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Effects of atrial natriuretic peptide on systemic haemodynamics and cardiac function in normal man
M J Allen1, S M Gilmour, M Singer
1Department of Medicine One, St. George's Hospital Medical School, London.
Insights
Atrial natriuretic peptides (ANP) lower blood pressure by dilating arterioles, not by negatively impacting heart contractility. ANP reduces cardiac output and plasma volume, with effects on blood pressure varying by body position.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
Background:
- Atrial natriuretic peptides (ANP) are known to reduce blood pressure.
- Animal studies suggest ANP's depressor effect stems from reduced cardiac output, but its impact on cardiac contractility (inotropic effect) in humans is unclear.
Purpose of the Study:
- To investigate the effects of Atrial natriuretic peptides (ANP) on cardiovascular parameters in normal humans.
- To determine if ANP has a negatively inotropic effect or primarily reduces cardiac output by affecting left ventricular filling.
Main Methods:
- Six healthy volunteers received placebo and incremental doses of ANP (0.25-12 µg/min) via infusion.
- Doppler measurements of ascending aortic blood flow were used to assess heart rate, cardiac output, and systemic vascular resistance in supine and erect positions.
Main Results:
- ANP caused dose-dependent increases in heart rate and maximal acceleration, and decreased systemic vascular resistance in both positions.
- In the erect position, ANP lowered systolic blood pressure. Post-infusion, cardiac output decreased, and systemic vascular resistance increased.
- Plasma volume significantly reduced (10.5%) despite minimal negative fluid balance.
Conclusions:
- Pharmacological doses of ANP act as an arteriolar dilator with rapid offset.
- ANP does not appear to have a negatively inotropic effect in humans.
- ANP reduces cardiac filling pressures through a slower offset mechanism, leading to decreased cardiac output and plasma volume.
Abstract:
Atrial natriuretic peptides (ANP) reduce blood pressure. Animal experiments suggest that this depressor action results from a reduction in cardiac output rather than peripheral vascular resistance but it is unresolved whether this is wholly due to their effect of reducing left ventricular filling or whether they have a negatively inotropic effect. We have therefore investigated the effects of ANP in normal man using Doppler measurements of ascending aortic blood flow. Six normal volunteers underwent infusions of placebo and incremental doses of ANP in the range 0.25 to 12 micrograms.min-1. Each infusion was given for 15 min and measurements made both in the supine and erect positions (passive tilt). In both positions ANP had dose dependent effects of increasing heart rate (HR) and maximal acceleration whilst lowering an index of systemic vascular resistance (ISVR). In the erect position ANP also lowered systolic blood pressure. In the 30 min after completion of the infusions there were significant decreases in peak velocity and cardiac output with increases in ISVR in both positions, but HR fell and diastolic pressure increased only when supine. During the course of the experiment mean haematocrit (SEM) increased from 43.9 (1.2) to 46.7 (1.0), indicating a mean reduction in plasma volume of 10.5%. This occurred despite a negative fluid balance of only 31(7) ml over the 2 h. These data suggest that ANP is not negatively inotropic and that, at pharmacological doses, it is an arteriolar dilator of rapid offset and reduces cardiac filling pressures by a mechanism of slower offset.