title: Autonomic control of the heart is altered in Sprague-Dawley rats with spontaneous hydronephrosis.
abstract: The renal medulla plays an important role in cardiovascular regulation, through interactions with the autonomic nervous system. Hydronephrosis is characterized by substantial loss of renal medullary tissue. However, whether alterations in autonomic control of the heart are observed in this condition is unknown. Thus we assessed resting hemodynamics and baroreflex sensitivity (BRS) for control of heart rate in urethane/chloralose-anesthetized Sprague-Dawley rats with normal or hydronephrotic kidneys. While resting arterial pressure was similar, heart rate was higher in rats with hydronephrosis (290 ± 12 normal vs. 344 ± 11 mild/moderate vs. 355 ± 13 beats/min severe; P < 0.05). The evoked BRS to increases, but not decreases, in pressure was lower in hydronephrotic rats (1.06 ± 0.06 normal vs. 0.72 ± 0.10 mild/moderate vs. 0.63 ± 0.07 ms/mmHg severe; P < 0.05). Spectral analysis methods confirmed reduced parasympathetic function in hydronephrosis, with no differences in measures of indirect sympathetic activity among conditions. As a secondary aim, we investigated whether autonomic dysfunction in hydronephrosis is associated with activation of the renin-angiotensin system (RAS). There were no differences in circulating angiotensin peptides among conditions, suggesting that the impaired autonomic function in hydronephrosis is independent of peripheral RAS activation. A possible site for angiotensin II-mediated BRS impairment is the solitary tract nucleus (NTS). In normal and mild/moderate hydronephrotic rats, NTS administration of the angiotensin II type 1 receptor antagonist candesartan significantly improved the BRS, suggesting that angiotensin II provides tonic suppression to the baroreflex. In contrast, angiotensin II blockade produced no significant effect in severe hydronephrosis, indicating that at least within the NTS baroreflex suppression in these animals is independent of angiotensin II.
authors: The Hypertension & Vascular Research Center, Wake Forest Univ. School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1032, USA. ddiz@wfubmc.edu
authors: Amy C
authors: AC
authors: Arnold
authors: Hossam A
authors: HA
authors: Shaltout
authors: Shea
authors: S
authors: Gilliam-Davis
authors: Nancy D
authors: ND
authors: Kock
authors: Debra I
authors: DI
authors: Diz
mesh_terms: D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology*; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D006869:Hydronephrosis / Q000503:physiopathology*; D007679:Kidney Medulla / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000502:physiology
chemical_list: D000804:Angiotensin II