Cerebrovascular reactivity to angiotensin and angiotensin-converting enzyme activity in cerebrospinal fluid.

The purpose of the present study was to test the vasomotor effect of angiotensin I (A I) and angiotensin II (A II) in feline cerebral arteries and to examine the presence of angiotensin converting enzyme (ACE) activity in the vessel wall and cerebrospinal fluid (CSF). A II (10(-8) -10(-5) M) induced concentration-dependent contractions of feline pial arteries (resting diameter, 98-286 microns) in situ with a maximum of 34% at 10(-4) M A II. A I produced dose-related contractions being approximately 20 times less potent than A II. The action of A I was significantly attenuated by the ACE inhibitor captopril (10(-5) M). These findings demonstrate the presence of ACE activity in the vessel wall and/or its surroundings. ACE activity was also found in feline CSF sampled from the cisterna cerebellomedullaris. Bradykinin (BK) was broken down and A I converted to A II by CSF, both effects being inhibited by captopril. This was demonstrated using bioassay and high-performance liquid chromatography. Considering the present and previous studies we conclude that the presence of ACE in the vessel wall and CSF is necessary for the conversion of A I to A II. Although ACE in CSF is able to degrade BK it appears not to be important for the metabolism of BK acting from the perivascular side of pial arteries in situ.