Central administration of angiotensin II receptor antagonists and arterial pressure regulation: a note of caution.
The blunting of arterial pressure increases to a variety of pressor agents or the lowering of arterial pressure in some models of hypertension following intracerebroventricular administration of an angiotensin II (AII) antagonist, has been interpreted as prima facie evidence for the involvement of the central AII system in these situations. Central administration of vasopressin or carbachol (a cholinergic agonist) produces pressor effects which have been reported to be due to an increase in the activity of the sympathetic nervous system. We now report that central administration of AII antagonists [either (Sar-1, Ile-8) AII or (Sar-1, Ala-8) AII] in rats prevents the majority (greater than 70%) of the pressor effects of intraventricular vasopressin or carbachol. These results can be interpreted in two ways. The first is that all of these pressor agents use a central angiotensinergic mechanism(s) to increase sympathetic nervous system activity. An alternative hypothesis is that centrally administered AII antagonists non-specifically inhibit sympathetic nervous system function.
Gruber
K A
KA
Department of Physiology & Biophysics, University of Puerto Rico, San Juan 00936-5067.
Callahan
M F
MF
Eskridge-Sloop
S L
SL
D015059:1-Sarcosine-8-Isoleucine Angiotensin II / Q000494:pharmacology*; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D001794:Blood Pressure; D002217:Carbachol / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012504:Saralasin / Q000494:pharmacology*; D014667:Vasopressins / Q000494:pharmacology
D057911:Angiotensin Receptor Antagonists; D014667:Vasopressins; D002217:Carbachol; D015059:1-Sarcosine-8-Isoleucine Angiotensin II; D012504:Saralasin