gms | German Medical Science

Background: Natriuretic peptides are important in the regulation of blood pressure. Recently, it was shown that physiological concentrations of atrial natriuretic peptide (ANP) induce a strong lipid mobilization. The response could be related to reflex mediated sympathetic activation and subsequent beta-adrenoreceptor stimulation.

Methods: We tested the metabolic response to ANP in 10 healthy normal weight men (31±1 years). Human ANP was infused at rates of 6.25, 12.5, and 25 ng/kg/min, with and without near complete i.v. beta-adrenoreceptor blockade with propranolol (0.20 mg/kg in four bolus doses followed by 0.033mg/kg/h infusion) in a cross over fashion. Blood samples for the determination of ANP, glycerol, non estrified fatty acids (NEFA) and insulin were obtained from an antecubital i.v. line. Microdialysis probes were inserted into abdominal subcutaneous adipose tissue (SCAT) and femoral skeletal muscle. Dialysate ethanol, glucose, lactate, pyruvate, and glycerol concentrations were analyzed. Indirect calorimetry was applied to monitor changes in energy expenditure and substrate oxidation rates.

Results: Without propranolol, heart rate increased from 55±2 bpm to 69±4 bpm (p< 0.01). With propranolol, heart rate was 53±2 bpm at baseline and 57±3 bpm at the highest ANP dose (ns). ANP elicited a dose dependent increase in serum NEFA and glycerol concentrations that was not suppressed with systemic propranolol infusion. The lipid mobilization of ANP was present in SCAT, but not in skeletal muscle. At high ANP concentrations, carbohydrate oxidation decreased (p<0.05) and lipid oxidation increased (p<0.01). This pattern of substate oxidation was not observed with propranolol.

Conclusion: We conclude that the ANP induced increase in lipid mobilization in humans is not mediated by beta-adrenoreceptor stimulation. Our data further support the idea that ANP induces lipolysis through natriuretic peptide receptor stimulation.