TY - JOUR A1 - Paakkari, I. A1 - Sirén, Anna-Leena A1 - Nurminen, M.-L. A1 - Svartström-Fraser, M. T1 - Injection of thyrotropin releasing hormone into the locus coeruleus increases blood pressure N2 - Thyrotropin releasing hormone (TRH), 10 pmol kg-1 injected in the region of locus coeruleus, caused a rapid (within 1 min) rise of mean arterial pressure in the urethane- naesthetized rat. No clear-cut effects in heart rate or ventilation were observed. When TRH was injected into the lateral ventricle, a dose more than 10-fold higher was required to achieve a comparable rise in arterial pressure. It is concluded that TRH may have a physiological rote in centrat cardiovascular regulation. KW - Thyreotropin-Releasinghormon KW - Blutdruck KW - Locus coeruleus KW - TRH KW - blood pressure KW - locus coeruleus Y1 - 1987 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-72894 ER - TY - JOUR A1 - Paakkari, P. A1 - Paakkari, I. A1 - Feuerstein, G. A1 - Sirén, Anna-Leena T1 - Evidence for differential opioid µ\(_1\)- and µ\(_2\)-receptor regulation of heart rate in the conscious rat N2 - The possibility that \(\mu\)Opioid-induced tachycardia and bradycardia could be mediated by different subtypes of the \(\mu\)·receptor was studied in conscious Sprague-Dawley rats. The selective \(\mu\)·receptor agonist dermorphin and its analog, TAPS (Tyr-o-Arg-Phe-sarcosine), a putative \(\mu _1\)-receptor agonist, were given centrally. Tyr-o-Arg-Phe-sarcosine increased the heart rate, the response being inversely correlated to the dose (an increase of 71 ± 22, 49 ± 14 and 30 ± 17 beats/min at doses of 0.3, 3 and 30 pmol, respectively). Dermorphin induced less clear changes in heart rate (maximum increase of 39 ± 14 beats/min at the dose of 1 pmol). Aftertreatment with the Jl 1-selective antagonist naloxonazine (NAZ), TAPS 30 pmol and dennorphin I pmol decreased heart rate by -22 ± 10 and -24 ± 7 bpm, respectively. The bradycardic effect oflarger doses of dennorphin was potentiated by NAZ (from -25 ± 8 to -97 ± 22 bpm) but abolished by the non-selective antagonist naloxone. These data suggest that the high affinity \(\mu _1\)-opioid receptors mediate tachycardic responses and \(\mu _2\)-receptors mediate bradycardic responses. KW - Neurobiologie KW - dennorphin KW - naloxonazine KW - naloxone KW - heart rate KW - blood pressure KW - µ·Opioid receptor subtypes Y1 - 1992 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63017 ER -