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  • 1
    Electronic Resource
    Electronic Resource
    Different responses of the isolated canine coronary artery superfused with blood or Krebs-Henseleit solution (1984)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 327 (1984), S. 156-158 
    Details
    ISSN: 1432-1912
    Keywords: Canine coronary artery ; Superfusion media ; Nifedipine ; Ca2+-channels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Responses of ring segments of the isolated canine coronary artery superfused with arterial blood from a donor dog were compared with responses of segments superfused with Krebs-Henseleit (K-H) solution. KCl (1–30 mg) caused contraction in a dose-dependent manner both in K-H solution- and in blood-superfused preparation. However, CaCl2 (1–100 mg) and nifedipine (0.1–30 μg) contracted and relaxed, respectively, only blood-superfused preparation but not K-H solution-superfused one. These results show that even in the same region of the coronary artery, different superfusates result in different responses to contracting or relaxing agents. This difference may be explained by the idea that Ca2+-channels are activated and endow basal tension in blood-superfused preparations, but not in K-H solution-superfused ones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500911
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of α- and β-sympathomimetic agonists on calcium-dependent slow action potential and force of contraction in the rabbit papillary muscle (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 318 (1982), S. 330-335 
    Details
    ISSN: 1432-1912
    Keywords: Rabbit papillary muscle ; Ca2+-dependent action potential ; α- + β-Adrenoceptors ; Positive inotropic effect
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of sympathomimetic α- and β-agonists on calcium-dependent slow action potential (SAP) and force of contraction were analyzed in the partially depolarized rabbit papillary muscle. 1. The effects of phenylephrine (3×10−6 mol/l) on SAP were compared with those of isoprenaline (5×10−8 mol/l) since the contractions that could be elicited at these concentrations were of similar amplitude. The maximum rate of rise (V max) of the slow action potential, which was taken to reflect the slow calcium inward current (Isi), was evidently smaller when elicited by phenylephrine than by isoprenaline. 2. V max of SAP induced by phenylephrine (3×10−6 mol/l) or isoprenaline (5×10−8 mol/l) was significantly increased in either case by additional application of isoprenaline. The positive inotropic effect induced by additional isoprenaline was associated with an increase in the rate of force development. 3. V max of SAP evoked by isoprenaline (5×10−8 mol/l) remained unchanged by additional application of phenylephrine (3×10−6 mol/l) whereas the duration of SAP was significantly prolonged. Additional phenylephrine markedly increased the time to peak force but left the rate of force development unchanged. These effects of phenylephrine on slow action potential and force of contraction were completely blocked by prazosin (10−8 mol/l). 4. The duration of SAP induced by dopamine was shortened by prazosin (10−8 mol/l) without alteration of V max, whereas force of contraction was reduced. 5. For further analysis of the mechanisms responsible for the prolongation of SAP by the α-mimetic effect of phenylephrine, additional experiments have been performed. In normal Tyrode solution containing MnCl2 (10 mmol/l), phenylephrine (3×10−6 mol/l) prolonged the duration of action potential without reestablishing force development. Prazosin (10−8 mol/l) completely antagonized this effect of phenylephrine. 6. These findings indicate that an increase in the slow calcium inward current induced by α-stimulation is much smaller than that induced by β-stimulation. The prolongation of the action potential evoked by α-stimulation seems to be induced by a suppression of the time-dependent outward current. This current may play an important role in the α-adrenoceptor-mediated positive inotropic effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501173
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  • 3
    Electronic Resource
    Electronic Resource
    Alpha-adrenoceptor-mediated restoration of calcium-dependent potential in the partially depolarized rabbit papillary muscle (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 301 (1978), S. 201-205 
    Details
    ISSN: 1432-1912
    Keywords: Phenylephrine ; α-Adrenoceptor ; Ca2+-dependent action potential ; Rabbit papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Electrophysiological and mechanical effects of phenylephrine were observed in the rabbit papillary muscle which was depolarized and rendered inexcitable by an elevation of potassium concentration to 27 mM in the presence of a β-adrenoceptor blocking drug, bufetolol (10−6 M). 1. Phenylephrine (10−6 to 10−4 M) restored the action potential and tension development. The amplitude, duration and maximum rate of rise of the action potential, and developed tension were augmented by an increase in the concentration of phenylephrine. 2. The amplitude of the action potential restored by phenylephrine was very sensitive to the Ca2+ concentration and increased by 29.2 mV/10-fold increase crease in external Ca2+ concentration. Nifedipine (10−6 M), a Ca2+ antagonist, completely suppressed the electrical and mechanical responses restored by phenylephrine (10−5 M), but tetrodotoxin (10−5 M) had little effect on these responses. 3. Phentolamine (10−6 M) suppressed both the action potential and developed tension restored by phenylephrine (10−5 M), but the elevation of the concentration of bufetolol from 10−6 M to 3×10−6 M was ineffective against these responses. In conclusion, the restoration by phenylephrine of Ca2+-dependent action potential may be ascribed to an enhancement of the inward Ca2+ current, mediated by α-adrenoceptors and this mechanism may play an important role in the α-adrenoceptor-mediated positive inotropic effect.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00507038
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  • 4
    Electronic Resource
    Electronic Resource
    Multiple effects of α-adrenoceptor stimulation on the action potential of the rabbit atrium (1984)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 325 (1984), S. 47-53 
    Details
    ISSN: 1432-1912
    Keywords: α-Adrenoceptors ; Phenylephrine ; Action potential ; Rabbit atrium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of α-adrenoceptor stimulation by phenylephrine (10−7–10−4 mol/l) in the presence of pindolol (10−7 mol/l) on the action potential and force of contraction were observed in the rabbit left atrium. 1. Phenylephrine reduced resting potential, prolonged action potential duration (APD), decreased maximum rate of rise of action potential ( $$\dot V_{{\text{max}}}$$ ) and increased force of contraction in a concentration-dependent manner. 2. Effects of phenylephrine (10−5 mol/l) were antagonized by prazosin (10−7 mol/l) or phentolamine (10−6 mol/l). 3. APD which had been prolonged by phenylephrine (10−5 mol/l) was slightly shortened by Ni2+ (0.3 mmol/l) at the level of 50% repolarization but almost unaffected at the level of 90% repolarization. TTX (10−6 mol/l) had no effect on ADP which had been prolonged by phenylephrine (10−5 mol/l). 4. Cs+ (10 mmol/l), which inhibits outward current i k 1, depolarized resting potential, but in contrast with phenylephrine Cs+ did not affect APD at 90% repolarization. 5. Phenylephrine (10−5 or 3×10−5 mol/l) restored Ca2+-dependent action potential and force of contraction in 20 mmol/l K+-Tyrode solution. These responses were suppressed by prazosin (10−7 mol/l) or Ni2+ (0.3 mmol/l). 6. Phenylephrine (10−5 or 10−4 mol/l) had no effect on steady-state membrane potential — $$\dot V_{{\text{max}}}$$ relationship. It is concluded that in the rabbit left atrium phenylephrine, via α-adrenoceptors may suppress outward currents perhaps i k 1 and i x, and might increase slow inward current.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00507053
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of acetylcholine on calcium-dependent electrical and mechanical responses in the guinea-pig papillary muscle partially depolarized by potassium (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 299 (1977), S. 1-7 
    Details
    ISSN: 1432-1912
    Keywords: Acetylcholine ; Ca2+-dependent action potential ; Isoproterenol ; Theophylline ; Gumea-pig papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of acetylcholine (ACh) on the Ca2+-dependent electrical and mechanical response restored by isoproterenol (10−8 M), theophylline (3 mM) or excess Ca2+ (7.2 mM) were investigated in the guinea-pig papillary muscle which was partially depolarized and rendered inexcitable by potassium (27 mM), and were compared with effects of nifedipine, a Ca2+ antagonist. Isoproterenol, theophylline and excess Ca2+ restored the Ca2+-dependent action potential and tension development. ACh at concentrations of 10−6–10−4 M decreased the maximum rate of rise of the action potential restored by isoproterenol or theophylline, but ACh (10−8–10−4 M) had no significant effect on the maximum rate of rise of the action potential restored by excess Ca2+. The actions of ACh on electrial and mechanical responses restored by isoproterenol or theophylline were increased by physostigmine (10−7 M) and were antagonized by atropine (10−7 M) but not by hexamethonium (3×10−4 M). Nifedipine (10−6M) significantly suppressed the maximum rate of rise of the action potential and tension development restored by isoproterenol, theophylline or excess Ca2+. It is concluded that ACh acting via muscarinic receptors suppresses the Ca2+-dependent action potential, that was previously restored by isoproterenol or theophylline, by an increase in calcium conductance (g Ca), which, in turn, may be due to an elevation of the level of cellular cAMP. However, ACh does not affect the action potential restored by excess Ca2+ which probably acts by an increase in the driving force for Ca2+. This mode of action of ACh is different from that of a Ca2+ antagonist, nifedipine. The antagonistic effect of ACh to positive inotropic effects induced by isoproterenol or theophylline may be attributed to this mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508630
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  • 6
    Electronic Resource
    Electronic Resource
    Restoration by histamine of the calcium-dependent electrical and mechanical response in the guinea-pig papillary muscle partially depolarized by potassium (1976)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 294 (1976), S. 261-269 
    Details
    ISSN: 1432-1912
    Keywords: Histamine ; Ca2+-dependent action potential ; H2-receptor ; cAMP ; Guinea-pig papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Electrophysiological and mechanical effects of histamine were observed in guinea-pig papillary muscle which had been depolarized and rendered inexcitable by elevation of potassium concentration in Tyrode solution to 27 mM. 1. Histamine (3×10−7 to 3×10−5 M) restored the action potential and tension development. The amplitude of the action potential was increased by 31.6 mV/10-fold increase in extracellular Ca2+ concentration. Nifedipine (10−6 M) abolished the electrical and mechanical responses which had been restored by histamine (10−5 M) but TTX (10−5 M) did not affect them. Reduction of the extracellular Na+ concentration to one half decreased the amplitude and the maximum rate of rise of the action potential restored by histamine (10−5 M) while the peak tension was increased and an after-contraction occurred. 2. The maximum rate of rise and the amplitude of the action potential restored by histamine (10−5 M) decreased with increase in stimulus frequency from 0.1–1.6 Hz. The peak tension decreased and then increased. The shape of the developed tension was also changed. In the presence of caffeine (1 mM), the only effect of an increase in stimulus frequency was a decrease in peak tension but the change in the shape of developed tension did not occur. 3. The electrical and mechanical responses restored by histamine (3×10−6 or 10−5 M) were depressed by metiamide (3×10−6 M) but not by diphenhydramine (10−5 M) or bufetolol (10−6 M). 4. The electrical response restored by histamine (10−6 or 10−5 M) was enhanced by papaverine (10−5 M) and depressed by N-methylimidazole (10 mM). It is concluded that histamine may enhance the slow inward Ca2+ current mediated by histamine H2-receptors and the adenylate cyclase system in ventricular muscle and that the positive inotropic action of histamine may be attributed to these mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508394
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  • 7
    Electronic Resource
    Electronic Resource
    Influence of acetycholine on the positive inotropic effect evoked by α- or β-adrenoceptor stimulation in the rabbit heart (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 320 (1982), S. 152-159 
    Details
    ISSN: 1432-1912
    Keywords: α- and β-Adrenoceptors ; Positive inotropic effect ; Acetylcholine ; Accentuated antagonism ; Rabbit papillary muscle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of acetylcholine (ACh) on the positive inotropic responses to α- as well as β-adrenoceptor stimulation was investigated in the isolated electrically driven rabbit ventricular muscle. 1. Stimulation of muscarinic receptors by ACh (10−9–10−4 mol/l) reduced the positive inotropic effect evoked by isoprenaline (10−8 mol/l) via β-adrenoceptor stimulation, but enhanced the positive inotropic effect of the α-adrenoceptor stimulating agent phenylephrine (10−6 mol/l) in the presence of pindolol (3×10−8 mol/l). 2. Sodium nitroprusside (SNP) (10−6–10−3 mol/l) reduced the β-adrenoceptor-mediated positive inotropic effect but did not effect the α-adrenoceptor-mediated one. 3. The depression by ACh (10−6 mol/l) or SNP (10−4 mol/l) of the positive inotropic effects evoked by β-adrenoceptor stimulation was accompanied by a decrease of the cAMP level which has been elevated by isoprenaline. However, the enhancement of the α-adrenoceptor mediated positive inotropic effect by ACh seems to be independent of changes in cAMP- and/or cGMP-levels. 4. ACh (10−6 mol/l) diminished the shortening of the action potential duration induced by isoprenaline (10−8 mol/l) in Tyrode solution and Ca2+-dependent potential restored by β-adrenoceptor stimulation in 27 mmol/l K+ Tyrode solution. In contrast, ACh (10−6 mol/l) affected neither the prolongation of action potential duration nor the Ca2+-dependent potential caused by α-adrenoceptor stimulation. The depression by acetylcholine of the β-adrenoceptor mediated positive inotropic effect may be due to the decrease in cAMP content and to the reduction of the slow inward current while the enhancement by ACh of the α-adrenoceptor mediated positive inotropic effect is not associated with changes in cAMP- and/or cGMP-levels and in electrophysiological phenomena. It is concluded that the accentuated antagonism (Levy 1971) between sympathomimetic and parasympathomimetic agents at the postsynaptic region results mainly from the interaction between β-adrenoceptor- and muscarinic receptor-mediated responses, and that the α-adrenoceptor-mediated responses are able to counteract the accentuated antagonism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00506315
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