title: Characteristics of renal sympathetic nerve single units in rabbits with angiotensin-induced hypertension.
abstract: We examined the effect of chronic angiotensin (Ang II)-induced hypertension on activity of postganglionic renal sympathetic units to determine whether altered whole renal nerve activity is due to recruitment or changes in firing frequency. Rabbits were treated with a low (20 ng kg(-1) min(-1), 8 weeks) or high dose (50 ng kg(-1) min(-1), 4 weeks) of Ang II before the experiment under chloralose-urethane anaesthesia. Spontaneously active units were detected from multiunit recordings using an algorithm that separated units by action potential shape using templates that matched spikes within a prescribed standard deviation. Multiunit sympathetic nerve activity was 40% higher in rabbits treated with low-dose Ang II than in sham (P = 0.012) but not different in high-dose Ang II. Resting firing frequency was similar in sham rabbits (1.00 ± 0.09 spikes s(-1), n = 144) and in those treated with high-dose Ang II (1.10 ± 0.08 spikes s(-1), n = 112) but was lower with low-dose Ang II (0.65 ± 0.08 spikes s(-1), n = 149, P < 0.05). Unit firing rhythmicity was linked to the cardiac cycle and was similar in sham and low-dose Ang II groups but 29-32% lower in rabbits treated with high-dose Ang II (P < 0.001). Cardiac linkage followed a similar pattern during hypoxia. All units showed baroreceptor dependency. Baroreflex gain and range were reduced and curves shifted to the right in Ang II groups. Firing frequency during hypoxia increased by +39% in low-dose Ang II and +82% in shams, but the greatest increase was in the high-dose Ang II group (+103%, P(dose) = 0.001). Responses to hypercapnia were similar in all groups. Increases in sympathetic outflow in hypertension caused by low-dose chronic Ang II administration are due to recruitment of neurons, but high-dose Ang II increases firing frequency in response to chemoreceptor stimuli independently of the arterial baroreceptors.
authors.affiliation: Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
authors.forename: Sandra L
authors.initials: SL
authors.lastname: Burke
authors.affiliation: Department of Cardiovascular Regulation, Russian Cardiology Research Centre, Moscow, Russia.
authors.forename: Elena V
authors.initials: EV
authors.lastname: Lukoshkova
authors.affiliation: Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.|Department of Pharmacology, Monash University, Clayton, Victoria, Australia.
authors.forename: Geoffrey A
authors.initials: GA
authors.lastname: Head
mesh_terms: D000200:Action Potentials; D000804:Angiotensin II / Q000008:administration & dosage; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000503:physiopathology; D017704:Baroreflex; D004305:Dose-Response Relationship, Drug; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology; D006439:Hemodynamics; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation* / Q000503:physiopathology*; D008297:Male; D011817:Rabbits; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014662:Vasoconstrictor Agents / Q000008:administration & dosage
chemical_list: D014662:Vasoconstrictor Agents; D000804:Angiotensin II