title: Low-dose B-type natriuretic peptide raises cardiac sympathetic nerve activity in sheep.
abstract: The reported effects of atrial natriuretic peptide (ANP) on sympathetic nerve activity (SNA) are variable, dependent on concomitant hemodynamic actions, and likely to be regionally differentiated. There are few reports of the effect of B-type natriuretic peptide (BNP) on SNA and none have measured cardiac SNA (CSNA) by direct microneurography. We measured the effects of low-dose ANP and BNP (2.4 pmol·kg(-1)·min(-1) infused for 120 min) on CSNA and hemodynamics in conscious sheep (n = 8). While there was a trend for mean arterial pressure and cardiac output to fall with both ANP and BNP, changes were not significant compared with vehicle control. However, BNP did significantly reduce systolic arterial (97 ± 4.2 vs. 107 ± 6.8 mmHg during control; P = 0.043) and pulse pressures (0.047) and increase heart rate (110 ± 6.7 vs. 96 ± 7.3 beats/min; P = 0.044). Trends for these hemodynamic parameters to change with ANP did not achieve statistical significance. ANP also had no significant effect on any CSNA parameters measured. In contrast, BNP induced a rise in both CSNA burst frequency (∼20 bursts/min higher than control, P = 0.011) and burst area (∼40% higher than control, P = 0.013). BNP-induced rises in burst incidence (bursts/100 beats), and burst area per 100 beats, however, were not significant. In conclusion, BNP infused at low doses that only had subtle effects on hemodynamics increased CSNA burst frequency and burst are per minute. This increase in CSNA may in large part be secondary to an increase in heart rate as CSNA burst incidence and burst area per 100 beats were not significantly increased. This study provides no evidence for inhibition of CSNA by natriuretic peptides.
authors.affiliation: Christchurch Heart Institute, University of Otago, Christchurch, New Zealand chris.charles@otago.ac.nz.
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Charles
authors.affiliation: Christchurch Heart Institute, University of Otago, Christchurch, New Zealand.
authors.forename: David L
authors.initials: DL
authors.lastname: Jardine
authors.affiliation: Christchurch Heart Institute, University of Otago, Christchurch, New Zealand.
authors.forename: Miriam T
authors.initials: MT
authors.lastname: Rademaker
authors.affiliation: Christchurch Heart Institute, University of Otago, Christchurch, New Zealand.
authors.forename: A Mark
authors.initials: AM
authors.lastname: Richards
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D005260:Female; D006321:Heart / Q000187:drug effects* / Q000294:innervation; D006339:Heart Rate / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D045283:Natriuretic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D020097:Natriuretic Peptide, Brain / Q000008:administration & dosage / Q000494:pharmacology*; D012756:Sheep; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology
chemical_list: D045283:Natriuretic Agents; D020097:Natriuretic Peptide, Brain
keywords: blood pressure; catecholamines; heart rate; hormones; sympathetic nervous system