To examine the role of prostaglandins (PGs) in the macula densa mechanism of renin release, rabbit afferent arteriole (Af) alone and afferent arteriole with macula densa attached (Af + MD) were microdissected and incubated consecutively. Hourly renin release rate from a single Af (or Af + MD) was calculated and expressed as ngAI·h-1·Af-1 (or Af + MD-1)/h (where AI is angiotensin I). Basal renin release rate from Af was 0.84± 0.14 ngAI·h-1·Af-1/h (X±SEM, n = 23) and remained stable throughout the incubations. Basal renin release rate from Af + MD was 0.33±0.04 ngAI·h-1Af + MD-1/h (n = 17), which was significantly lower (p<0.01) than that from Af. When furosemide (1.5mM) was added to Af, no significant change in renin release rate was observed. However, when furosemide was added to Af + MD, renin release rate increased from 0.40±0. 05 to 1.59± 0.15 ngAI·h-1·Af + MD-1/h (n = 10, p<0.01). After the pretreatment with indomethacin, a cyclooxygenase inhibitor, furosemide still increased renin release rate from 0.17 + 0.02 to 0. 56±0. 09 ng Al·h-1·Af+ MD-1/h (n = 5, p<0.05); however, indomethacin pretreatment reduced both basal and furosemide-stimulated renin release rate (p<0.05). In the presence of PGI2 (IOεM), renin release rate from Af increased from 0.45±0.14 to 1.49± 0.53ng AI·h-1Af-1/h (n = 9, p<0. 05), and further increased to 4.50±1.24ng AI·h-1Af-1/h (p<0. 02) after removal from PGI2. When PGE2 (10 ε M) was added to Af + MD, renin release rate increased from 0.54 + 0.09 to 1.26±0.24ng AI·h-1·Af+ MD-1/h (n = 8, p<0.05). However PGE2 had no effect on renin release rate from Af alone. We concluded that (1) the prostaglandin system may be a modulating factor of response in the macula densa mechanism of renin release, (2) PGI2 has direct action on renin release from afferent arteriole, and (3) PGE2 may participate in the control of renin release through the action on the macula densa.
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