Abstract
Adenosine analogs selective for the A 1 subclass of adenosine receptors, such as N 6-cyclohexyladenosine (CHA), inhibit renin secretion in vitro preparations. Ca chelation blocks the inhibitory effect, consistent with mediation by increased intracellular free Ca 2+, and it has been suggested that intracellular Ca 2+ could increase as a result of receptor-induced inhibition of adenylate cyclase followed by decreased Ca efflux from the renin-secreting cells. Pertussis toxin blocks receptor-induced inhibition of adenylate cyclase in many cells, and in others, it blocks receptor-induced phosphotidylinositol response. In the present studies, pertussis toxin treatment stimulated the basal renin secretory rate of rat renal cortical slices and blocked the inhibitory effect of CHA but not the inhibitory effect of K-depolarization. These data support the hypothesis that a pertussis toxin substrate, such as N i, is involved in CHA-, but not in K-depolarization, -induced inhibition of renin secretion.
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