Cerebral postischemic hypoperfusion is mediated by ETA receptors

• Published in: Brain research Vol. 726; no. 1-2; pp. 242 - 246
• Main Authors: SPATZ, M, YASUMA, Y, STRASSER, A, MCCARRON, R. M
• Format: Journal Article
• Language: English
• Published: London Elsevier 08-07-1996; Amsterdam; New York, NY
• Subjects: Animals; Biological and medical sciences; Blood Pressure - drug effects; Cerebrovascular Circulation - drug effects; Cerebrovascular Circulation - physiology; Endothelin Receptor Antagonists; Enzyme Inhibitors - pharmacology; Female; Gerbillinae; Ischemic Attack, Transient - physiopathology; Medical sciences; Neurology; Nitric Oxide Synthase - antagonists & inhibitors; Nitroarginine - pharmacology; Peptides, Cyclic - pharmacology; Receptor, Endothelin A; Receptors, Endothelin - physiology; Temperature; Vascular diseases and vascular malformations of the nervous system; Regional blood flow; Nervous system diseases; Endothelin; Rodentia; Cardiovascular disease; Cerebral disorder; Vascular disease; Vertebrata; Experimental disease; Mammalia; Ischemia; Animal; Central nervous system disease; Nitrogen monoxide; Peptidergic receptor; Hemodynamics; Antagonist; Gerbil; Cerebrovascular disease; Brain (vertebrata)
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/0006-8993(96)00409-X

Effect of ETA-receptor antagonist, BQ123, on postischemic hypoperfusion in the presence or absence of nitric oxide synthetase inhibitor, N omega-nitro-L-arginine (NLA), was investigated in Mongolian gerbils. BQ123 given prior to ischemia reversed the early incomplete recovery of cerebral blood flow observed with NLA without affecting the late postischemic hypoperfusion. Additional postischemic administration of BQ123 also reversed (P < 0.01) the late postischemic hypoperfusion seen in NLA-, N omega-nitro-D-arginine methyl ester- or Ringer's-treated animals.