Vasomotor effects of atrial natriuretic peptides on feline pial arterioles.

Vasomotor responses to atrial natriuretic peptide (ANP), atriopeptin I and atriopeptin II were examined on individual pial vessels on the cortical surface of chloralose-anaesthetized cats. The peptides were administered by subarachnoid perivascular microapplication in an open skull preparation. Changes in vessel calibre were quantified and compared to those of the vehicle, artificial cerebrospinal fluid, which was without significant vasomotor effect. All 3 atrial peptides significantly increased pial arteriolar calibre. ANP, the most potent, gave rise to a maximum increase in arterial calibre of 33 +/- 4% (mean +/- S.E.M., n = 7, P less than 0.05) at 10(-6) M. The concentration of ANP effecting half the maximum response was approximately 7 nmol. Atriopeptin I and II were equipotent with a maximum increase in calibre at 10(-6) M of 21 +/- 4% (n = 10) and 23 +/- 2% (n =6), respectively. The concentration of these peptides effecting half the maximum response was, similar to ANP, in the nanomolar range. Samples of pial arterioles along with middle cerebral and basilar arteries were processed for immunohistochemistry using a polyclonal antibody raised against human ANP. No specific ANP-immunoreactivity was found associated with these vessels. However, dense granular ANP-immunoreactive deposits were clearly demonstrated in sections of feline atria. We conclude that all 3 peptides studied are vasoactive in the cerebral circulation, ANP being the most potent. Since there is no evidence for perivascular ANP nerves around these vessels, the physiological significance of these findings must await identification of the source of ANP.