This study was designed to examine the effect of α-human atrial natriuretic polypeptide (α-hANP) on renin release in the absence of tubules, glomeruli and macula densa. Rabbit afferent arterioles were microdissected and incubated for two consecutive, 20 minute periods. Hourly renin release rate from a single arteriole was calculated. Basal renin release rate was 0.97 ± 0.13 ng AI·hr-1·Af-1/hr (x±SEM, N = 18) and remained stable throughout the incubations. When afferent arterioles were exposed to α-hANP (0.01, 0.1 or 1 μM), renin release rate did not change significantly. Isoproterenol (5 μM) increased renin release rate from 0.92 ± 0.28 to 1.50 ± 0.46 ng AI·hr-1·Af-1/hr (N = 7, P<0.01). After pretreatment of afferent arterioles with α-hANP (1 μM), isoproterenol still increased renin release rate from 0.98 ± 0.24 to 1.64 ± 0.37 ng AI·hr-1·Af-1/hr (N = 7, P<0.01). The increases in renin release rate induced by isoproterenol were not different between the two groups. Pretreatment of rabbits with furosemide for two days before experiments resulted in greater basal renin release rates from microdissected afferent arterioles (1.70 ± 0.35 ng AI·hr-1·Af-1/hr, N = 14). However, exposure to α-hANP (1 μM) did not alter this elevated renin release rate. It is concluded that atrial natriuretic factor may not have a direct action on juxtaglomerular cells.
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