Decreased Facilitation by Angiotensin II of Noradrenergic Neurotransmission in Isolated Mesenteric Artery of Rabbits with Chronic Heart Failure

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Abstract
Both in human and in experimental heart failure (HF), the renin-angiotensin system and the sympathetic nervous system are activated. In a previous study a facilitatory action of angiotensin II (Ang II) was shown in the rabbit mesenteric artery, which was mediated via prejunctionally located Ang II type 1 (AT1) receptors. Very little is known about the effects of Ang II on sympathetic neurotransmission at the peripheral level in congestive heart failure (CFH). Accordingly, in the isolated mesenteric arteries obtained from rabbits with experimentally induced CHF, as well as in age-matched control rabbits, the effect of Ang II on contractions provoked by electrical field stimulation was investigated in the presence and absence of the AT1 receptor antagonist eprosartan. Additionally, to investigate a possible postjunctional facilitation, the effects of Ang II on α-adrenoceptor-mediated responses were studied using noradrenaline (NA). Lastly, the vasoconstrictor effects of Ang II were compared between HF rabbits and controls, by constructing concentration-response curves to Ang II. In control rabbits, Ang II 0.5 n M caused an enhancement of stimulation-induced responses by a factor 3.2 ± 0.5, 2.4 ± 0.3, and 1.5 ± 0.08, at 1, 2, and 4 Hz, respectively (P M