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  • Title: Lymphocytes from spontaneously hypertensive rats exhibit enhanced adenylyl cyclase-Gi protein signaling.
    Author: Marcil J, Anand-Srivastava MB.
    Journal: Cardiovasc Res; 2001 Jan; 49(1):234-43. PubMed ID: 11121816.
    Abstract:
    OBJECTIVE: We have previously demonstrated an augmented activation of Gialpha proteins in heart and aorta from spontaneously hypertensive rats (SHRs), which was attributed to an enhanced expression of Gialpha proteins. Since immortalized lymphoblasts derived from lymphocytes of hypertensive patients have been shown to have enhanced Gi activation, the present studies were undertaken to investigate if lymphocytes from SHRs also exhibit enhanced Gi activation and whether this activation is related to enhanced expression of Gi proteins. METHODS: The levels of G-proteins and mRNA were determined by immunoblotting and Northern blotting techniques, using specific antibodies and cDNA probes, respectively. Adenylyl cyclase activity stimulated or inhibited by agonists was determined to examine the functions of G-proteins. RESULTS: The levels of Gialpha-2, Gialpha-3, Gbeta but not of Gs(alpha45) and Gs(alpha47) were significantly increased in lymphocytes from SHRs as compared to their control Wistar Kyoto (WKY) rats. Similarly the mRNA levels of Gialpha-2 and Gialpha-3 were significantly augmented in SHRs as compared to their age-matched WKYs. The increased levels of Gialpha were reflected in increased functions of Gi in SHRs as indicated by increased inhibition of forskolin-stimulated adenylyl cyclase activity by GTPgammaS. The activity of adenylyl cyclase stimulated by GTPgammaS, isoproterenol, NECA, NaF and forskolin was significantly decreased in SHRs as compared to their age-matched WKY rats. On the other hand, inhibitory hormones, atrial natriuretic peptide and angiotensin II inhibited adenylyl cyclase activity to a greater extent in SHRs as compared to their age-matched WKY rats. CONCLUSIONS: These results indicate that lymphocytes from spontaneously hypertensive rats exhibit enhanced Gi activation (function) which may be attributed to the enhanced expression of Gi proteins. It may be suggested that enhanced Gi expression and associated signaling may be one of the factors responsible for enhanced lymphoblasts proliferation observed in hypertension.
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