Effect of adrenaline on serum mid‐regional pro‐atrial natriuretic peptide and central blood volume. Issue 9 (21st August 2022)

• Record Type: Journal Article
• Authors: Sejersen, Casper; Bjerre‐Bastos, Jonathan J.; Goetze, Jens P.; Nielsen, Henning B.; Bihlet, Asger R.; Secher, Niels H.
• Is Part Of: Experimental physiology. Volume 107:Issue 9(2022)
• Page Start: 1037
• Page End: 1045
• Publication Date: 2022-08-21
• Subjects: adrenaline -- central blood volume -- mid‐regional pro‐atrial natriuretic peptide; Physiology, Experimental -- Periodicals; 571.0724
• DOI: 10.1113/EP090516
• Languages: English
• ISSNs: 0958-0670

Abstract

Abstract : New Findings: What is the central question in this study? Atrial natriuretic peptide (ANP) is secreted in response to atrial wall distension and thus allows for evaluation, albeit indirect, of the central blood volume. Adrenaline has chronotropic and inotropic effects. We evaluated whether the chronotropic and inotropic effects of adrenaline were reflected in mid‐regional proANP. What is the main finding and its importance? Central blood volume remained stable with infusion of adrenaline and yet mid‐regional proANP increased. Thus, the chronotropic and inotropic state of the heart or adrenaline directly induces release of ANP variants from the myocytes. Abstract: Atrial natriuretic peptide (ANP) has vasodilatory, natriuretic and diuretic properties. It is secreted in response to atrial wall distension and thereby provides an indirect evaluation of central blood volume (CBV). Adrenaline has chronotropic and inotropic effects that increase cardiac output. In the present study, we evaluated whether these effects were influenced by an increase in CBV and reflected in mid‐regional proANP (MR‐proANP) concentrations in the circulation, a stable proxy marker of bioactive ANP. Changes in CBV were evaluated by thoracic electrical admittance and haemodynamic variables monitored by pulse‐contour analysis during two intervals with graded infusion of adrenaline. Adrenaline infusion increased heart rate (by 33 ± 18%) and stroke volume (by 6 ± 13%), hence cardiac output (by 42 ± 23%; all P < 0.05). The increase in cardiac output did not result from an increase in CBV, because thoracic electrical admittance remained stable (−3 ± 17%; P = 0.230). Serum MR‐proANP concentrations were increased (by 26 ± 25%; P < 0.001) by adrenaline infusion and remained elevated 60 min postinfusion. We conclude that MR‐proANP in the circulation is affected not only by CBV, but also by increased chronotropy/inotropy of the heart, or that adrenaline directly induces release of ANP variants from the myocytes.