Angiotensin and CNS regulation of blood pressure.
It appears that angiotensin II (AII) has access to the CNS by three routes: endogenous formation within the brain, passage into CSF, or transfer across "gaps" in the blood-brain barrier. The mode of access influences both the characteristics and the magnitude of the cardiovascular effects exerted by AII within the CNS. In the dog the effects of blood-borne AII on the area postrema (AP) in the IV ventricle seem to have the most physiological significance. In recent experiments we have characterized both the histological composition of this structure and its physiological effects. While electrical stimulation of the AP, in similarity to the pressor effects of intravertebral AII, produces a hypertensive response dependent on sympathetic vasomotor outflow, ablation of this structure results in mild hypotension associated with decreased hemodynamic variability and altered vascular responsiveness to intravenous AII and norepinephrine. Recent data suggest that the sympatho-facilitative action of AII on the AP may involve endogenous opiates in the brainstem.
D000320:Adrenergic Fibers / Q000502:physiology; D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001921:Brain / Q000502:physiology*; D001933:Brain Stem / Q000166:cytology / Q000502:physiology / Q000601:surgery; D002302:Cardiac Output; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D009638:Norepinephrine / Q000494:pharmacology; D014655:Vascular Resistance
D000804:Angiotensin II; D009638:Norepinephrine