Role of Angiotensin II Receptors in Tail Skin Temperature Response to Isoproterenol

Abstract

The objective of these experiments was to assess the possibility that the increase in tail skin temperature (TSK) accompanying administration of the beta-adrenergic agonist isoproterenol (ISO) was mediated by angiotensin II (AngII) as a result of stimulation of renin release by ISO. Although AngII is known to be a potent vasoconstrictor in mammals, acute administration of this peptide to rats induces a vasodilation of blood vessels in the tail and an increase in TSK. The objective was approached in several (DuP 753); ways: (i) use of the nonpeptide AngII receptor antagonist losartan potassium (DuP 753); (ii) use of the peptide AngII receptor antagonist saralasin; (iii) use of the AngI-converting enzyme inhibitor captopril, and (iv) chronic administration of AngII. The rationale for these experiments was that blockade of AngII receptors (Experiments 1 and 2), inhibition of the enzyme that converts AngI to AngII (Experiment 3), or down-regulation of the AngII receptors (Experiment 4) would be expected to prevent any contribution to the ISO-induced increase in TSK by AngII. The results of these experiments are consistent in revealing that the response of TSK to ISO administration is due in part (approximately 55%) to a direct effect of ISO and in part (approximately 45%) to an indirect effect resulting from the ISO-stimulated release of renin from the kidneys and the formation of AngII in the blood.