Temperature sensitivity of angiotensin-induced inotropic effects

Temperatures in the range of 30 to 37 degrees C were examined for effects on angiotensin (Ang) peptide-induced inotropic actions in rabbit isolated aortic rings and left atria. Both transmurally-stimulated and punctate-stimulated atria were employed to examine neurogenic and direct cardiac actions of the Ang, respectively. The peptides examined were Ang II, Ang III, and sarcosyl1-Ang II. Ang III was more potent at 33 degrees C than at 37 degrees C in the transmurally stimulated atria, in which the Ang III concentration-response curve was shifted roughly 10-fold to the left at 33 degrees C in comparison to 37 degrees C. Sarcosyl1-Ang II responses were maximal at 37 degrees C and significantly reduced at lower temperatures in aortic rings (30 degrees C) and in transmurally stimulated atria (30 and 33 degrees C). Ang II actions were not significantly altered by temperature changes in the 30 to 37 degrees C range except in transmurally stimulated atria, in which angiotensin II was more potent at 30 degrees C than at 33 degrees C. The results indicate that relatively small temperature alterations can profoundly affect potency ratios and maximal responses among the angiotensin peptides particularly when the angiotensin response is mediated in part by activation of sympathetic neurons, as in the transmurally stimulated atria. The data are consistent with either different mechanisms of cellular stimulation or multiple populations of receptors for the angiotensins. The greater effect of temperature alterations on angiotensin responses in the transmurally stimulated atria suggests that the peptides influence sympathetic nerves and cardiac or smooth muscle differently.