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

Abstract

Abstract

The objective of these experiments was to assess the possibility that the increase in tail skin temperature (T_SK) accompanying administration of the β-adrenergic agonist isoproterenol (ISO) was mediated by angiotensin II (Angll) as a result of stimulation of renin release by ISO. Although Angll 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 T_SK. The objective was approached in several ways: (i) use of the nonpeptide Angll receptor antagonist losartan potassium (DuP 753); (ii) use of the peptide Angll receptor antagonist saralasin; (iii) use of the Angl-converting enzyme inhibitor captopril, and (iv) chronic administration of Angll. The rationale for these experiments was that blockade of Angll receptors (Experiments 1 and 2), inhibition of the enzyme that converts Angl to Angll (Experiment 3), or down-regulation of the Angll receptors (Experiment 4) would be expected to prevent any contribution to the ISO-induced increase in T_SK by Angll. The results of these experiments are consistent in revealing that the response of T_SK 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 Angll in the blood.