Modulation of protein kinase C by adenosine: Involvement of adenosine A1 receptor-pertussis toxin sensitive nucleotide binding protein system

1995 ◽  
Vol 149-150 (1) ◽  
pp. 51-58 ◽  
Author(s):  
Ravi B. Marala ◽  
S. Jamal Mustafa
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Pertussis Toxin ◽  
Binding Protein ◽  
Nucleotide Binding ◽  
Adenosine A1 Receptor ◽  
Protein System ◽  
Kinase C ◽  
Adenosine A1 ◽  
A1 Receptor

Adenosine A1 receptor-induced upregulation of protein kinase C: role of pertussis toxin-sensitive G protein(s)

1995 ◽  
Vol 269 (5) ◽  
pp. H1619-H1624 ◽  
Author(s):  
R. B. Marala ◽  
S. J. Mustafa
Keyword(s):  
Protein Kinase C ◽  
Coronary Artery ◽  
Protein Kinase ◽  
G Protein ◽  
Pertussis Toxin ◽  
Protein S ◽  
Porcine Coronary Artery ◽  
Kinase C ◽  
Adenosine A1 ◽  
A1 Receptor

Biochemical and pharmacological studies have established that adenosine modulates protein kinase C (PKC), which plays an important role in the maintenance of vascular tone. Our earlier studies [Marala and Mustafa. Am. J. Physiol. 268 (Heart Circ. Physiol. 37): H271-H277, 1995. Marala, R. B., K. Ways, and S. J. Mustafa. Am. J. Physiol. 264 (Heart Circ. Physiol. 33): H1465-H1471, 1993] have shown the involvement of adenosine A1 receptors and not the A2 receptors in the upregulation of PKC in porcine coronary artery. The mechanism(s) by which adenosine upregulates PKC is not yet clearly understood. We now report the increased expression of PKC by adenosine A1 receptor through an upstream activation of pertussis toxin-sensitive G protein(s). Incubation of porcine coronary artery for 24 h with a relatively specific A1-receptor agonist (2S)-N6-(2-endo-norbornyl)adenosine (ENBA) elevated the contractile responses to endothelin-1 by about twofold, probably due to an increased expression of PKC. Incubation of porcine coronary artery with ENBA also protected against the phorbol 12,13-dibutyrate (PDBu)-induced depletion of PKC. Inclusion of pertussis toxin in the incubation medium completely blocked both the upregulatory and the protective effects of ENBA. Incubation with pertussis toxin did not alter the PKC activity as judged by the contractile responses to PDBu. On the contrary, incubation of porcine coronary artery with cholera toxin for 24 h did not alter any of the ENBA responses (upregulation of PKC and the protection against PDBu-induced PKC depletion). Incubation conditions of coronary arteries with toxins are sufficient to cause ADP ribosylation of respective G proteins as judged by back ADP ribosylation studies.(ABSTRACT TRUNCATED AT 250 WORDS)

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