AT1-receptor antagonists dose-dependently counteracted the Ang II-induced facilitation of noradrenergic neurotransmission in isolated rat mesenteric arteries, with telmisartan being the most potent.
Do AT1-receptor antagonists (losartan, irbesartan, telmisartan) reduce Angiotensin II-induced facilitation of sympathetic neurotransmission in isolated rat mesenteric arteries?
AT1-receptor antagonists dose-dependently inhibit Angiotensin II-facilitated sympathetic neurotransmission in rat mesenteric arteries, with telmisartan showing the highest potency.
valor p: p=<0.05
SUMMARY: The effect of the AT1-receptor antagonists losartan, irbesartan, and telmisartan on angiotensin II (Ang II)-induced facilitation of noradrenergic neurotransmission was investigated in the isolated rat mesenteric artery under isometric conditions. Electrical field stimulation (2, 4, and 8 Hz) caused a frequency-dependent increase of contractile force. At stimulation frequencies of 2, 4, and 8 Hz, Ang 11 (10 nM) increased the stimulation-induced vasoconstrictor responses by a factor 4.8 +/- 0.9, 2.9 +/- 0.7, and 1.3 +/- 0.1, respectively (p irbesartan > losartan (p < 0.05 between linear regression lines). Contractile responses to exogenous noradrenaline were unaltered in the presence of Ang II 10 nM. We conclude that the facilitating effect of Ang II on noradrenergic neurotransmission is mediated by presynaptically located AT1-receptors. Conversely, this facilitating effect can be dose-dependently counteracted by blockade of these receptors. Sympathoinhibitory properties are likely to contribute to the therapeutic effect of AT1-blockers, in particular in conditions in which the sympathetic nervous system is activated, such as congestive heart failure and hypertension.
Balt et al. (Sun,) reported a other. AT1-receptor antagonists (losartan, irbesartan, telmisartan) vs. Control (Ang II alone) was evaluated on Ang II-induced facilitation of noradrenergic neurotransmission (stimulation-induced vasoconstrictor responses) (p=<0.05). AT1-receptor antagonists dose-dependently counteracted the Ang II-induced facilitation of noradrenergic neurotransmission in isolated rat mesenteric arteries, with telmisartan being the most potent.