From the Department of Internal Medicine, University of Texas Medical
Branch, Galveston, Texas.
Correspondence to Donna H. Wang, MD, Department of Internal Medicine, 8.104 Medical Research Bldg, University of Texas Medical Branch, Galveston, TX 77555-1065. E-mail dwang{at}utmb.edu
Abstract—To test the novel
hypothesis that neonatal degeneration of capsaicin-sensitive sensory
nerves causes the rat to respond to a salt load with a significant and
sustained rise in blood pressure, newborn Wistar rats were given 50
mg/kg capsaicin subcutaneously on the 1st and 2nd day of life. Control
rats were treated with vehicle. Immediately after the weanling period,
male rats were divided into 4 groups and fed different sodium diets for
2 weeks: capsaicin pretreatment plus high sodium diet (4%, CAP-HS),
capsaicin plus normal sodium diet (0.5%, CAP-NS), control plus high
sodium diet (CON-HS), and control plus normal sodium diet (CON-NS).
Both tail-cuff systolic blood pressure and mean
arterial pressure with anesthesia were
significantly higher in CAP-HS than in CAP-NS, CON-HS, and CON-NS
(P<0.05), but they were not different among the latter
3 groups. Radioimmunoassay revealed that levels of calcitonin
gene–related peptide in dorsal root ganglia were markedly decreased by
capsaicin treatment (P<0.05). Twenty-four-hour urine
volume and urine sodium excretion were significantly lower in CAP-HS
than in CON-HS but were higher in CAP-HS and CON-HS compared with
CAP-NS and CON-NS (P<0.05). Urine potassium excretion
was not different among the 4 groups. Thus, this study provides the
first evidence that neonatal degeneration of capsaicin-sensitive
sensory nerves renders the rat salt-sensitive in terms of blood
pressure regulation. Furthermore, our data suggest that neonatal
capsaicin treatment may impair renal sodium and water excretion
responses to high sodium intake. This model will provide a novel
experimental paradigm for exploring underlying molecular mechanisms
linked with salt-sensitive hypertension and sensory nerve
function.
© 1998 American Heart Association, Inc.
Scientific Contributions
Rapid Communication: Salt-Sensitive Hypertension Induced by Sensory Denervation
Introduction of a New Model
Key Words: capsaicin • sodium, dietary • nervous system • hypertension • renal circulation
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