α2-Adrenergic mediation of the effects of angiotensin II on rat renal artery in vitro

Angiotensin II (ANG II) is a major influence on renal blood flow, acting directly on the renal vasculature and upon other controllers. In vivo observations suggest that ANG II affects renal artery resistance, although explicit in vitro studies have produced negative results. To resolve this issue, potential interactive effects of ANG II on renal artery in vitro were tested. Renal arteries were harvested from ketamine-anesthetized Sprague–Dawley rats and perfused in vitro at constant flow. Resistance was determined from the axial pressure drop while downstream pressure was held constant at ≈80 mmHg (1 mmHg = 133.3 Pa). ANG II, per se, had only a trivial effect on arterial diameter (−5.5 ± 1.5% at 10−7 M ANG II) and failed to affect resistance at concentrations ranging from 10−11 to 10−7 M. Norepinephrine caused strong concentration-dependent constriction, increasing resistance from 0.32 ± 0.04 to 1.86 ± 0.73 mmHg∙mL−1∙min at 10−6 M and 3.27 ± 0.88 mmHg∙mL−1∙min at 10−5 M. In the presence of 10−8 M ANG II, these responses were significantly increased to 3.31 ± 1.00 and 5.02 ± 1.22 mmHg∙mL−1∙min, respectively. Similarly, in the presence of 10−6 M norepinephrine, ANG II caused significant, concentration-dependent constriction of renal artery. In a separate experiment, 10−7 M yohimbine, a relatively specific antagonist of α2-adrenergic receptors, reversed the resistance increment due to ANG II, but not that due to norepinephrine. When yohimbine was applied before norepinephrine and ANG II, it did not affect the response to norepinephrine, but again blocked potentiation of the response by ANG II. The results indicate that, as occurs in some other vascular beds, ANG II "uncovers" vascular constriction that is mediated by α2-adrenergic receptors.Key words: vascular, resistance, interaction, norepinephrine, yohimbine.