SEPARATION OF PERIPHERAL AND CENTRAL CARDIOVASCULAR ACTIONS OF ANGIOTENSIN-II

The presser and vasoconstrictor action of angiotensin II (ANG II) is c onsidered to be caused by a combination of its direct and indirect vas cular effects, the latter mediated by the sympathetic nervous system. The purpose of this study was to determine the extent to which the dir ect and indirect actions of ANG II contribute to its presser and vascu lar effects. Blood pressure, cutaneous vascular, and plasma norepineph rine responses to intravenous ANG II were measured in conscious rabbit s before and after inhibition of central sympathetic outflow with intr avenous and intracisternal clonidine and after ganglionic blockade wit h intravenous pentolinium. Intravenous ANG II caused a similar dose-re lated rise in blood pressure before and after sympathetic blockade wit h intravenous clonidine, intracisternal clonidine, and intravenous pen tolinium. In contrast, the dose-related fall in cutaneous ear blood fl ow and cutaneous ear temperature and rise in cutaneous ear vascular re sistance induced by intravenous ANG II were abolished after intravenou s clonidine, intracisternal clonidine, and intravenous pentolinium. He art rate was unchanged after ANG II. There were no changes in back ski n or rectal temperature. There was a nonsignificant fall in plasma nor epinephrine and no change in epinephrine after ANG II. These results d emonstrate that the acute presser response to intravenous ANG II is me diated by its direct vascular effects and is not dependent on central or ganglionic stimulation of the sympathetic nervous system, in contra st to the effect of ANG II on cutaneous ear vasoconstriction, which is predominantly caused by a centrally mediated increase in sympathetic nervous activity. Our results separate, in conscious rabbits, the dire ct vascular effects of ANG II from its indirect vascular actions, whic h are mediated by central sympathetic stimulation in the brain.