TY - JOUR A1 - Eimerl, J. A1 - Sirén, Anna-Leena A1 - Feuerstein, G. T1 - Systemic and regional hemodynamic effects of leukotrienes D\(_4\) and E\(_4\) in the conscious rat N2 - No abstract available KW - Neurobiologie Y1 - 1986 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63317 ER - TY - JOUR A1 - Sirén, Anna-Leena A1 - Feuerstein, G. T1 - Effect of PAF and BN 52021 on cardiac function and regional blood flow in the conscious rat N2 - No abstract available KW - Neurobiologie Y1 - 1989 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63145 ER - TY - JOUR A1 - Sirén, Anna-Leena A1 - Feuerstein, G. T1 - Thyrotropin releasing hormone-induced hindquarter vasodilation is mediated by \(\beta _2\)-adrenoceptors N2 - No abstract available KW - Neurobiologie Y1 - 1989 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63155 ER - TY - JOUR A1 - Sirén, Anna-Leena A1 - Feuerstein, G. T1 - Hemodynamic effects of endothelin after systemic and central nervous System administration in the conscious rat N2 - No abstract available KW - Neurobiologie Y1 - 1989 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63165 ER - TY - JOUR A1 - Feuerstein, G. A1 - Letts, G. A1 - Sirén, Anna-Leena T1 - N-Ac-Leukotriene E\(_4\): Unique vascular activity in the conscious rat N2 - No abstract available KW - Neurobiologie Y1 - 1988 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63171 ER - TY - JOUR A1 - Sirén, Anna-Leena A1 - Lake, C. R. A1 - Feuerstein, G. T1 - Hemodynamic and neural mechanisms of action of thyrotropin releasing hormone in the rat N2 - Tbe mechanisms mediating the etl'ects ofthyrotropin-releasing hormone (TRH) on the cardiovascular system were studied in the conscious rat. Intracerebroventricolar (i.c. v.) injection of TRH (8 pmol-80 nmollkg) induced dose-dependent lncreases in mean arterial pressure, heart rate, and cardiac index. Rindquarter blood Oow increased due to vasodilation, while an lncrease in renal and mesenteric vascular resistance caused a decrease in blood Oow in the respective organs. The plasma Ievels of norepinephrine a~d epinephrine were increased by TRH, while there was no change in plasma renin activity or vasopressin. Tbe cardiovascular actions of i.c. v. TRH were not in.fluenced by blockade of the renin-angiotensin system or vasopressin receptors. Tbe ganglion blocker chlorisondamine and the a 1- aod al-adrenoreceptor antagooist phentolamlne (2 mg/kg i.v.) abolished the increase in blood pressure and mesenteric vasoconstriction after i.c. v. TRH. Propranolol (2 mg/kg i. v.) blocked the TRH-ioduced increase in cardiac index, heart rate, and hindquarter blood flow. The hindquarter vasodllatlon lnduced by TRH was also blocked by the selective ß1-adrenocept9r antagonist ICI 188,551 (1 or 2 mg/kg i.v.), while tbe ,8,-adrenoceptor blocker practolol (10 mg/kg i.v.) had no eft'ect on the hindquarter vasodiJation produced by TRH but totally blocked the increase in cardiac Index. In adrenal demedullated rats, the systemic hemodynamic eft'ects ofi.c. v. TRH were dimlnished along with the decrease in renal blood flow and lncrease in renal vascular resistance; however, the iocrease in hfndquarter blood flow was attenuated only in adrenal demedullated rats pretreated with the sympathetlc blocker bretylium. The renal vasoconstriction induced by i.c. v. TRH was not abolished by renal denervation. In sinoaortic debufl'ered rats, the pressor, tachycardic, and mesenteric vasoconstrictor responses to centrally administered TRH were significantly potentiated. Taken together, these data soggest that the putative rieurotransmitter TRH may play a role in central regulation of cardiac functions and organ blood flow distribution through both tbe sympathetic nerves and the adrenal medulla. A pivotal roJe for ß1-adrenoceptors in mediation ofhindquarter vasodilation ls also demonstrated. KW - Neurobiologie Y1 - 1988 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63183 ER - TY - JOUR A1 - Sirén, Anna-Leena A1 - Letts, G. A1 - Feuerstein, G. T1 - N-Acetyl-leukotriene E\(_4\) is a potent constrictor of rat mesenteric vessels N2 - N-Acetyl-leukotriene E\(_4\) administered to conscious freely moving rats produced a dose-dependent vasoconstriction in the mesenteric vessels which led to profound reduction of blood flow to the gut. Renal and hindquarter blood flow and vascular resistance were not affected even by high doses of N-acetyl-leukotriene E\(_4\) . N-Acetyl-leukotriene E\(_4\) was 10-fold more potent than the thromboxane analog U-46619 and 1000-fold more potent than prostaglandin F\(_{2a}\) but 2-5-fold less potent than leukotriene D\(_4\)/E\(_4\) to induce mesenteric vasoconstriction. These data indicatc that N-acetylleukotriene E\(_4\) is a biologically active metabolite of peptide leukotrienes, and might play a role in cardiovascular derangements mediated by leukotrienes. KW - Neurobiologie KW - Peptide-leukotrienes KW - N-Acetyl-leukotriene E4 KW - Prostaglandins KW - Mesenteric circulation KW - Anaphylactic shock Y1 - 1988 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63196 ER - TY - JOUR A1 - Feuerstein, G. A1 - Sirén, Anna-Leena T1 - Mesenteric vascular responses to i.v. administration of lipoxin A\(_4\) and lipoxin B\(_4\) in the conscious rat N2 - Lipoxin A (LXA\(_4\)) and lipoxin B\(_4\)(LXB\(_4\)) are newly discovered lipoxygenase-interacting products of leukocytes which might have a role in cardiovascular events associated with anaphylaxis. We have tested this possibility by systemic administration of both LXA\(_4\) and LXB\(_4\) to the conscious rat while monitaring systemic and regional hemodynamic changes. LXA\(_4\) and' LXB\(_4\) (l-100 pg/kg) produced dose-dependent constriction of the mesenteric vessels, up to + 123±23% and +50±9% for LXA\(_4\)/B\(_4\) , respectively. Dose-related changes were not observed in arterial blood pressure, heart rate, renal (LXB\(_4\)) and hindquarter blood ftow. We suggest that LXA\(_4\) and LXB\(_4\) might affect selective vascular beds, such as the mesenteric vessels, and contribute to variations in blood flow in specific pathophysiological states. KW - Neurobiologie KW - Lipoxin KW - Anaphylaxis KW - Mesenteric circulation KW - Renal circulation KW - Icosanoid Y1 - 1988 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63200 ER - TY - JOUR A1 - Feuerstein, G. A1 - Sirén, Anna-Leena T1 - Hypothalamic µ-receptors in the cardiovascular control: a review N2 - The endogenous opioid system includes three major families of peptides [22): dynorphins (derived from pre-proenkephalin B); endorphins (derived from pre-proopiomelanocortin) and enkephalins (derived from pre-proenkephalin A). Multiple species of opioid peptides are derived from these major precursors and many of them possess potent cardiovascular properties. Multiple forms of opioid receptors have been defined in the central nervous system. Although the relationship of these receptors to the multiple actions of the opioid systems is not weil understood, some predications can be made: in vitro the dynorphin-related peptidesbind preferentially to kappa-opioid receptors; the enkephalins bind preferentially to delta and JL-opioid receptors and while beta-endorphin binds to mu- and delta-, but not to kappa-opioid receptors. While littleis known on the roJe ofthe opioid system in normal cardiovascular regulation, it has become clear that cardiovascular stress situations substantially modify the activity ofthe endogenous opioid system. This review focuses on the mu-opioid system in the hypothalamus with special emphasis on its potential roJe in cardiovascular control of both normal and pathophysiologic states. KW - Neurobiologie KW - µ opioid receptors KW - Hypothalamus KW - Cardiovascular system KW - Sympathetic nervous system Y1 - 1988 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63228 ER - TY - JOUR A1 - Sirén, Anna-Leena A1 - Feuerstein, G. T1 - Cardiovascular effects of rat calcitonin gene-related peptide in the conscious rat KW - Neurobiologie Y1 - 1988 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63236 ER -