Abstract

We investigated the effect of the NO donor SNAP (6.7 nM) on basal and stretch-induced ANF release from isolated perfused rat atria. There was no significant difference in basal ANF secretion between the vehicle- and SNAP-infused atria (SNAP: 388±63 pg. 100 μl −1, n=13 vs. vehicle: 349±26 pg. 100 μl −1, n=5). Atrial distention caused an increase in ANF secretion in both the buffer- and SNAP-treated groups. SNAP greatly attenuated the stretch-induced increase in ANF (SNAP: 225±7 pg. 100 μl −1, n=5 vs. vehicle: 448±72 pg. 100 μl −1, n=13, P<0.05). The compliance of atria treated with SNAP was lower than that of the vehicle-perfused atria ( P<0.05). Thus, although SNAP appeared to attenuate stretch-induced ANF secretion, there was in fact no significant difference in the ratio of Δ[ANF] to Δintraluminal volume (SNAP: 5.8±1.3 pg. 100 μl −1. μl −1 vs. vehicle: 8.2±1.4 pg. 100 μl −1. μl −1.). In conclusion, we found no evidence that NO alters the control of basal or stretch-induced ANF secretion. NO can however reduce ANF release by shifting the pressure–volume curve, so that a given increase in atrial pressure is associated with a smaller increase in intraluminal volume and reduced atrial distention.

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