TY - JOUR A1 - Labroo, V. M. A1 - Cohen, L. A. A1 - Lozovsky, D. A1 - Sirén, Anna-Leena A1 - Feuerstein, G. T1 - Dissociation of the cardiovascular and prolactin-releasing activities of TRH by histidine replacement N2 - No abstract available KW - Neurobiologie Y1 - 1987 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63253 ER - TY - JOUR A1 - Feuerstein, G. A1 - Sirén, Anna-Leena T1 - Opioid peptides: A role in hypertension? [Brief Review] N2 - 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. KW - Neurobiologie Y1 - 1987 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63262 ER - TY - JOUR A1 - Feuerstein, Giora A1 - Sirén, Anna-Leena T1 - The Opioid System in cardiac and vascular regulation of normal and hypertensive states N2 - 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. KW - Medizin Y1 - 1987 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-47418 ER - TY - JOUR A1 - Feuerstein, G. A1 - Sirén, Anna-Leena T1 - Cardiovascular effects of enkephalins N2 - 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. KW - Medizin Y1 - 1987 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-49048 ER - TY - JOUR A1 - Sirén, Anna-Leena A1 - Feuerstein, Giera T1 - Central autonomic pharmacology of thyrotropin releasing hormone N2 - 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. KW - Medizin Y1 - 1987 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-49051 ER - 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 - 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 - Paakkari, I. A1 - Nurminen, M-L. A1 - Sirén, Anna-Leena T1 - Cardioventilatory effects of TRH in anesthetized rats: role of the brainstem N2 - Cardioventilator responses were studied in anaesthetized rats after injections of TRH into either the lateral (i.c.v. lat) or the fourth (i.c.v. IV) cerebral ventricles. TRH induced a morerapid hypertensive effect i.c.v. IV than i.c.v. lat. Blocking of the cerebral aqueduct abolished the hypertensive and tachypnoeic effects of TRH i.c.v. lat but not those of TRH i.c.v. IV. It is concluded that TRH increased blood pressure and ventilation rate via brain stem structures close to the fourtli ventricle. KW - Neurobiologie KW - TRH KW - Cardiovascular KW - Ventilation KW - Brain stem Y1 - 1986 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63277 ER - TY - JOUR A1 - Sirén, Anna-Leena A1 - Powell, E. A1 - Feuerstein, G. T1 - Thyrotropin releasing hormone in hypovolemia: a hemodynamic evaluation in the rat N2 - ln the present study the effects of thyrotropin releasing hormone (TRH) and its stable analogue, CG3703, on cardiac output (thermodilution, Cardiomax) and regional blood flow (BF; directional pulsed Doppler technique) were investigated in hypovolemic hypotension in the rat. In urethan-anesthetized rats TRH (0.5 or 2 mg/ kg ia) or CG3703 (0.05 or 0.5 mg/kg ia) reversed the bleeding (27% of the blood volume)-induced decreases in mean arterial ... KW - Neurobiologie KW - cardiac output KW - total peripheral resistance KW - regional blood flow Y1 - 1986 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63288 ER - TY - JOUR A1 - Sirén, Anna-Leena A1 - Feuerstein, G. T1 - Effect of T-2 toxin on regional blood flow and vascular resistance in the conscious rat N2 - The acute effect ofT-2 toxemia on local blood flow and vascular resistance in hindquarter. mesenteric. and renal vascular beds was continuously measured by the directional pulsed Doppler technique in conscious, male Sprague-Dawley rats. Intravenous injection ofT-2 toxin (I mg/kg) in the conscious rat reduced blood flow and increased vascular resistance in all blood vessels studied but had no significant effect on mean arterial pressure or heart rate. The blood flow in hindquarters gradually decreased to a minimum of -77 ± 9% (mean ±SE) 6 hr after the toxin injection. The hindquarter vascular resistance concomitantly increased to a maximum value of + 323 ± 69% above thc resistance before toxin administration. Mesenteric and renal blood flow initially increased (slightly) and then gradually decreased. The maximum drop of blood flow, -90 ± 13% and -76 ± 13% for the mesenteric and renal vascular beds, respectively, was achieved 4 hr after T-2 toxin injection and the blood flow values remained low for up to 6 hr. Simultaneously with the impairment of KW - Neurobiologie Y1 - 1986 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-63293 ER -