Angiotensin modulation of vascular tone and adrenergic neurotransmission in cat femoral arteries.
1. AI and AII induced contractions in cat femoral arteries, which were inhibited by saralasin. 2. The response to AI was reduced by captopril and endothelium removal and by chymostatin in endothelium-denuded segments. 3. AII contractions were increased by indomethacin, L-NAME and endothelium removal. 4. AII and AI facilitated the adrenergic neurotransmission. This facilitation was inhibited by saralasin and/or captopril. 5. These data suggest: (1) AI is converted into AII in the endothelial and adventitial layer; (2) the contractions caused by AI and AII are mediated by AII receptors and are modulated by endothelial release of NO and PGI2; and (3) the existence of presynaptic AII receptors mediating the facilitation of neurotransmission caused by AI and AII.
Encabo
A
A
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.
Ferrer
M
M
Marín
J
J
Balfagón
G
G
D000704:Analysis of Variance; D000803:Angiotensin I / Q000378:metabolism*; D000804:Angiotensin II / Q000096:biosynthesis / Q000502:physiology*; D000818:Animals; D002415:Cats; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D005263:Femoral Artery / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D009638:Norepinephrine / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
D000804:Angiotensin II; D000803:Angiotensin I; D009638:Norepinephrine