Related Experiment Video
Updated: Aug 14, 2026
Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Subpressor calcium infusion increases isovolumic left ventricular relaxation time and atrial natriuretic peptide in
W L Finn1, R D Gordon, B I Seneviratne
1University of Queensland Department of Medicine, Greenslopes Hospital, Brisbane, Australia.
Insights
Elevated calcium levels directly stimulate atrial natriuretic peptide (ANP) release from atrial myocytes, independent of blood pressure or atrial stretch. This suggests a direct cellular mechanism for ANP regulation by calcium.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
Background:
- Atrial natriuretic peptide (ANP) plays a crucial role in cardiovascular homeostasis.
- The precise mechanisms regulating ANP secretion, particularly the direct effects of extracellular calcium, require further elucidation.
Purpose of the Study:
- To investigate the direct effect of acute calcium infusion on plasma and urinary ANP levels.
- To explore the potential mechanisms mediating ANP release, differentiating between hemodynamic and direct cellular effects.
Main Methods:
- Subpressor infusion of calcium in normal subjects to achieve upper limit normal calcium levels.
- Monitoring of heart rate, plasma and urinary ANP, noradrenaline, blood pressure, and cardiac output.
- Assessment of atrial dimensions and left ventricular filling dynamics to evaluate atrial stretch.
Main Results:
- Calcium infusion significantly increased plasma and urinary ANP levels.
- Heart rate and noradrenaline decreased, while total peripheral resistance (TPR) increased, without a significant rise in blood pressure.
- No evidence of increased atrial stretch was observed, ruling out this mechanism for ANP elevation.
- Increased left ventricular relaxation time and decreased early filling velocity indicated increased cardiac muscle tone.
Conclusions:
- Acute calcium infusion directly stimulates ANP release from atrial myocytes.
- This stimulation appears to be independent of changes in blood pressure, heart rate, or atrial stretch.
- Calcium may exert a direct effect on atrial myocytes, influencing ANP secretion through contractile or secretory pathways.
Abstract:
1. Subpressor calcium infusion for 1 h, which raised calcium levels to the upper limit of normal in normal subjects, increased plasma and urinary levels of atrial natriuretic peptide (ANP). 2. Heart rate fell, presumably due to carotid baroreflex stimulation (supported by the fall in noradrenaline) and the resultant fall in cardiac output prevented the expected rise in blood pressure due to the rise in total peripheral resistance (TPR). Thus the increase in ANP was not explained by an increase in blood pressure or noradrenaline. 3. There was no evidence for increased atrial stretch (no increase in atrial area or early velocity of left ventricular filling) as a mechanism for increased ANP. 4. Isovolumic left ventricular relaxation time increased, early velocity of ventricular filling decreased and TPR increased, consistent with increased tone in left ventricular and arteriolar muscle. 5. This suggests a direct effect of calcium on the atrial myocyte, stimulating ANP either through contractile or secretory mechanisms.
Related Concept Videos
01:27Feedback Regulation of Calcium Concentration
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
01:18Antihypertensive Drugs: Action of Calcium Channel Blockers
01:26Heart Failure Drugs: Inotropic Agents
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:27Regulation of Stroke Volume
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
01:29Heart Failure II: Pathophysiology