@article{Siren1988, author = {Sir{\´e}n, Anna-Leena}, title = {Cardiovascular pharmacology of thyrotropin releasing hormone}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63214}, year = {1988}, subject = {Neurobiologie}, language = {en} } @article{FeuersteinSiren1988, author = {Feuerstein, G. and Sir{\´e}n, Anna-Leena}, title = {Hypothalamic µ-receptors in the cardiovascular control: a review}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63228}, year = {1988}, abstract = {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.}, subject = {Neurobiologie}, language = {en} } @article{SirenFeuerstein1988, author = {Sir{\´e}n, Anna-Leena and Feuerstein, G.}, title = {Cardiovascular effects of rat calcitonin gene-related peptide in the conscious rat}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63236}, year = {1988}, subject = {Neurobiologie}, language = {en} } @article{HallenbeckDutkaKochaneketal.1988, author = {Hallenbeck, JM and Dutka, AJ and Kochanek, PM and Sir{\´e}n, Anna-Leena and Pezeskpour, GH and Feuerstein, G.}, title = {Stroke risk factors prepare rat brainstem tissues for a modified localized Shwartzman reaction}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47971}, year = {1988}, abstract = {Stroke risk factors such as hypertension, diabetes, advanced age, and genetic predisposition to stroke were demonstrated to prepare rat brainstem tissues for a modified local Shwartzman reaction. A single intracisternal injection of endotoxin provoked the reaction, and affected rats manifested neurologie deficits accompanied by pathologie lesions. Brainstem infarcts developed in only a small proportion of rats without recognized risk factors after intracisternal injection of endotoxin. Thus, stroke risk factors, whieh are ordinarily regarded as operating through acceleration of atherosclerosis, may predispose to brain ischemia by local effects on brain mierocirculation such as those thought to underlie preparation of a tissue for the local Shwartzman reaction.}, subject = {Gehirn}, language = {en} } @article{FeuersteinLeaderSirenetal.1987, author = {Feuerstein, G. and Leader, P. and Sir{\´e}n, Anna-Leena and Braquet, P.}, title = {Protective effect of PAF-acether antagonist, BN 52021, in trichothecen toxicosis}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63244}, year = {1987}, abstract = {Trichothecenes are mycotoxins which produce Iethai toxicosis in humans and animals, yet no adequate therapeutic regimen has been developed. This study provides evidence that the selective platelet activating factor (PAF) antagonist, BN 52021 (5-15 mg/kg i.v.) can prolong the survival of conscious rats exposed to a highly Iethai T -2 toxicosis. These data also suggest that P AF is an important mediator of this unique toxicosis.}, subject = {Neurobiologie}, language = {en} } @article{LabrooCohenLozovskyetal.1987, author = {Labroo, V. M. and Cohen, L. A. and Lozovsky, D. and Sir{\´e}n, Anna-Leena and Feuerstein, G.}, title = {Dissociation of the cardiovascular and prolactin-releasing activities of TRH by histidine replacement}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63253}, year = {1987}, abstract = {No abstract available}, subject = {Neurobiologie}, language = {en} } @misc{FeuersteinSiren1987, author = {Feuerstein, G. and Sir{\´e}n, Anna-Leena}, title = {Opioid peptides: A role in hypertension? [Brief Review]}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63262}, year = {1987}, abstract = {This review is an attempt to highlight evidence that may implicate the endogenaus opioid system in the pathogenesis of hypertension in humans. The evidence raised includes biochemical, physiological, pharmacological, and behavioral studies con~ucted in in vitro andin vivo systems, experimental models of hypertension, and hornans with essential hypertension. While the compelling biochemical and pharmacological evidence in experimental animals clearly shows the presence of opioid peptides and their receptors in strategic sites of cardiovascular control and potent cardiovascular response to opioid peptides, opioid antagonists show no consistent blockade or reversal of hypertension in experimental animals or humans. One possible explanation for this phenomenon could be the vast redundancy in systems regulating blood pressure (i.e., the blockade ofone system stillleaves many other systerils fully able to rapidly offset the eliminated system). Regarding the opioid system, the situation is much more complex, since some opioid receptors (\(\mu\)-type) niediate pressor responses, while other receptors (\(\kappa\)type) mediate depressor responses. Therefore, nonselective opioid receptor antagonists (e.g., naloxone), which block both types ofreceptors, can be devoid ofany cardiovascular activity, while a selective \(\mu\)-receptor antagonist or a selective arid potent \(\kappa\)-receptor agonist may produce the desired antihypertensive elfect. A combination of both actions (i.e., a drug that is both \(\mu\)antagonist and a \(\kappa\)antagonist) might be even more advantageous. Until such compounds are developed, this hypothesis will be hard to prove.}, subject = {Neurobiologie}, language = {en} } @article{FeuersteinSiren1987, author = {Feuerstein, Giora and Sir{\´e}n, Anna-Leena}, title = {The Opioid System in cardiac and vascular regulation of normal and hypertensive states}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47418}, year = {1987}, abstract = {The endogenous opioid system includes three major families of peptides: 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. Opioid peptides and opioid receptors, of which multiple forms have been defined, are present in the central nervous system and peripheral neural elements. In the central nervous system, opioid peptides and receptors are found in forebrain and hindbrain nuclei involved in baroregulation, sympathoadrenal activation, and several other vital autonomic functions. In the periphery, opioid peptides are found in autonomic ganglia, adrenal gland, heart, and other organs; multiple opioid receptors are also found in vascular tissue, heart, and kidneys. Although little is known to date on the regulatory mechanisms of the opioid system in normal cardiovascular states, it became clear that cardiovascular stress situations substantially modify the activity of the endogenous opioid system. The purpose of this review is to clarify the sites of interaction of the opioid system with all major components of the cardiovascular system and indicate the potential role of this system in the ontogenesis of cardiac malfunction, vascular diseases, and hypertension.}, subject = {Medizin}, language = {en} } @article{FeuersteinSiren1987, author = {Feuerstein, G. and Sir{\´e}n, Anna-Leena}, title = {Cardiovascular effects of enkephalins}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-49048}, year = {1987}, abstract = {Enkephalins and their receptors are found in neurons and nerve terminals known to be involved in central cardiovascular control as well as the peripheral sympathetic and parasympathetic systems. Enkephalins and opioid receptors were also iden tified in the heart, kidneys, and blood vessels. The enkephalins interact with several specific receptors, of which p, 0, and K have been best characterized. Enkephalins administered to humans or animals produce cardiovascular effects which depend on the spedes, route of administration, anesthesia, and the selectivity for receptor subtype. While little information exists on the role of enkephalins in normal cardiovascular control, current data suggest that enkephalins might have a role in cardiovascular stress responses such os in shock and trauma.}, subject = {Medizin}, language = {en} } @article{SirenFeuerstein1987, author = {Sir{\´e}n, Anna-Leena and Feuerstein, Giera}, title = {Central autonomic pharmacology of thyrotropin releasing hormone}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-49051}, year = {1987}, abstract = {Thyrotropin releasing hormone (TRH, I-pyroglutamyl-l-histidyl-l-prolinamide) was the fIrst hypothalamic releasing SUbstance to be isolated, chemically characterized and synthetized /1/. The studies to date have revealed that the thyrotropin release from the pituitary gland is only one of the numerous actions of TRH. In addition to its endocrine actions (TSH and prolactin release) this tripeptide has central nervous system actions totally unrelated to its effects on the hypothalamo-pituitary axis. This review aims to summarize the studies on the central nervous system' actions of TRH with special emphasis on the autonomic pharmacology of this peptide.}, subject = {Medizin}, language = {en} }