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  • 1
    ISSN: 1432-1912
    Schlagwort(e): α-Adrenoceptors ; Isoprenaline ; Renin ; Sympathetic nervous system
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 303 (1978), S. 139-144 
    ISSN: 1432-1912
    Schlagwort(e): α-Adrenoceptors ; Renin ; Isoprenaline ; Tyramine
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 290 (1975), S. 315-321 
    ISSN: 1432-1912
    Schlagwort(e): Isoprenaline ; Renin ; Vasoconstrictors ; Macula densa
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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