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Adrenergic Receptors

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Ruth H. Strasser – One of the best experts on this subject based on the ideXlab platform.

  • Regulation of β-Adrenergic Receptors in acute myocardial ischemia: subtype-selective increase of mRNA specific for β1-Adrenergic Receptors
    Journal of molecular and cellular cardiology, 1995
    Co-Authors: Renate Ihl-vahl, R. Marquetant, J. Bremerich, Ruth H. Strasser
    Abstract:

    Acute myocardial ischemia leads to a rapid increase of cardiac β-Adrenergic Receptors in plasma membranes despite the release of large and desensitizing amounts of endogenous catecholamines. Part of this increase has been shown to occur at the expense of intracellular Receptors. To investigate whether an additional expressional regulation of β-Adrenergic Receptors due to an increase of mRNA levels is involved, the mRNA levels specific for β 1 – and β 2 –Adrenergic Receptors were determined after various periods of global ischemia in isolated perfused rat hearts. The subtype-specific quantification of mRNA for β 1 – and β 2 –Adrenergic Receptors was determined using reverse-transcription followed by PCR (RT-PCR) and RNA protection assays. RT-PCR resulted in single amplification products of the expected sizes (159 by for β 1 –Adrenergic Receptors and 240 by for β 2 –Adrenergic Receptors). The specificity of these amplification products was confirmed by specific restriction digests, Southern blot hybridizations with internal oligonucleotides and sequencing using the dideoxy chain termination method. For quantification purposes, the mRNAs of housekeeping gene GAPDH and of cardiac α-actin were determined as internal standards. Additionally, cRNAs specific for β 1 – and β 2 –Adrenergic Receptors were used as external standards. Brief periods of global ischemia induced a rapid increase in the steady state level of mRNA for β 1 –Adrenergic Receptors. There was a statistically significant rise already after 15 min by 57% compared to controls. After 30 min of ischemia the mRNA levels had almost doubled. After 60 min of ischemia, the mRNA levels specific for β 1 –Adrenergic Receptors tended to decrease, but remained significantly above normoxic controls. In contrast, the mRNA levels specific for β 2 –Adrenergic Receptors remained constant up to 60 min of global myocardial ischemia. To investigate, whether agonist occupancy of the Receptors may contribute to this regulation, the effect of preperfusion with the β-blocker alprenolol was determined. Contrary to expectation, β-blockade did not influence the ischemia-induced increase of mRNA levels specific for β 1 –Adrenergic Receptors. These data demonstrate for the first time, that acute myocardial ischemia induces a rapid, and subtype-selective regulation of mRNA levels for β 1 –Adrenergic Receptors. However, occupation or activation of β-Adrenergic Receptors by an agonist is not involved in this newly characterized regulation of mRNA for β 1 –Adrenergic Receptors in acute myocardial ischemia.

Peter J Rice – One of the best experts on this subject based on the ideXlab platform.

  • Relaxation of isolated human myometrial muscle by β2 –Adrenergic Receptors but not β1 –Adrenergic Receptors
    American Journal of Obstetrics and Gynecology, 1998
    Co-Authors: Uchenna C. Nwosu, Peter J Rice
    Abstract:

    Abstract Objective: Human myometrium contains both β 1 –Adrenergic and β 2 –Adrenergic Receptors. This study was designed to assess the importance of each β-Adrenergic receptor subtype in relaxation of human myometrial muscle strips. Study Design: Radioligand binding studies were used to establish the presence of each β-Adrenergic receptor subtype, whereas highly selective β 1 -antagonists and β 2 -antagonists were used to assess the contribution of β-Adrenergic receptor subtypes to myometrial relaxation after exposure to (–)–isoproterenol. Results: Membranes prepared from myometrium contained 82% ± 4% β 2 –Adrenergic Receptors. After contraction produced by exposure to potassium chloride (35 mmol/L), isoproterenol produced relaxation with half maximal effect at 0.02 μmol/L and a maximal relaxation of 52% ± 3%. β 1 -Antagonist CGP-20712A had no significant effect, whereas β 2 -antagonist ICI-118551 produced a characteristic rightward shift of the isoproterenol concentration-relaxation relationship. Conclusions: Although both β 1 –Adrenergic Receptors and β 2 –Adrenergic Receptors are present in human myometrial tissue at term, relaxation by nonselective β-agonist isoproterenol is mediated exclusively by β 2 –Adrenergic Receptors. (Am J Obstet Gynecol 1998;179:895-8.)

Renate Ihl-vahl – One of the best experts on this subject based on the ideXlab platform.

  • Regulation of β-Adrenergic Receptors in acute myocardial ischemia: subtype-selective increase of mRNA specific for β1-Adrenergic Receptors
    Journal of molecular and cellular cardiology, 1995
    Co-Authors: Renate Ihl-vahl, R. Marquetant, J. Bremerich, Ruth H. Strasser
    Abstract:

    Acute myocardial ischemia leads to a rapid increase of cardiac β-Adrenergic Receptors in plasma membranes despite the release of large and desensitizing amounts of endogenous catecholamines. Part of this increase has been shown to occur at the expense of intracellular Receptors. To investigate whether an additional expressional regulation of β-Adrenergic Receptors due to an increase of mRNA levels is involved, the mRNA levels specific for β 1 – and β 2 –Adrenergic Receptors were determined after various periods of global ischemia in isolated perfused rat hearts. The subtype-specific quantification of mRNA for β 1 – and β 2 –Adrenergic Receptors was determined using reverse-transcription followed by PCR (RT-PCR) and RNA protection assays. RT-PCR resulted in single amplification products of the expected sizes (159 by for β 1 –Adrenergic Receptors and 240 by for β 2 –Adrenergic Receptors). The specificity of these amplification products was confirmed by specific restriction digests, Southern blot hybridizations with internal oligonucleotides and sequencing using the dideoxy chain termination method. For quantification purposes, the mRNAs of housekeeping gene GAPDH and of cardiac α-actin were determined as internal standards. Additionally, cRNAs specific for β 1 – and β 2 –Adrenergic Receptors were used as external standards. Brief periods of global ischemia induced a rapid increase in the steady state level of mRNA for β 1 –Adrenergic Receptors. There was a statistically significant rise already after 15 min by 57% compared to controls. After 30 min of ischemia the mRNA levels had almost doubled. After 60 min of ischemia, the mRNA levels specific for β 1 –Adrenergic Receptors tended to decrease, but remained significantly above normoxic controls. In contrast, the mRNA levels specific for β 2 –Adrenergic Receptors remained constant up to 60 min of global myocardial ischemia. To investigate, whether agonist occupancy of the Receptors may contribute to this regulation, the effect of preperfusion with the β-blocker alprenolol was determined. Contrary to expectation, β-blockade did not influence the ischemia-induced increase of mRNA levels specific for β 1 –Adrenergic Receptors. These data demonstrate for the first time, that acute myocardial ischemia induces a rapid, and subtype-selective regulation of mRNA levels for β 1 –Adrenergic Receptors. However, occupation or activation of β-Adrenergic Receptors by an agonist is not involved in this newly characterized regulation of mRNA for β 1 –Adrenergic Receptors in acute myocardial ischemia.

Kenneth E White – One of the best experts on this subject based on the ideXlab platform.

Martin J Lohse – One of the best experts on this subject based on the ideXlab platform.