PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7495925-3 1995 MK-212 induced a significant increase in plasma concentrations of cortisol and PRL. 6-chloro-2-(1-piperazinyl)pyrazine 0-6 prolactin Homo sapiens 79-82 7495925-0 1995 Effect of pindolol pretreatment on MK-212-induced plasma cortisol and prolactin responses in normal men. 6-chloro-2-(1-piperazinyl)pyrazine 35-41 prolactin Homo sapiens 70-79 7495925-4 1995 The MK-212-induced response in plasma cortisol was not diminished by pindolol pretreatment, whereas the MK-212-induced PRL response was significantly inhibited by pindolol pretreatment. 6-chloro-2-(1-piperazinyl)pyrazine 104-110 prolactin Homo sapiens 119-122 7495925-5 1995 These data suggest that the MK-212-induced cortisol response may be mediated by 5-HT2A or 5-HT2C receptor activation, or both, despite 5-HT1A inhibition; however, PRL secretion by MK-212 requires 5-HT1A receptor availability as well as 5-HT2A/5-HT2C receptor activation, since blockade of the former appears to blunt the PRL responses to MK-212. 6-chloro-2-(1-piperazinyl)pyrazine 28-34 prolactin Homo sapiens 163-166 7495925-5 1995 These data suggest that the MK-212-induced cortisol response may be mediated by 5-HT2A or 5-HT2C receptor activation, or both, despite 5-HT1A inhibition; however, PRL secretion by MK-212 requires 5-HT1A receptor availability as well as 5-HT2A/5-HT2C receptor activation, since blockade of the former appears to blunt the PRL responses to MK-212. 6-chloro-2-(1-piperazinyl)pyrazine 28-34 prolactin Homo sapiens 321-324 7495925-5 1995 These data suggest that the MK-212-induced cortisol response may be mediated by 5-HT2A or 5-HT2C receptor activation, or both, despite 5-HT1A inhibition; however, PRL secretion by MK-212 requires 5-HT1A receptor availability as well as 5-HT2A/5-HT2C receptor activation, since blockade of the former appears to blunt the PRL responses to MK-212. 6-chloro-2-(1-piperazinyl)pyrazine 180-186 prolactin Homo sapiens 163-166 7495925-5 1995 These data suggest that the MK-212-induced cortisol response may be mediated by 5-HT2A or 5-HT2C receptor activation, or both, despite 5-HT1A inhibition; however, PRL secretion by MK-212 requires 5-HT1A receptor availability as well as 5-HT2A/5-HT2C receptor activation, since blockade of the former appears to blunt the PRL responses to MK-212. 6-chloro-2-(1-piperazinyl)pyrazine 180-186 prolactin Homo sapiens 163-166 1756196-4 1991 The plasma PRL, but not the plasma cortisol response, following MK-212 was also significantly lower in the alcoholics. 6-chloro-2-(1-piperazinyl)pyrazine 64-70 prolactin Homo sapiens 11-14 7956751-5 1994 However, the plasma cortisol and PRL responses to MK-212 did not differ between the two groups. 6-chloro-2-(1-piperazinyl)pyrazine 50-56 prolactin Homo sapiens 33-36 3365458-0 1988 Stimulation of serum cortisol and prolactin secretion in humans by MK-212, a centrally active serotonin agonist. 6-chloro-2-(1-piperazinyl)pyrazine 67-73 prolactin Homo sapiens 34-43 3365458-5 1988 The cortisol and prolactin responses to the 40-mg dose of MK-212 were positively correlated (rho = + 0.85, p less than 0.02). 6-chloro-2-(1-piperazinyl)pyrazine 58-64 prolactin Homo sapiens 17-26 3365458-8 1988 MK-212 may stimulate the secretion of cortisol and prolactin in humans via a serotonin (5-HT2) receptor mechanism and may be a valuable tool with which to study 5-HT receptor sensitivity in humans. 6-chloro-2-(1-piperazinyl)pyrazine 0-6 prolactin Homo sapiens 51-60