Modulation of adrenergic transmission by angiotensins in the perfused rat mesentery. Am J Physiol 1979 Feb;236(2):H211-7 PMID: 217278
Pubmed ID
217278Abstract
Isolated rat mesenteric arteries perfused with a modified Krebs solution were utilized to study the effects of angiotensin II (AII), angiotensin III (AIII), and [des-Asp1-Arg2]AII on adrenergic transmission. Angiotensin II potentiated vasoconstrictor responses to both sympathetic nerve stimulation and to exogenous norepinephrine, whereas AIII and [des-Asp1-Arg2]AII potentiated vasoconstrictor responses to exogenous norepinephrine only. When the responses to exogenous norepinephrine were compared, the order of agonist potency was AIII greater than AII greater than [des-Asp1-Arg2]AII. The potentiation of sympathetic nerve stimulation by AII was inhibited by simultaneous administration of AIII (25%), [des-Asp1-Arg2]AII (51%), [Sar1-Ile8]AII (83%), and (Ile7)AIII (80%). The potentiation of exogenous norepinephrine by AII, AIII, and [des-Asp1-Arg2]AII was inhibited by [Sar1-Ile8]AII (110%, 113%, and 108%, respectively) and by [Ile7]AIII (50%, 64%, 91%, respectively). We conclude that AII possesses the capacity both to increase norpinephrine release during sympathetic nerve stimulation and to decrease norepinephrine reuptake, whereas AIII and [des-Asp1-Arg2]AII decrease norepinephrine release and reuptake. Also, under conditions of increased N-terminal degradation of AII, blockade of norepinephrine reuptake would be increased while the release of norepinephrine by nerve stimulation would be reduced.
Author List
Campbell WB, Jackson EKAuthor
William B. Campbell PhD Chair, Professor in the Pharmacology and Toxicology department at Medical College of WisconsinScopus
2-s2.0-0018433703 38 CitationsMESH terms used to index this publication - Major topics in bold
Angiotensin IIAngiotensin III
Animals
Male
Mesenteric Arteries
Norepinephrine
Perfusion
Rats
Sympathetic Nervous System
Synaptic Transmission
Vasoconstriction
Vasomotor System
