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  • 1
    Electronic Resource
    Electronic Resource
    Defective ANF-R2/ANP-C receptor-mediated signalling in hypertension (1995)
    Springer
    Molecular and cellular biochemistry 149-150 (1995), S. 223-231 
    Details
    ISSN: 1573-4919
    Keywords: G-proteins ; adenylyl cyclase ; ANF receptors ; hypertensive rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract In the present studies we have shown that atrial natriuretic factor (peptide) receptor of ANF-R2/ANP-C type is coupled to adenylyl cyclase/cAMP signal transduction system through Gi-regulatory protein and is implicated in mediating some of the physiological responses of atrial natriuretic factor or peptide (ANP). ANF-R2/ANP-C receptor-mediated adenylyl cyclase inhibition was altered in hypertension. This alteration was tissue specific. In heart, aorta, brain and adrenal, the extent of inhibition of adenylyl cyclase by ANP was enhanced in SHR as compared to age-matched WKY, whereas in platelets, the ANP-mediated inhibition was completely attenuated. The enhanced inhibition of adenylyl cyclase by ANP was also observed in heart and aorta from DOCA-salt hypertensive rats. In addition, the augmented inhibition of adenylyl cyclase by ANP was observed in 2 weeks and older ANP but not in 3–5 days old SHR. Similarly, in DOCA-salt hypertensive rats, the enhanced inhibition of adenylyl cyclase by ANP was observed after 2 weeks of DOCA-salt treatment when the blood pressure was also enhanced, however one week of DOCA-salt treatment did not result in an augmented blood pressure and augmented ANP-mediated inhibition of adenylyl cyclase, suggesting that blood pressure increase may be responsible for the enhanced responsiveness of ANP to adenylyl cyclase inhibition. However, in genetic model of hypertension, the increased inhibition of adenylyl cyclase by ANP at 2 weeks of age (when the blood pressure is normal) may be implicated in the pathogenesis of hypertension. The augmented inhibition of adenylyl cyclase in cardiovascular tissues from SHR and DOCA-salt hypertensive rats may be due to the upregulation of ANF-R2/ANP-C receptors or due to the amplification of post-receptor signalling mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01076581
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Differential regulation of G-protein expression by vasoactive peptides (1997)
    Springer
    Molecular and cellular biochemistry 176 (1997), S. 21-27 
    Details
    ISSN: 1573-4919
    Keywords: atrial natriuretic peptide ; angiotensin II ; G-proteins ; adenylyl cyclase ; vascular smooth muscle cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Vasoactive peptides such as angiotensin II (AII), atrial natriuretic peptide (ANP) and vasopressin play an important role in the regulation of blood pressure. We have recently shown an augmentation of Giα levels in heart and aorta from genetic and experimentally-induced hypertensive rats, which may be attributed to the increased levels of vasoactive peptides. We have therefore investigated the effect of AII and ANP on the expression of G-proteins (Giα and Gsα) in cultured vascular smooth muscle cells (VSMC) and their relationship with adenylyl cyclase activity. Exposure of VSMC with AII resulted in the augmentation of the levels of Giα-2 and Giα-3 proteins and Giα-2 and Giα-3 mRNA and not of Gsα as determined by immunoblotting and Northern blotting techniques respectively. However, the stimulatory effects of N-ethylcarboxamide adenosine (NECA) and isoproterenol on adenylyl cyclase was diminished by AII treatment, whereas the inhibitory effects of AII and C-ANP4-23 were completely attenuated. On the other hand, pretreatment of the cells with C-ANP4-23 resulted in the reduction of the levels of Giα-2 and Giα-3 and not of Gsα. The inhibitory responses of adenylyl cyclase to C-ANP4-23 and AII were also attenuated and the stimulatory effects of GTPgS and other agonists were significantly augmented. These data indicate that AII and ANP modulate the expression of Gia protein in a different manner. It may be suggested that the enhanced levels of Giα protein observed in hypertension may be attributed to the augmented levels of AII and not to ANP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006810508860
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    G-protein and Membrane Signaling in Cardiovascular Disease (1997)
    Springer
    Heart failure reviews 2 (1997), S. 85-94 
    Details
    ISSN: 1573-7322
    Keywords: G-proteins ; adenylyl cyclase ; hypertension ; hypertrophy ; cardiovascular system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Guanine nucleotide regulatory proteins (G-proteins) play a key role in the regulation of various signal transduction systems, which are implicated in the modulation of a variety of physiological functions such as platelet functions, including platelet aggregation, secretion, and clot formation, and cardiovascular functions, including arterial tone and reactivity. Several abnormalities in adenylyl cyclase activity, cAMP levels, and G-protein levels have shown to be responsible for the altered cardiac performance and vascular functions observed in cardiovascular disease states. The enhanced or unaltered levels of inhibitory G-proteins(Giα-2 and Giα-3) and mRNA have been reported in different models of hypertension, whereas Gsα levels were shown to be unaltered. These changes in G-protein were associated with functions. The enhanced levels of Giα proteins precede the development of blood pressure and suggest that over expression of Gi proteins may be one of the contributing factors for the pathogenesis of hypertension. On the other hand, the levels of Gsα and not of Giα proteins were decreased in volume- or pressure-overload hypertrophy. The responsiveness of adenylyl cyclase to β-adrenergic agonists was also attenuated. Similarly, is chemia was shown to be associated with decreased, increased,or unaltered levels of Gsα, with decreased levels of Giα, and with decreased responsiveness of adenylyl cyclase to various stimuli such as β-adrenergic agonists, guanine nucleotides, forskolin, etc. Thus,the altered levels of G-proteins and cAMP levels may be responsible for the impaired cardiovascular functions observed in hypertension, hypertrophy,and cardiac failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009767810044
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    G-proteins and adenylyl cyclase signalling in hypertension (1996)
    Springer
    Molecular and cellular biochemistry 157 (1996), S. 163-170 
    Details
    ISSN: 1573-4919
    Keywords: G-proteins ; adenylyl cyclase ; heart ; aorta ; spontaneously hypertensive rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The present studies were undertaken to examine if adenylyl cyclase activity and the levels of G-proteins (Gsα and Giα) are altered in cardiovascular tissues in hypertension. Adenylyl cyclase activity and its responsiveness to stimulatory and inhibitory hormones as well as the expression of G-proteins (Gs and Gi) were determined at protein and mRNA levels by using specific antibodies and cDNA probes in hearts and aorta from 12 week old spontaneously hypertensive rats (SHR) and their age-matched control Wistar Kyoto (WKY) rats. The stimulatory effects of guanine nucleotides, isoproterenol, glucagon etc. on adenylyl cyclase activity were decreased in SHR rats as compared to the WKY rats, whereas, the inhibitory hormones inhibited enzyme activity to a grater extent in SHR rats as compared to WKY rats. Furthermore, the levels of Giα-2 and Giα-3 proteins and Giα-2 and Giα-3 mRNA as determined by immunoblotting and Northern blotting techniques respectively were higher in SHR as compared to WKY rats. However, the levels of Gsa were unaltered in SHR. To further investigate if these alterations are the cause or effect of hypertension, the SHRs at various ages of the development of blood pressure (3–5 days, 2, 4 and 8 weeks) and their age-matched WKY were used for G-protein expression and adenylyl cyclase activity. The increased expression of Giα−2 and Giα−3 protein and mRNA levels in hearts and aorta were observed as early as in 2-weeks old SHR as compared to WKY, when the blood pressure was still normal. However, the levels of Gsα in SHR were not different from WKY rats. In addition, the altered responsiveness of adenylyl cyclase to hormone stimulation and inhibition was also observed as early as in 2 week old SHR. These results suggest that the increased expression of Giα−2 and Giα−3 and decreased levels of cAMP precedes the development of blood pressure and may be one of the contributing factors in the pathogenesis of hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00227895
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    Paper (German National Licenses)
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