats. 2 In SH-rats the dose-related falls in blood pressure to bromocriptine, 3 to 30 mg/kg orally or intraperitoneally, were biphasic, an initial fall at 1 h being followed by some recovery at 2 h and a subsequent fall in blood pressure at 4 and 6 h. 3 The dopamine antagonists, metoclopramide, sulpiride, haloperidol and pimozide, had little or no effect on the hypotensive response to bromocriptine, 10 mg/kg orally, in SH-rats. 4 Pretreatment with alpha-methyl-p-tyrosine augmented the hypotensive response to bromocriptine, 10 mg/kg orally, in SH-rats. 5 In adrenal demedullated SH-rats, the hypotensive response to bromocriptine, 3 to 30 mg/kg orally, was abolished. 6 In SH-rats the hypotensive response to bromocriptine, 10 mg/kg orally, was prevented by the beta-adrenoceptor blocking drugs, propranolol and oxprenolol, but was unaffected by (+)-propranolol and by the cardio-selective beta-adrenoceptor blocking drug, atenolol. 7. In SH-rats pretreated with bromocriptine, 10 mg/kg orally, and then anaesthetized, the pressor responses to low doses of intravenous adrenaline were reversed to depressor, indicating that bromocriptine possesses alpha-adrenoceptor blocking activity. 8 The results suggest that hypotensive response to bromocriptine in conscious SH-rats is mediated by adrenaline released from the adrenal medullae which, in the presence of alpha-adrenoceptor blockade, stimulates vascular beta-adrenoceptors producing vasodilatation.  相似文献   

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