Facilitation of noradrenergic transmission by locally generated angiotensin II in guinea-pig isolated atria and in the perfused caudal artery of the rat.
In guinea-pig isolated atria, angiotensin I and angiotensin II produced concentration dependent increases in the rate of spontaneous beating and in the release of noradrenaline produced by field stimulation of sympathetic nerves. In rat isolated caudal artery preparations, both angiotensin I and angiotensin II had direct vasoconstrictor actions and also produced concentration dependent increases in constrictor responses to periarterial sympathetic stimulation. All the above effects of angiotensin I and angiotensin II were blocked by the receptor antagonist saralasin, but only those of angiotensin I were blocked by the converting enzyme inhibitor enalaprilat (MK-422). The findings confirm that angiotensin II generated locally from precursor angiotensin I within cardiac and vascular tissues may modulate noradrenergic transmitter release.
D000803:Angiotensin I / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D001158:Arteries / Q000378:metabolism; D003891:Desipramine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012504:Saralasin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects
D000804:Angiotensin II; D000803:Angiotensin I; D012504:Saralasin; D003891:Desipramine; D009638:Norepinephrine