Neuronal responses in subfornical organ and other regions to angiotensin II applied by various routes

• Published in: Brain research bulletin Vol. 14; no. 4; p. 307
• Main Authors: Ishibashi, S, Oomura, Y, Gueguen, B, Nicolaidis, S
• Format: Journal Article
• Language: English
• Published: United States 01.01.1985
• Subjects: Action Potentials - drug effects; Angiotensin II - administration & dosage; Angiotensin II - pharmacology; Animals; Carotid Arteries; Dinoprost; Injections, Intra-Arterial; Injections, Intraventricular; Iontophoresis; Male; Neurosecretory Systems - drug effects; Prostaglandins F - pharmacology; Rats; Rats, Inbred Strains; Sodium Nitrite - pharmacology; Subfornical Organ - drug effects
• ISSN: 0361-9230
• DOI: 10.1016/0361-9230(85)90190-X

Effects of Angiotensin II (AII) and of signals of hydromineral deficiencies on neuronal firing in the subfornical organ (SFO) and the surrounding regions of the rat were examined. AII was applied in three ways: electrophoresis, intracarotid injection, or intracerebroventricular injection. Seventeen SFO neurons (52%) were facilitated by electrophoretic AII and one (3%) was inhibited (AII-responding neurons). Neurons in other regions (cerebral cortex, nucleus triangularis septi, hippocampus, nucleus periventricularis) were also facilitated (23%) or inhibited (14%). Prostaglandin (PG)F2, a universal vasoconstrictor, produced an effect similar to that by AII on neuronal activity of the SFO and surrounding regions, and this effect was antagonized by (NO2-), a vasoplegic agent. Intracarotid injection of AII caused biphasic facilitation of SFO activity. The second increase correlates with changes in blood pressure. Intraventricular injection of AII caused drastic and long lasting excitation of SFO activity. Simultaneous intraventricular application of NO2- blocked the AII effect on SFO neurons but not on blood pressure. Hypovolemia or cerebrospinal fluid withdrawal that might cause mechanical stimulation of circumventricular organs increased SFO neuronal activity. These results are compatible with the vasoconstriction hypothesis of an indirect effect of AII through change in diameter of the vasa that surround neurons.