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  • 2015-2019
  • 1985-1989  (1)
  • 1975-1979  (3)
  • 1960-1964
  • 1915-1919
  • 1900-1904
  • 1830-1839
  • Isoprenaline
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 303 (1978), S. 139-144 
    ISSN: 1432-1912
    Keywords: α-Adrenoceptors ; Renin ; Isoprenaline ; Tyramine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of the indirect sympathomimetic agent tyramine on the isoprenaline-induced increase in plasma renin concentration was investigated in conscious rats. Tyramine caused a dose-dependent decrease in the isoprenaline-induced elevation of plasma renin concentration. Pretreatment of the rats with reserpine abolished this effect of tyramine, indicating that tyramine released catecholamines which acted on the inhibitory adrenoceptors. Pretreatment with phenoxybenzamine, an α-adrenoceptor antagonist, also abolished the inhibitory effect of tyramine on renin release, indicating that α-adrenoceptors mediated the observed inhibition of renin release. In rats with chronically denervated kidneys tyramine did not inhibit renin release. It is concluded that catecholamines which are released from renal sympathetic nerve endings can suppress renin release by activating α-adrenoceptors.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1912
    Keywords: α-Adrenoceptors ; Isoprenaline ; Renin ; Sympathetic nervous system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The importance of the sympatho-adrenal system for the isoprenaline-induced increase in plasma renin concentration was investigated in conscious rats. Ganglionic blockade by trimethidinium (10 mg kg−1) increased the dose-dependent elevation of plasma renin concentration induced by isoprenaline (0.03–0.48 μg kg−1 min−1). Also treatment of the rats with guanethidine (6 mg kg−1) or reserpine (2.5 mg kg−1, given 16 and 7 h prior to the experiments) further increased the effect of isoprenaline (0.5 μg kg−1 min−1) on plasma renin concentration. Unilateral renal denervation combined with contralateral nephrectomy doubled the effect of the β-sympathomimetic amine on renin release. The α-adrenoceptor antagonist phenoxybenzamine (3 mg kg−1) also enhanced the effect of isoprenaline on this parameter. It is concluded that apart from a stimulation of renin release via β-adrenoceptors the sympathetic nervous system may inhibit renin release via stimulation of α-adrenoceptors.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1912
    Keywords: Adenosine ; (−)-N6-phenylisopropyladenosine ; Ca2+ channels ; Bay K 8644 ; Isoprenaline ; Amrinone ; Heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of the present study was to characterize the positive inotropic effect of the Ca2+ channel activator Bay K 8644. In isolated guinea-pig papillary muscles we investigated whether adenosine and the R site adenosine receptor agonist (−)-N6-phenylisopropyladenosine (PIA) were able to antagonize the positive inotropic effect of Bay K 8644. The effect of Bay K 8644 and adenosine or PIA on myocardial cAMP content was also measured. The influence of adenosine and PIA on the positive inotropic effect of the β-adrenoceptor agonist isoprenaline and of the phosphodiesterase inhibitor amrinone was studied for comparison. Adenosine and PIA antagonized the positive inotropic effects of isoprenaline and amrinone in a concentration-dependent manner. In contrast, adenosine or PIA did not affect the positive inotropic effect of Bay K 8644. The positive inotropic effect of Bay K 8644 was not accompanied by a change in the cAMP content of the papillary muscles. Additionally applied adenosine or PIA also failed to affect the cAMP content. It is concluded that an increased myocardial cAMP content is not involved in the positive inotropic effect of Bay K 8644. Moreover, the results support the view that adenosine and PIA only antagonize the positive inotropic effects of drugs known to increase myocardial cAMP content and that an increased myocardial cAMP content is a prerequisite for the manifestation of a negative inotropic effect of the nucleosides in ventricular cardiac muscle.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 290 (1975), S. 315-321 
    ISSN: 1432-1912
    Keywords: Isoprenaline ; Renin ; Vasoconstrictors ; Macula densa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism of the increase in plasma renin concentration caused by the β-sympathomimetic agent isoprenaline has been further investigated. Rats were pretreated by occluding the left renal artery for 2 hrs, thus rendering the macula densa cells of this kidney nonfunctioning. After contralateral nephrectomy infusion of isoprenaline (1.5 μg/kg min) still caused a strong increase in plasma renin concentration. This increase was significantly suppressed by simultaneous infusion of angiotensin II (1.0 μg/kg min), the α-sympathomimetic amine phenylephrine (60 μg/kg min) or octapressin (10 mU/kg min). The results exclude any mediator-role of the macula densa receptors in the isoprenaline-induced release of renin. The possibility of a stimulation of renin release via the baroreceptors or a direct “secretomotoric” action of isoprenaline is discussed.
    Type of Medium: Electronic Resource
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