EFFECTS OF ADENOSINE AND ANGIOTENSIN ON MACULA DENSA-STIMULATED RENINSECRETION

The present studies were performed to assess, in the isolated perfused juxtaglomerular apparatus of the rabbit kidney, the effect of exogeno us adenosine on renin secretion stimulated by a low NaCl concentration at the macula densa. Addition of adenosine to the bath resulted in a change of renin secretion from 30.4 to 23.9 nGU/min at an adenosine co ncentration of 10(-6) M (n = 7; P = NS), from 38.6 to 17.9 nGU/min at a concentration of 10(-4) M (n = 7; P = 0.038), and from 18.4 to 5.8 n GU/min at 10(-2) M (P = 0.0053). Addition of the Al receptor antagonis t 8-cyclopentyl-1,3-dipropylxanthine at 10(-5) M fully reversed the ef fect of adenosine at 10(-4) M, but not at 10(-2) M. Inhibition of aden osine breakdown by the adenosine deaminase inhibitor pentostatin (10(- 6) M) enhanced the inhibitory effect of adenosine with renin secretion falling from 61.7 to 19.5 nGU/min at 10(-6) M adenosine (P = 0.035) a nd from 44.7 to 13.5 nGU/min at 10(-4) M adenosine (n = 0.027). A mark ed inhibition of NaCl-dependent renin secretion was caused by both ang iotensin II (P = 0.011) and angiotensin III (P = 0.006), both at 10(-8 ) M. These results show that adenosine is capable of reducing macula d ensa-mediated renin secretion, but that this effect, even at very high concentrations or during adenosine deaminase blockade, does not fully mimic the inhibitory potency of increasing luminal NaCl concentration . Because the marked effect caused by angiotensins establishes the pot ential of this preparation to demonstrate inhibitory hormonal influenc es, it is concluded that adenosine does not appear to be the sole para crine factor responsible for the NaCl-induced reduction of renin secre tion.