Synthetic atrial natriuretic factor does not directly dilate splanchnic or cerebral resistance-sized arteries, indicating its hypotensive effects are not due to direct vasodilation in these vascular beds.
ANF lacks direct dilator effects on cerebral and mesenteric arteries; leaves open alternative mechanisms for its hypotensive action and requires higher-level confirmation.
The effects of synthetic atrial natriuretic factor and atriopeptin III on induced tone in resistance-sized arteries from the rat were examined in vitro. Cylindrical segments of small mesenteric or cerebral arteries were mounted on a microcannula and pressurized to a transmural pressure of 75 mm Hg. After equilibration, the level of tone in cerebral arteries was on the order of - 35 change in diameter; addition of atrial natriuretic factor or atriopeptin III in cumulative doses from 10(-10) to 10(-7) M did not produce any transient or sustained changes in diameter. Similarly, atrial natriuretic factor or atriopeptin III did not alter the contractile responses of cerebral vessels to serotonin or prostaglandin F2 alpha. Mesenteric arteries, which do not possess an intrinsic myogenic tone, were precontracted with potassium (30 mM), norepinephrine (10(-6) M), or prostaglandin F2 alpha (1.1 X 10(-5) M) and exposed to the synthetic natriuretic peptides, also without effect. Transmural electrical stimulation (0.3-msec pulses; 180 mA; 4/second) relaxed cerebral and contracted mesenteric arteries; preincubation in 10(-7) M atrial natriuretic factor or atriopeptin III did not alter subsequent responses. These observations suggest that the hypotensive action of atrial natriuretic factor cannot be attributed to direct vasodilation of splanchnic or cerebral resistance-sized arteries.
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Osol et al. (1986) studied this question.
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