Ulrike Poller
Martin Luther University of Halle-Wittenberg
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Ulrike Poller.
Journal of the American College of Cardiology | 1997
Ulrike Poller; Gesine Nedelka; Joachim Radke; Klaus Pönicke; Otto-Erich Brodde
OBJECTIVES This study was conducted to determine possible age-dependent changes in the responsiveness of human cardiac muscarinic receptors. BACKGROUND It is well known that the baroreflex activity decreases with aging. However, the mechanisms underlying this phenomenon are not completely understood at present. METHODS In six healthy young (mean [+/-SEM] age 26 +/- 2 years) and six healthy older volunteers (mean age 60 +/- 2 years), we determined 1) the effects of graded doses of atropine (bolus application, six doses, each for 20 min, range 0.03 to 0.96 mg) and the M1-cholinoceptor selective antagonist pirenzepine (bolus application, eight doses, each for 20 min, range 0.04 to 10 mg) on heart rate, blood pressure and systolic time intervals (as measure of inotropism); and 2) the baroreflex activity by assessing the bradycardic response to phenylephrine. RESULTS Atropine and pirenzepine caused biphasic effects on heart rate: At lower doses (< 0.12 mg for atropine, < 5 mg for pirenzepine) they decreased heart rate, whereas at higher doses they increased heart rate. Heart rate decreases induced by both antimuscarinic drugs were significantly larger in the young volunteers than in the older volunteers, whereas heart rate increases were not significantly different for both drugs. Atropine and pirenzepine did not significantly affect blood pressure and systolic time intervals. Infusion of graded doses of phenylephrine (four doses ranging from 0.1 to 1.0 microgram/kg body weight per min for 15 min each) caused a higher increase in systolic blood pressure and a smaller decrease in heart rate at each dose in the older volunteers than in the young volunteers. The slopes of the regression lines were 16 +/- 2.3 ms/mm Hg for the young and 6 +/- 0.5 ms/mm Hg for the older volunteers (p < 0.01). CONCLUSIONS Human cardiac muscarinic receptor activity is diminished with increasing age; such decreased cardiac muscarinic receptor activity could contribute to the decrease in baroreflex activity with aging. In contrast, antimuscarinic drugs seem to have no effect on human cardiac contractility.
Naunyn-schmiedebergs Archives of Pharmacology | 1997
Rafael F. Schäfers; Ulrike Poller; Klaus Pönicke; M. Geissler; Anton Daul; Martin C. Michel; Otto-Erich Brodde
Abstract This study aimed firstly to compare the in vivo cardiovascular effects of exogenously administered and of endogenously released noradrenaline; secondly to characterize the adrenoceptors mediating these responses; thirdly to assess the influence of parasympathetic tone on the cardiovascular effects of noradrenaline. In two randomised placebo-controlled studies, healthy, young, male volunteers received intravenous (i.v.) infusions of noradrenaline at six incremental doses of 10–160 ng/kg/min and – in order to release endogenous noradrenaline – tyramine at four incremental doses of 5–20 μg/kg/min. Noradrenaline and tyramine were administered in the absence and presence of α1-adrenoceptor blockade with doxazosin (2 mg p.o.), α2-adrenoceptor blockade with yohimbine (15 mg p.o.), selective β1-adrenoceptor blockade with bisoprolol (15 mg p.o.) and muscarinic receptor blockade with atropine (15 μg/kg i.v. loading dose followed by 0.15 μg/kg/min by i.v. infusion). Vasoconstrictor effects were assessed by measurement of diastolic blood pressure (Pdiast) and myocardial effects by measurement of systolic time intervals, namely the duration of electromechanical systole corrected for heart rate (QS2c). I.v. noradrenaline increased Pdiast (Δmax 17 mmHg) and this was nearly completely suppressed by doxazosin but only slightly blunted by yohimbine. Noradrenaline also slightly shortened QS2c (Δmax –22 ms), and this was potentiated by both doxazosin and yohimbine and completely blocked by bisoprolol. I.v. tyramine reduced Pdiast (Δmax –7 mmHg), which was not affected by α1-adrenoceptor blockade, and profoundly shortened QS2c (Δmax -104 ms) which was significantly correlated with a marked increase in systolic blood pressure (Psyst) (Δmax 57 mmHg). The shortening of QS2c and the rise in Psyst were not influenced by α-adrenoceptor blockade but were antagonized by bisoprolol. Atropine potentiated the blood pressure rise and the shortening of QS2c induced by i.v. noradrenaline and converted the fall in Pdiast induced by i.v. tyramine into an increase. Thus the cardiovascular effects of exogenous noradrenaline are mainly characterized by α1-adrenoceptor-mediated vasoconstriction and the actions of endogenous noradrenaline (released by i.v. tyramine) by β1-adrenoceptor-mediated positive inotropic effects. The rise in Psyst with i.v. tyramine most likely reflects positive inotropism and not a vascular ‘pressor’ response.
Journal of Cardiovascular Pharmacology | 1999
Jens Jakubetz; Saskia Schmuck; Ulrike Poller; Birgit Fuchs; Antje Gorf; J. Radke; Klaus Pönicke; Otto-Erich Brodde
The aim of this study was to find out whether cardiac responses to the beta-adrenoceptor antagonists with intrinsic sympathomimetic activity (ISA) xamoterol and celiprolol are mediated by cardiac beta1- or beta2-adrenoceptors or both. For this purpose we assessed, in six healthy male volunteers, the effects of xamoterol (100 and 200 mg, p.o.) and celiprolol (200, 600, and 1,200 mg, p.o.) on blood pressure, heart rate, and heart rate-corrected duration of the electromechanical systole (QS2c, as a measure of inotropism). Xamoterol, in both doses, increased systolic blood pressure and heart rate, transiently decreased diastolic blood pressure, and shortened QS2c; all these effects were attenuated after pretreatment of the volunteers with the beta1-adrenoceptor antagonist bisoprolol. Celiprolol, in all three doses, increased heart rate, decreased diastolic blood pressure, and shortened QS2c but only marginally increased systolic blood pressure. Bisoprolol did not attenuate these celiprolol effects but rather enhanced celiprolol effects on systolic blood pressure and heart rate. In a further set of experiments, we studied cardiovascular effects of celiprolol in six healthy volunteers whose beta2-adrenoceptors had been desensitized by a 2-week treatment with 3x5 mg/day terbutaline. Under these conditions, celiprolol failed to increase heart rate or to shorten QS2c. We conclude that, under resting conditions, in healthy volunteers, beta-adrenoceptor antagonists with ISA can exert increases in heart rate and contractility that are mediated by either cardiac beta1-adrenoceptor (xamoterol) or cardiac beta2-adrenoceptor (celiprolol) stimulation. Thus in the human heart, the ISA of beta-adrenoceptor antagonists can be a beta1- or beta2-adrenoceptor agonistic component.
Naunyn-schmiedebergs Archives of Pharmacology | 1995
A. E. Daul; M. Elter-Schulz; Ulrike Poller; F. Jockenhövel; Klaus Pönicke; F Boomsma; A. J. Man in't Veld; R. F. Schäfers; O.-E. Brodde
Epinine (N-methyl-dopamine, the active metabolite of ibopamine), is a full agonist at dopamine (DA)-receptors and α- and \-adrenoceptors. To study whether in vivo DA-receptor mediated effects can be separated from α- and \-adrenoceptor effects we compared in 10 male volunteers the effects of i.v. epinine (0.5; 1; 2; 4 μg/kg/min for 15 min each) on DA-receptor (changes in serum prolactin)- and α- and \-adrenoceptor (changes in systolic [Psyst] and diastolic blood pressure [Pdiast] and heart rate)-mediated effects with those of dopamine before and after propranolol (5 mg i.v. 45 min pre-infusion), bisoprolol (15 mg p.o. 2 h preinfusion) and domperidone (10 mg p.o. 1 h pre-infusion). At the 0.5 and 1 μg doses dopamine and epinine did not affect Psyst Pdiast and heart rate but significantly decreased prolactin levels. At the higher dose both dopamine and epinine significantly increased Psyst and heart rate, while only epinine significantly increased Pdiast. In addition both dopamine and epinine significantly increased diuresis and natriuresis; in contrast, only dopamine, but not epinine, dose-dependently increased plasma noradrenaline levels. Domperidone did not affect dopamine- and epinine-evoked blood pressure-and heart rate-changes, but antagonized their prolactin-effects (at least at the lower doses). Bisoprolol and propranolol significantly reduced dopamine-induced Psyst- and heart rate-increases to about the same extent. Propranolol enhanced epinine-induced Psyst-and Pdiast-increases while bisoprolol reduced epinine-evoked Psyst-increase but not Pdiast-increase. Epinine-induced heart rate-increase was abolished by bisoprolol and was converted into a heart rate-decrease by propranolol. We conclude that in 0.5 and 1 μg doses (plasma levels of 20–80 nmol/1) epinine acts only at DA-receptors. Thus, ibopamine in therapeutically recommended doses (3 × 100 mg/day with peak plasma epinine-levels of 50–80 nmol/1) very likely activates only DA-receptors. In higher doses, however, epinine -like dopamine - activates α- and \-adrenoceptors whereby epinine has a stronger α-adrenoceptor agonistic activity than dopamine. Moreover, part of the dopamine-effects are indirect via release of endogenous noradrenaline whereas epinine-effects do not appear to include an indirect component.
Naunyn-schmiedebergs Archives of Pharmacology | 1997
Ulrike Poller; R. F. Schäfers; Saskia Schmuck; Jens Jakubetz; J. Radke; A. E. Daul; Klaus Pönicke; Otto-Erich Brodde
Abstract The aim of this study, carried out in six elder healthy volunteers (mean age: 61 years), was to determine the influence of muscarinic receptor blockade with atropine (15 µg/kg i.v. loading dose followed by 0.15 µg/kg/min by i.v. infusion) on the effects of i.v. infusions of noradrenaline (5 incremental doses of 10-120 ng/kg/min) or tyramine, that releases endogenous noradrenaline (4 incremental doses of 5-20 µg/kg/min), on blood pressure, heart rate and systolic time intervals (STI’s, as a measure of positive inotropism). These results were compared with those recently published for young healthy volunteers (mean age: 26 years; Schäfers et al. 1997). Noradrenaline caused increases in systolic and diastolic blood pressure, decreases in heart rate and a shortening of STI’s that were not different from those in young volunteers. Atropine did not significantly affect these hemodynamic responses to noradrenaline, while in young volunteers it significantly enhanced noradrenaline-induced blood pressure increases and converted the heart rate decrease into an increase. In the present study in elder volunteers, tyramine caused a smaller increase in systolic blood pressure than in the previous study in young volunteers; in addition, it slightly increased diastolic blood pressure while it decreased diastolic blood pressure in young volunteers. Atropine did not significantly affect the hemodynamic effects of tyramine in the elder volunteers, while in the young volunteers it enhanced the increase in systolic blood pressure and converted the decreases in diastolic blood pressure and heart rate into increases. These results indicate a) that ageing is accompanied by a blunted baroreflex-mediated parasympathetic activation resulting in reduced cholinergic vasodilation and decreases in heart rate, and b) that ageing is associated with a decreased responsiveness of (cardiac) β-adrenoceptors and (vascular) α1-adrenoceptors which is only unmasked when the counterregulatory action of parasympathetic activation is removed.
Clinical Pharmacology & Therapeutics | 2000
Jens Jakubetz; Saskia Schmuck; Germar Wochatz; Barbara Ruhland; Ulrike Poller; J. Radke; Otto-Erich Brodde
The M1‐muscarinic receptor antagonist pirenzepine in low doses (<1 mg intravenously) decreases heart rate. We investigated whether these effects of pirenzepine differ in volunteers with activated cardiac β1‐adrenergic receptors versus activated cardiac β2‐adrenergic receptors.
Naunyn-schmiedebergs Archives of Pharmacology | 2004
Heike Bruck; Ulrike Poller; Hendrik Lüssenhop; Klaus Pönicke; Thomas Temme; Gerd Heusch; Thomas Philipp; Otto-Erich Brodde
The intrinsic sympathomimetic activity (ISA) of a β-adrenoceptor blocker can be mediated by β1- or β2-adrenoceptors. The aim of this study was to characterize the ISA of the β-adrenoceptor blocker carteolol in healthy volunteers. Two approaches were employed. First, we assessed the effects of carteolol (20, 40 or 80 mg p.o.) on blood pressure, heart rate and heart-rate corrected duration of electromechanical systole (QS2c, a measure of cardiac contractility) in the volunteers. Carteolol dose-dependently increased systolic blood pressure, heart rate and contractility and decreased diastolic blood pressure. The β1-adrenoceptor blocker bisoprolol did not attenuate these carteolol effects, but rather enhanced the effects on heart rate and systolic blood pressure. Second, we treated volunteers for 7 days with 1×20 mg/day carteolol and assessed lymphocyte β2-adrenoceptor density (by (−)-[125I]-iodocyanopindolol binding) and functional responsiveness (by 10 μM isoprenaline-induced increase in lymphocyte cyclic AMP content). Carteolol significantly reduced lymphocyte β2-adrenoceptor density and function. After withdrawal of carteolol lymphocyte β2-adrenoceptor density and function recovered only very slowly and had not returned to control levels 11 days after carteolol withdrawal. In conclusion, the fact that, on the one hand, the cardiovascular effects of carteolol were not attenuated by the β1-adrenoceptor blocker bisoprolol and, on the other, carteolol significantly decreased lymphocyte β2-adrenoceptor density and function is in favour of the idea that the ISA of carteolol is mediated by β2-adrenoceptors. Involvement of an additional receptor site (e.g. the propranolol-resistant state of the β1-adrenoceptor), however, cannot be excluded.
Journal of the American College of Cardiology | 2000
Stefan Dhein; Peter Röhnert; Silke Markau; Emanuel Kotchi-Kotchi; Karin Becker; Ulrike Poller; Bernd Osten; Otto-Erich Brodde
Cardiovascular Research | 1998
Ulrike Poller; Birgit Fuchs; Antje Gorf; Jens Jakubetz; J. Radke; Klaus Pönicke; Otto-Erich Brodde
Journal of the American College of Cardiology | 1998
J. Jakubetz; Ulrike Poller; J. Radke; Klaus Pönicke; Otto-Erich Brodde