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Alpha-Adrenergic Mechanisms in the Cardiovascular Hyperreactivity to Norepinephrine-Infusion in Essential Hypertension

Alpha-Adrenergic Mechanisms in the Cardiovascular Hyperreactivity to Norepinephrine-Infusion in Essential Hypertension

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WALTHER, Lisa-Marie, Roland VON KÄNEL, Nadja HEIMGARTNER, Claudia ZUCCARELLA-HACKL, Guido STIRNIMANN, Petra H. WIRTZ, 2022. Alpha-Adrenergic Mechanisms in the Cardiovascular Hyperreactivity to Norepinephrine-Infusion in Essential Hypertension. In: Frontiers in endocrinology. Frontiers Media SA. 13, 824616. eISSN 1664-2392. Available under: doi: 10.3389/fendo.2022.824616

@article{Walther2022Alpha-58307, title={Alpha-Adrenergic Mechanisms in the Cardiovascular Hyperreactivity to Norepinephrine-Infusion in Essential Hypertension}, year={2022}, doi={10.3389/fendo.2022.824616}, volume={13}, journal={Frontiers in endocrinology}, author={Walther, Lisa-Marie and von Känel, Roland and Heimgartner, Nadja and Zuccarella-Hackl, Claudia and Stirnimann, Guido and Wirtz, Petra H.}, note={Article Number: 824616} }

Zuccarella-Hackl, Claudia Heimgartner, Nadja Stirnimann, Guido Alpha-Adrenergic Mechanisms in the Cardiovascular Hyperreactivity to Norepinephrine-Infusion in Essential Hypertension von Känel, Roland Walther, Lisa-Marie 2022-08-16T12:42:03Z Zuccarella-Hackl, Claudia Heimgartner, Nadja von Känel, Roland Stirnimann, Guido Walther, Lisa-Marie Attribution 4.0 International 2022 2022-08-16T12:42:03Z Wirtz, Petra H. Wirtz, Petra H. eng Aims: Essential hypertension (EHT) is characterized by cardiovascular hyperreactivity to stress but underlying mechanism are not fully understood. Here, we investigated the role of α-adrenergic receptors (α-AR) in the cardiovascular reactivity to a norepinephrine (NE)-stress reactivity-mimicking NE-infusion in essential hypertensive individuals (HT) as compared to normotensive individuals (NT).<br />Methods: 24 male HT and 24 male NT participated in three experimental trials on three separate days with a 1-min infusion followed by a 15-min infusion. Trials varied in infusion-substances: placebo saline (Sal)-infusions (trial-1:Sal+Sal), NE-infusion without (trial-2:Sal+NE) or with non-selective α-AR blockade by phentolamine (PHE) (trial-3:PHE+NE). NE-infusion dosage (5µg/ml/min) and duration were chosen to mimic duration and physiological effects of NE-release in reaction to established stress induction protocols. We repeatedly measured systolic (SBP) and diastolic blood pressure (DBP) as well as heart rate before, during, and after infusions.<br />Results: SBP and DBP reactivity to the three infusion-trials differed between HT and NT (p’s≤.014). HT exhibited greater BP reactivity to NE-infusion alone compared to NT (trial-2-vs-trial-1: p’s≤.033). Group differences in DBP reactivity to NE disappeared with prior PHE blockade (trial-3: p=.26), while SBP reactivity differences remained (trial-3: p=.016). Heart rate reactivity to infusion-trials did not differ between HT and NT (p=.73).<br />Conclusion: Our findings suggest a mediating role of α-AR in DBP hyperreactivity to NE-infusion in EHT. However, in SBP hyperreactivity to NE-infusion in EHT, the functioning of α-AR seems impaired suggesting that the SBP hyperreactivity in hypertension is not mediated by α-AR.

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