Does angiotensin II and atrial natriuretic peptide alter cerebral blood flow and vascular resistance in anesthetized rabbits?
High doses of angiotensin II produce cerebral vasodilatation, particularly in small vessels, while atrial natriuretic peptide selectively dilates large cerebral arteries without interfering with ANG II-induced CBF increases.
The purpose of the present study was to determine effects of angiotensin (ANG) II on the cerebral circulation. We measured the pial artery pressure (PAP) and CBF in anesthetized rabbits. ANG II (5 micrograms/min) was infused into each carotid artery, and systemic arterial pressure was maintained constant. During infusion of ANG II, there was a significant increase in CBF and fall of PAP, with no change in the large artery resistance (LAR) and a significant decrease in the small vessel resistance (SVR). To investigate whether prostaglandin modulated the ANG II-induced increase in CBF, indomethacin was administered (10 mg/kg i.v.) in another group of animals. Indomethacin itself reduced PAP and increased LAR significantly without changing CBF or SVR. Indomethacin did not attenuate the effects of ANG II on the cerebral circulation. The CMRO2 was assessed during ANG II intracarotid infusion in another group of rabbits. CMRO2 did not change during infusion of ANG II. We also investigated effects of alpha-atrial natriuretic peptide (ANP) on the cerebral circulation. Infusion of ANP (1 microgram/min) decreased LAR by 28% (p less than 0.05) without altering SVR. Administration of ANG II after ANP tended to reduce LAR (p greater than 0.05), with a significant decrease in SVR. The results of the present study suggest that high doses of ANG II can produce cerebral vasodilatation, particularly of small vessels. Blood-borne ANP dilated the large arteries of the cerebral circulation selectively and neither interfered with nor reversed the ANG II-induced increase in CBF.
Tamaki et al. (Sun,) studied this question.