mr-2266 and beta-funaltrexamine

mr-2266 has been researched along with beta-funaltrexamine* in 3 studies

Other Studies

3 other study(ies) available for mr-2266 and beta-funaltrexamine

ArticleYear
Electric muscle stimulation in the spontaneously hypertensive rat induces a post-stimulatory reduction in activity: role of different opioid receptors.
    Acta physiologica Scandinavica, 1990, Volume: 140, Issue:4

    We have previously shown that prolonged low-frequency muscle stimulation, inducing contractions of the gastrocnemius muscle, in conscious spontaneously hypertensive rats leads to an opioid-mediated post-stimulatory reduction in blood pressure and analgesia. In the present study we investigated whether muscle stimulation would also induce a post-stimulatory reduction in behavioural activity in the spontaneously hypertensive rats. Selective opioid receptor antagonists were used to analyse the involvement of endogenous opioids. Muscle stimulation, lasting 60 min, induced a post-stimulatory sedation that outlasted the stimulation for hours. Sniffing, locomotor activity and total behavioural activity were significantly reduced. The post-stimulatory reduction in activity was reversed back to control levels by a high dose of naloxone (15 mg kg-1 i.v.). The selective mu-receptor antagonist beta-funaltrexamine, given intracerebroventricularly before stimulation, did not influence the development of the post-stimulatory drop in activity. The delta-receptor antagonist ICI 154,129 had no effect at all on the already developed sedation, whereas MR 2266 BS, a kappa-receptor antagonist (3 mg kg-1 i.v.), completely reversed the drop in activity. These results show that muscle stimulation gives rise to an opioid-mediated post-stimulatory reduction in activity in spontaneously hypertensive rats. The results also indicate the involvement of the opioid kappa-receptor in the behavioural response.

    Topics: Animals; Benzomorphans; Electric Stimulation; Hypertension; Male; Motor Activity; Muscles; Naloxone; Naltrexone; Rats; Rats, Inbred SHR; Receptors, Opioid

1990
Role of opioid receptors in the long-lasting blood pressure depression after electric muscle stimulation in the hind leg of the rat.
    Acta physiologica Scandinavica, 1990, Volume: 140, Issue:2

    In a previous study, electrically induced contractions of the gastrocnemius muscle in conscious spontaneously hypertensive rats were shown to induce a blood pressure reduction of 15-20 mmHg lasting several hours. We showed in that study that endogenous opioid systems were involved. In this study, drugs with selective affinity for different opioid receptors were used to analyse further the involvement of endogenous opioid systems in the post-stimulatory drop in blood pressure in spontaneously hypertensive rats. Prestimulatory intracerebroventricular administration of beta-FNA (a mu-receptor antagonist) did not significantly influence the response at all, nor did a lower intravenous dose of naloxone reverse the post-stimulatory drop in blood pressure. High-dose naloxone (15 mg kg-1) increased post-stimulatory blood pressure by around 10 mmHg. About 50% of the drop thus remained after this treatment. A similar, partial reversal of the decreased blood pressure was seen after intravenous administration of a delta-receptor antagonist, ICI 154,129. However, the depressor response was completely reversed by a low intravenous dose of MR 2266 BS (a kappa-receptor antagonist). These results suggest that the reduction in blood pressure after muscle stimulation is mainly mediated by the opioid kappa-receptor. A certain involvement of the delta-receptor is also indicated.

    Topics: Animals; Benzomorphans; Blood Pressure; Electric Stimulation; Enkephalin, Leucine; Heart Rate; Hindlimb; Male; Naloxone; Naltrexone; Physical Conditioning, Animal; Rats; Rats, Inbred SHR; Receptors, Opioid; Regional Blood Flow

1990
Antagonistic and rate-suppressing effects of opioid antagonists in the pigeon.
    The Journal of pharmacology and experimental therapeutics, 1985, Volume: 235, Issue:2

    Pigeons trained to peck a key on a fixed-ratio 20 schedule of food presentation were used to evaluate the antagonistic and rate-suppressing effects of several opioid antagonists. Antagonism was measured as an increase in the dose of morphine necessary to suppress responding. Antagonist pretreatments increased the suppressing dose of morphine, although the magnitude of the increase varied markedly among different antagonists. Rank order of the maximum increase in the suppressing dose of morphine that each antagonist produced was: naltrexone = WIN 44,441 greater than beta-funaltrexamine greater than naloxone = buprenorphine greater than MR 2266 greater than diprenorphine. The time course of morphine antagonism also differed among antagonists. For example, buprenorphine was not an effective antagonist when administered 10 min before morphine, but was effective when administered either 2 or 12 hr before morphine. beta-Funaltrexamine and WIN 44,441 had the longest durations of antagonist action; each antagonized the rate-suppressing effects of morphine from 10 min to 24 hr. The effective antagonistic dose range (i.e., doses which blocked the rate-suppressing effects of morphine without affecting response rate when administered alone) and maximum increase in the suppressing dose of morphine were highly correlated, suggesting that the direct effects of most of these antagonists on responding may limit their effectiveness as morphine antagonists.

    Topics: Animals; Azocines; Benzomorphans; Buprenorphine; Columbidae; Conditioning, Operant; Diprenorphine; Dose-Response Relationship, Drug; Morphine; Naloxone; Naltrexone; Narcotic Antagonists

1985