Mechanisms of exaggerated renal sympathoinhibition during volume loading in spontaneously hypertensive rats.
OBJECTIVE
This investigation examined the central portion of the cardiac volume receptor reflex, which mediates the exaggerated renal sympathoinhibitory response to isotonic saline volume loading observed in spontaneously hypertensive rats, and compared the findings with those in normotensive Wistar-Kyoto control rats.


METHODS
Wistar-Kyoto and spontaneously hypertensive rats were fed either a normal diet or one high in sodium chloride for 4 weeks and subjected to sinoaortic denervation. To evaluate the central gain of the cardiopulmonary baroreflex, electrical stimulation of the central portion of the cut vagus was used to provide a standardized stimulus that simulates activation of cardiac volume receptors. To evaluate central alpha 2-adrenoceptor regulation of renal sympathetic nerve activity, volume loading was performed in rats pretreated with intracerebroventricular guanabenz, which decreased the elevated basal values of arterial pressure, heart rate and renal sympathetic nerve activity in spontaneously hypertensive rats towards those of Wistar-Kyoto rats.


RESULTS
Vagal stimulation produced frequency-dependent decreases in arterial pressure, heart rate and renal sympathetic nerve activity that were similar in the two strains of rats on either a normal- or a high-sodium diet. Volume administration in rats pretreated with guanabenz resulted in similar decreases in renal sympathetic nerve activity in the two strains of rats.


CONCLUSIONS
The mechanism of exaggerated renal sympathoinhibition during volume administration in spontaneously hypertensive rats involves an alteration in central alpha 2-adrenoceptor regulation of renal sympathetic nerve activity.
Rodriguez-Martinez
M
M
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242, USA.
Jones
S Y
SY
DiBona
G F
GF
D000818:Animals; D017704:Baroreflex / Q000502:physiology; D001810:Blood Volume / Q000187:drug effects*; D001921:Brain / Q000503:physiopathology; D004525:Efferent Pathways / Q000503:physiopathology; D006143:Guanabenz / Q000494:pharmacology; D007276:Injections, Intraventricular; D007668:Kidney / Q000294:innervation*; D008297:Male; D009433:Neural Inhibition / Q000502:physiology*; D010952:Plasma Substitutes / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology*; D011921:Rats, Inbred WKY; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D012965:Sodium Chloride / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D010952:Plasma Substitutes; D011942:Receptors, Adrenergic, alpha; D012965:Sodium Chloride; D006143:Guanabenz