Why the study?
Does intravenous captopril alter cerebral blood flow autoregulation in normotensive and hypertensive rats?
Does intravenous captopril alter cerebral blood flow autoregulation in normotensive and hypertensive rats?
Intravenous captopril resets the limits of cerebral blood flow autoregulation to lower mean arterial pressures in rats, suggesting a role for local angiotensin II in large cerebral artery resistance.
Should not alter clinical ACE inhibitor use; leaves open translation of angiotensin II effects on cerebral autoregulation.
The cerebrovascular effects of converting enzyme inhibition were examined in normotensive and hypertensive rats. Cerebral blood flow was measured using the intracarotid 133xenon injection method in halothane/nitrous oxide anaesthetized animals. The main finding was that following intravenous administration of captopril (10 mg/kg), cerebral blood flow autoregulation was markedly altered. Although cerebral blood flow was unchanged from baseline levels, both the lower and upper limits of autoregulation were reset to lower mean arterial pressure and the autoregulatory plateau shortened. The lower limit was shifted 20-30 mmHg, the upper limit 50-60 mmHg, and the plateau shortened by 20-40 mmHg. The effect was interpreted as being a consequence of compensatory autoregulatory constriction of small resistance vessels in the brain following captopril-induced dilatation of large resistance vessels. It was inferred that locally produced angiotensin II might play a role in the resistance of large cerebral arteries.
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Barry et al. (1984) studied this question.