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  • 1
    Electronic Resource
    Electronic Resource
    HMR 1098: An Inhibitor of Cardiac ATP-Sensitive Potassium Channels (2000)
    Oxford, UK : Blackwell Publishing Ltd
    Cardiovascular drug reviews 18 (2000), S. 0 
    Details
    ISSN: 1527-3466
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1527-3466.2000.tb00040.x
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  • 2
    Electronic Resource
    Electronic Resource
    Ramipril (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Cardiovascular drug reviews 5 (1987), S. 0 
    Details
    ISSN: 1527-3466
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1527-3466.1987.tb00502.x
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  • 3
    Electronic Resource
    Electronic Resource
    Technetium-99m-Labeled HOE 140: A Potential Bradykinin B2 Receptor Imaging Agent (1995)
    s.l. : American Chemical Society
    Journal of medicinal chemistry 38 (1995), S. 2799-2801 
    Details
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jm00015a001
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  • 4
    Electronic Resource
    Electronic Resource
    Differences in acetylcholine- and bradykinin-induced vasorelaxation of the mesenteric vascular bed in spontaneously hypertensive rats of different ages (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 38-43 
    Details
    ISSN: 1432-1912
    Keywords: SHR ; Endothelium-dependent relaxation ; Rat mesenteric vascular bed ; Rat thoracic aorta ; Bradykinin Acetylcholine ; Age dependency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study examined whether alterations of endothelium-dependent vasorelaxation in spontaneously hypertensive rats (SHR) in response to the endothelium-dependent vasodilators acetylcholine and bradykinin ran parallel. We tried to find out the age at which endothelium-dependent vasorelaxation in response to each agonist became impaired and compared three different groups of SHR aged 7, 21 and 51 weeks. To be able to separate hypertension-induced alterations from age-dependent changes age-matched normotensive Wistar rats were included. Endothelium-dependent vasorelaxation was studied in the mesenteric vascular bed precontracted with noradrenaline, a typical resistance vessel, which showed relaxation to both acetylcholine and bradykinin, and the precontracted thoracic aorta, which only responded to acetylcholine. There were major differences in the agonist-dependent vasorelaxation between bradykinin and acetylcholine in SHR as a function of age. A surprising finding was that acetylcholine-induced relaxation was preserved, even slightly improved not only in young SHR (7 weeks) with developing hypertension but also in adult SHR (21 weeks) with established hypertension, which can be interpreted as a compensatory mechanism. As expected, in old SHR (51 weeks) acetylcholine induced vasorelaxation was impaired as a consequence of the detrimental effects of long-term hypertension on endothelium. The parallel changes observed with acetylcholine in the mesenteric vascular bed and thoracic aorta provided mutual confirmation. In clear contrast to acetylcholine bradykinin-induced vasorelaxation was already impaired in young SHR with developing hypertension suggesting that bradykinin-induced vasorelaxation is either much more sensitive to detrimental effects of (even slightly) increased blood pressure or, more likely, that there is a basic deficiency in the action of bradykinin in SHR. Thus, our study allows to conclude that impairment of acetylcholine-induced endothelium-dependent vasorelaxation in the mesenteric vascular bed of SHR is a secondary phenomenon developing as a consequence of long-term hypertension while the impaired bradykinin-induced vasorelaxation seems to be a primary phenomenon that could be closely related to the development of hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168704
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  • 5
    Electronic Resource
    Electronic Resource
    Differences in acetylcholine- and bradykinin-induced vasorelaxation of the mesenteric vascular bed in spontaneously hypertensive rats of different ages (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 38-43 
    Details
    ISSN: 1432-1912
    Keywords: Key words SHR ; Endothelium-dependent relaxation ; Rat mesenteric vascular bed ; Rat thoracic aorta ; Bradykinin Acetylcholine ; Age dependency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The present study examined whether alterations of endothelium-dependent vasorelaxation in spontaneously hypertensive rats (SHR) in response to the endothelium-dependent vasodilators acetylcholine and bradykinin ran parallel. We tried to find out the age at which endothelium-dependent vasorelaxation in response to each agonist became impaired and compared three different groups of SHR aged 7, 21 and 51 weeks. To be able to separate hypertension-induced alterations from age-dependent changes age-matched normotensive Wistar rats were included. Endothelium-dependent vasorelaxation was studied in the mesenteric vascular bed precontracted with noradrenaline, a typical resistance vessel, which showed relaxation to both acetylcholine and bradykinin, and the precontracted thoracic aorta, which only responded to acetylcholine. There were major differences in the agonist-dependent vasorelaxation between bradykinin and acetylcholine in SHR as a function of age. A surprising finding was that acetylcholine-induced relaxation was preserved, even slightly improved not only in young SHR (7 weeks) with developing hypertension but also in adult SHR (21 weeks) with established hypertension, which can be interpreted as a compensatory mechanism. As expected, in old SHR (51 weeks) acetylcholine-induced vasorelaxation was impaired as a consequence of the detrimental effects of long-term hypertension on endothelium. The parallel changes observed with acetylcholine in the mesenteric vascular bed and thoracic aorta provided mutual confirmation. In clear contrast to acetylcholine bradykinin-induced vasorelaxation was already impaired in young SHR with developing hypertension suggesting that bradykinin-induced vasorelaxation is either much more sensitive to detrimental effects of (even slightly) increased blood pressure or, more likely, that there is a basic deficiency in the action of bradykinin in SHR. Thus, our study allows to conclude that impairment of acetylcholine-induced endothelium-dependent vasorelaxation in the mesenteric vascular bed of SHR is a secondary phenomenon developing as a consequence of long-term hypertension while the impaired bradykinin-induced vasorelaxation seems to be a primary phenomenon that could be closely related to the development of hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168704
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of the Na+/H+-exchange inhibitor Hoe 642 on intracellular pH, calcium and sodium in isolated rat ventricular myocytes (1996)
    Springer
    Pflügers Archiv 433 (1996), S. 26-34 
    Details
    ISSN: 1432-2013
    Keywords: Key words Na+/H+-exchange ; Hoe 642 ; Cardiomyocyte ; Hypoxia ; Fluorescence technique ; BCECF ; Fura-2 ; SBFI
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The inhibitors of the Na+/H+-exchange (NHE1) system Hoe 694 and Hoe 642 possess cardioprotective effects in ischaemia/reperfusion. It is assumed that these effects are due to the prevention of intracellular sodium (Nai) and calcium (Cai) overload. The purpose of the present study was to investigate the effects of Hoe 642 on intracellular pH, Na+ and Ca2+ (pHi, Nai and Cai) in isolated rat ventricular myocytes under anoxic conditions or in cells in which oxidative phosphorylation had been inhibited by 1.5 mmol/l cyanide. In cells which were dually loaded with the fluorescent dyes 2,7-biscarboxyethyl-5,6-carboxyfluorescein (BCECF) and Fura-2, anoxia caused acidification of the cells (from pHi 7.2 to pHi 6.8) and an increase in Cai from about 50 nmol/l to about 1 μmol/l. The decrease in pHi began before the cells underwent hypoxic (rigor) contracture, whereas Cai only began to rise after rigor shortening had taken place. After reoxygenation, pHi returned to its control value and Cai oscillated and then declined to resting levels. It was during this phase that the cells rounded up (hypercontracture). When 10 μmol/l Hoe 642 was present from the beginning of the experiment, pHi and Cai were not significantly different from control experiments. At reoxygenation, pHi did not recover, but Cai oscillated and returned to its resting level. To monitor Nai, the cells were loaded with the dye SBFI. After adding 1.5 mmol/l cyanide or 100 μmol/l ouabain, Nai increased from the initial 8 mmol/l to approximately 16 mmol/l. Hoe 642 or Hoe 694 (10 μmol/l) did not prevent the increase in Nai. In contrast, the blocker of the persistent Na+ current R56865 (10 μmol/l) attenuated the CN–-induced rise in Nai. The substance ethylisopropylamiloride was not used because it augmented considerably the intensity of the 380 nm wavelength of the cell’s autofluorescence. In conclusion, the specific NHE1 inhibitor Hoe 642 did not attenuate anoxia-induced Cai overload, nor CN–-induced Nai and Cai overload. Hoe 642 prevented the recovery of pHi from anoxic acidification. This low pHi maintained after reoxygenation may be cardioprotective. Other possible mechanisms of NHE1 inhibitors, such as prevention of Ca2+ overload in mitochondria, cannot be ruled out. The increase in Nai during anoxia is possibly due to an influx of Na+ via persistent Na+ channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050244
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  • 7
    Electronic Resource
    Electronic Resource
    Angiotensin converting enzyme inhibitors, left ventricular hypertrophy and fibrosis (1995)
    Springer
    Molecular and cellular biochemistry 147 (1995), S. 89-97 
    Details
    ISSN: 1573-4919
    Keywords: left ventricular hypertrophy ; fibrosis ; ramipril ; autocrine-paracrine actions ; ACE inhibitors ; bradykinin ; prostacyclin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract From pharmacological investigations and clinical studies, it is known that angiotensin converting enzyme (ACE) inhibitors exhibit additional local actions, which are not related to hemodynamic changes and which cannot be explained only by interference with the renin angiotensin system (RAS) by means of an inhibition of angiotensin II (ANG II) formation. Since ACE is identical to kininase II, which inactivates the nonapeptide bradykinin (BK) and related kinins, potentiation of kinins might be responsible for these additional effects of ACE inhibitors. a) In rats made hypertensive by aortic banding, the effect of ramipril in left ventricular hypertrophy (LVH) was investigated. Ramipril in the antihypertensive dose of 1 mg/kg/day for 6 weeks prevented the increase in blood pressure and the development of LVH. The low dose of ramipril (10 μg/kg/day for 6 weeks) had no effect on the increase in blood pressure or on plasma ACE activity but also prevented LVH after aortic banding. The antihypertrophic effect of the higher and lower doses of ramipril, as well as the antihypertensive action of the higher dose of ramipril, was abolished by coadmistration of the kinin receptor antagonist icatibant. In the regression study the antihypertrophic actions of ramipril were not blocked by the kinin receptor antagonist. Chronic administration of BK had similar beneficial effects in a prevention study which were abolished by icatibant and NG-nitro-L-arginine (L-NNA). In a one year study the high and low dose of ramipril prevented LVH and fibrosis. Ramipril had an early direct effect in hypertensive rats on the mRNA expression for myocardial collagen I and III, unrelated to its blood pressure lowering effect. b) In spontaneously hypertensive rats (SHR) the preventive effects of chronic treatment with ramipril on myocardial LVH was investigated. SHR were treated in utero and, subsequently, up to 20 weeks of age with a high dose (1 mg/kg/day) or with a low dose (10 μg/kg/day) of ramipril. Animals on a high dose remained normotensive, whereas those on a low dose developed hypertension in parallel to vehicle-treated controls. Left ventricular mass was reduced only in high-dose-treated, but not in low-dose treated animals but both groups revealed an increase in myocardial capillary length density. In SHR stroke prone animals cardiac function and metabolism was improved by ramipril and abolished by coadministration of icatibant. In contrast to the prevention studies, in a regression study ramipril reduced cardiac hypertrophy also by low dose treatment. c) In rats chronic nitric oxide (NO) inhibition by NG-nitro-L-arginine-methyl ester (L-NAME) treatment induced hypertension and LVH. Ramipril protected against blood pressure increase and partially against myocardial hypertrophy. These experimental findings in different models of LVH characterise ACE inhibitors as remarkable antihypertrophic and antifibrotic substances.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00944788
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  • 8
    Electronic Resource
    Electronic Resource
    Cardiac arrhythmias are ameliorated by local inhibition of angiotensin formation and bradykinin degradation with the converting-enzyme inhibitor ramipril (1989)
    Springer
    Cardiovascular drugs and therapy 3 (1989), S. 873-882 
    Details
    ISSN: 1573-7241
    Keywords: angiotensin-converting enzyme ; bradykinin ; ramipril ; bradykinin antagonist ; arrhythmias ; isolated ischemic rat hearts ; cardioprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the influence of the angiotensin-converting enzyme (ACE) inhibitor ramipril on cardiac arrhythmias in guinea pigs and rats. Ramiprilat, the active moiety of ramipril, did not influence action potentials of isolated guinea-pig papillary muscle or rabbit sinus node, thereby excluding cellular electrophysiological evidence of anti-arrhythmic properties. Ramipril protected against cardiac arrhythmias induced by digoxin infusion in guinea pigs. This effect was comparable with that of lidocaine. In isolated perfused ischemic working rat hearts, angiotensin (ANG) I (3×10−9 M/l) and ANG II (1×10−9 M/l) aggravated reperfusion arrhythmias, accompanied by deterioration of cardiodynamic and metabolic events. Bradykinin (BK) (1×10−10−1×10−8 M/l), in contrast, protected against reperfusion arrhythmias, which corresponded to an increase in energy-rich phosphates and glycogen stores and a decrease in lactate levels in myocardial tissue. Identical changes were seen in hearts from rats pretreated with ramipril (1 mg/kg PO) or perfused with ramiprilat (2.58 ×10−7−2.58×10−5 M/l). Local ACE inhibition in these ischemic hearts antagonized ANG I but not ANG II effects and enhanced BK effects. The BK antagonist D-Arg-(Hyp2, Thi5,8, D-Phe7) BK abolished the beneficial effects of BK, ramipril, and ramiprilat. Increased concentrations of BK or ramiprilat were able to reverse the antagonism. The antiarrhythmic agent nicainoprol, a fast-sodiumchannel blocking drug (class Ib), also protected isolated rat hearts against reperfusion arrhythmias, but was without beneficial effects on cardiac hemodynamics and biochemical parameters, in contrast to the ACE inhibitor. These results suggest that the beneficial effects of the ACE inhibitor ramipril on digoxin and reperfusion arrhythmias are not mediated by their direct actions on ionic channels in the cell membrane. It seems that other factors are responsible for its beneficial effects on reperfusion arrhythmias, cardiac function, and metabolism, which are associated with a reduction in ANG II generation and BK degradation by local ACE inhibition in the heart.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869575
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  • 9
    Electronic Resource
    Electronic Resource
    Bradykinin antagonists with dehydrophenylalanine analogues at position 5 (1998)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Peptide Science 4 (1998), S. 92-100 
    Details
    ISSN: 1075-2617
    Keywords: bradykinin ; antagonists ; dehydrophenylalanine ; smooth muscle contraction ; radio-ligand binding studies ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: Continuing the studies on structural requirements of bradykinin antagonists, it has been found that analogues with dehydrophenylalanine (ΔPhe) or its ring-substituted analogues (ΔPhe(X)) at position 5 act as antagonists on guinea pig pulmonary artery, and on guinea pig ileum. Because both organs are considered to be bradykinin B2receptor tissues, the analogues with ΔPhe or ΔPhe(X) at position 5, but without any replacement at position 7, seem to represent a new structural type of B2receptor antagonist. All the analogues investigated act as partial antagonists; they inhibit the bradykinin-induced contraction at low concentrations and act as agonists at higher concentrations. Ring substitutions by methyl groups or iodine reduce both the agonistic and antagonistic activity. Only substitution by fluorine gives a high potency. Incorporation of ΔPhe into different representative antagonists with key modifications at position 7 does not enhance the antagonist activity of the basic structures, with one exception. Only the combination of ΔPhe at position 5 with DPhe at position 7 increases the antagonistic potency on guinea pig ileum by about one order of magnitude. Radio-ligand binding studies indicate the importance of position 5 for the discrimination of B2receptor subtypes. The binding affinity to the low-affinity binding site (KL) was not significantly changed by replacement of Phe by ΔPhe. In contrast, ring-methylation of ΔPhe results in clearly reduced binding to KL. The affinity to the high-affinity binding site (KH) was almost unchanged by the replacement of Phe in position 5 by ΔPhe, whereas the analogue with 2-methyl-dehydrophenylalanine completely failed to detect the KH-site. The peptides were synthesized on the Wang-resin according to the Fmoc/Butstrategy using Mtr protection for the side chain of Arg. The dehydrophenylalanine analogues were prepared by a strategy involving PyBop couplings of the dipeptide unit Fmoc-Gly-ΔPhe(X)-OH to resin-bound fragments. © 1998 European Peptide Society and John Wiley & Sons, Ltd.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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