Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reports of ephedrine-induced psychoses resembling amphetamine psychosis prompted studies of this classic sympathomimetic agent in systems that indicate central dopaminergic actions. Ephedrine induced dose-related stereotyped behavior in rats. This behavior was antagonized by haloperidol, but not by alpha- or beta-adrenergic blockers. Pretreatment with AMPT, but not reserpine, attenuated the stereotypy induced by ephedrine under one of two sets of conditions. Consistent prolactin suppression in humans was not seen. These findings are discussed in the context of clinical and pharmacologic data regarding other dopamine agonist drugs (the central nervous system stimulants, apomorphine, ET 495). These data suggest the possibility that synergistic noradrenergic and dopaminergic facilitation may be important in the induction of the stimulant psychoses.
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PMID:Dopaminergic agonist properties of ephedrine--theoretical implications. 41 69

The effects of pindolol on the prolactin (PRL) and growth hormone (GH) responses to intravenous tryptophan (LTP) were studied in eight healthy male volunteers. Pindolol pretreatment (40 mg over 48 h) markedly attenuated the GH response to LTP and modestly, but significantly, reduced the LTP-induced increase in plasma PRL. The disposition of LTP following infusion was not altered by pindolol. While the data are consistent with 5-HT1A receptor mediation of PRL and GH responses to LTP, the intrinsic sympathomimetic actions of pindolol might also be involved in the attenuation of the endocrine responses to LTP.
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PMID:Pindolol decreases prolactin and growth hormone responses to intravenous L-tryptophan. 200 40

Pharmacotherapy of male reproductive disorders is applicable to the majority of men seeking treatment for infertility. Since a favorable prognosis is associated with specific medical measures directed toward enhancing sperm quality, a comprehensive clinical and laboratory assessment of the infertile male is essential. This treatment may consist of replacement therapy for pituitary or hypothalamic dysfunction (i.e., exogeneous gonadotropins or GnRH), suppression of prolactin excess, antimicrobial therapy, sympathomimetic agents for ejaculatory disorders, or immunosuppressive treatment of sperm autoimmunity. Finally, the possibility of multiple causes of male reproductive dysfunction and their specific forms of treatment should be considered.
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PMID:Pharmacologic therapy of male infertility: specific treatment. 267 Apr 13

After an appropriate clinical and laboratory assessment of a patient's fertility status, the clinician must often decide whether specific and empiric treatment is indicated. Specific treatment may take the form of replacement therapy (exogenous gonadotropins or GnRH) for pituitary or hypothalamic failure, inhibition of prolactin secretion, antimicrobial therapy, or immunosuppressive therapy for demonstrable immunologic infertility. Finally, ejaculatory dysfunction often requires sympathomimetic agents. Alternatively, in the normogonadotropic oligospermic patient, the major form of empiric therapy relies on the enhancement of physiologic hormone levels that influence spermatogenesis. Such "stimulation" therapy may be achieved by GnRH analogues, antiestrogens, exogenous gonadotropins, or androgens.
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PMID:Medical treatment of male infertility. 355 93

Plasma prolactin concentrations were measured in unanaesthetized male rats before and after stereotaxic microinjection of adrenergic agents into the mediobasal and preoptic-anterior hypothalamus. In the mediobasal hypothalamus injection of the alpha 2 agonist clonidine produced a dose-dependent increase in prolactin secretion over the dose range 0.1 to 10 nmoles, the stimulation due to 1 nmole being blocked by idazoxan (alpha 2 antagonist). Stimulation of prolactin release was also caused by isoprenaline (beta agonist) and was significantly reduced by the beta antagonist propranolol. The beta 2 agonist salbutamol was also effective in stimulating prolactin secretion. However, the adrenergic agonists, noradrenaline (mixed alpha and beta), phenylephrine (alpha 1) and tyramine (sympathomimetic) failed to affect prolactin secretion. In the preoptic-anterior hypothalamus clonidine caused a dose-dependent increase in prolactin secretion over the dose range 0.001 to 10 nmoles, the stimulation due to 0.1 nmole being abolished by idazoxan. While prolactin levels were significantly elevated by noradrenaline and tyramine, phenylephrine was ineffective. We conclude that the activation of alpha 2 and beta 2 adrenoceptors in the mediobasal hypothalamus and of alpha 2 adrenoceptors in the preoptic-anterior hypothalamus, on or near prolactin-regulating neurons, results in increased prolactin secretion. An alpha 1 inhibitory action in the mediobasal hypothalamus has however not been ruled out. Adrenergic inputs in the preoptic-anterior hypothalamus appear to exert a predominant facilitatory effect on prolactin secretion.
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PMID:Alpha 2 and beta adrenoceptors in the mediobasal hypothalamus and alpha 2 adrenoceptors in the preoptic-anterior hypothalamus stimulate prolactin secretion in the conscious male rat. 809 44

It is known that prolactin (PRL) is produced within the brain and numerous central actions of the hormone have been reported. In anesthetized lactating rats, central administration of PRL, i.e., intracerebroventricular (icv) or intrathecally (it), facilitated milk ejection (ME) by depressing the sympathetically mediated facilitatory tone of the mammary ductal system. However, it is not known whether or not the same effects and similar mechanisms take place in conscious rats after PRL administration. In the present study, the effects of centrally administered PRL, i.e., icv or it, on ME was determined in both conscious and anesthetized rats. In conscious rats, the rate of ME was determined by applying a 15-min period of suckling by the litter, following a 6-h period of isolation. In anesthetized rats, intramammary pressure (IMP) responses of the mammary glands to exogenous oxytocin (OT) were recorded. The results showed that, whereas in anesthetized rats, increased responsiveness of the mammary glands to OT were observed after PRL administration, an intense inhibition of ME occurred in conscious rats. Because, in conscious and anesthetized rats, these effects were prevented by prior administration of the beta-adrenergic blocker propranolol (PROP) to the mothers, this suggests that the PRL effects on ME are modulated through sympathomimetic and sympatholytic actions in conscious and anesthetized rats, respectively. Thus, as shown by ductal tone measurements, in conscious, but not in anesthetized rats, the effect of PRL was associated with increased ductal constriction within the mammary glands; an effect that was mimicked by icv administration of the beta-adrenergic agonist isoproterenol (ISOP) and that was prevented by PROP. Further, the sympatholytic action of icv-PRL in anesthetized rats prevented the effect on ductal tone of both icv-PRL in conscious rats and of ISOP in anesthetized rats. Taken together, these results clearly suggest that the central effects of PRL on ME are modulated by adrenergic mechanisms.
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PMID:beta-adrenergic mechanisms modulate central nervous system effects of prolactin on milk ejection. 1156 59

A sudden loud sound evokes an electromyographic (EMG) response from the orbicularis oculi muscle in humans together with an auditory evoked potential (AEP) and an increase in skin conductance (SC). Startle responses are inhibited by weak prepulses (prepulse inhibition, (PPI)) and may also be modified by the level of alertness. We compared the sedative drug clonidine and the alerting drug modafinil on sound-evoked EMG, AEP, and SC responses, on the PPI of these responses and on level of arousal and autonomic functions. Sixteen healthy male volunteers participated in four weekly sessions (clonidine 0.2 mg, modafinil 400 mg, their combination, placebo) in a double-blind, cross-over, balanced design. Responses were evoked by sound pulses of 115 and 85 dB (PPI) for 40 ms and recorded conventionally. Level of alertness, autonomic functions (pupil diameter, blood pressure, heart rate, salivation, temperature) and the plasma levels of the hormones prolactin, thyroid-stimulating hormone and growth hormone were also measured. Data were analyzed with analysis of variance with multiple comparisons. Both prepulses and clonidine attenuated all three startle responses and modafinil antagonized clonidine's effects on the EMG and AEP responses. None of the drugs affected PPI. Clonidine showed sedative and sympatholytic effects, and modafinil showed alerting and sympathomimetic effects. In conclusion, startle responses were susceptible not only to PPI but also to the level of arousal.
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PMID:Modulation of the acoustic startle response by the level of arousal: comparison of clonidine and modafinil in healthy volunteers. 1734 69