Why the study?
Does AT1 or AT2 receptor inhibition affect noradrenaline sensitivity and blood pressure in normotensive rats treated with angiotensin II?
Does AT1 or AT2 receptor inhibition affect noradrenaline sensitivity and blood pressure in normotensive rats treated with angiotensin II?
Both AT1 and AT2 receptor activation appear important in controlling noradrenaline sensitivity of rat portal vein smooth muscle.
Preclinical findings on AT1/AT2 modulation of noradrenaline sensitivity warrant no clinical change; leaves open human relevance in hypertension.
Short term treatments of normotensive Wistar Kyoto rats with angiotensin II (ANGII) or in combination with the AT1 receptor antagonist, losartan or PD123319, the AT2 receptor antagonist on systemic arterial blood pressure (MABP) and their influence on noradrenaline sensitivity in isolated mesenteric portal vein were evaluated. ANGII increased MABP as well as the contractile response to noradrenaline in vessels from ANGII-treated animals. MABP and the maximal effect of the concentration response curve for noradrenaline were prevented by losartan. However, PD123319 did not influence the blood pressure, but completely removed the vessels sensitivity to noradrenaline. ANGII combined with the AT1 and/or AT2 receptors blockade completely prevented the pressure response to ANGII, but the concentration response curve for noradrenaline did not differ from the vehicle-treated control curve. In conclusion both AT1- and AT2 receptor activation seems to be important in controlling noradrenaline sensitivity of rat portal vein smooth muscle.
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Datté et al. (2001) studied this question.
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