(Hypertension. 1999;33:499-503.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Antihypertensive Mechanisms Underlying a Novel Salt-Sensitive Hypertensive Model Induced by Sensory Denervation
From the Department of Internal Medicine, University of Texas Medical Branch, Galveston.
Correspondence to Donna H. Wang, MD, Department of Internal Medicine, 8.104 Medical Research Building, University of Texas Medical Branch, Galveston, TX 77555-1065. E-mail dwang{at}utmb.edu
Abstract—A novel model of
hypertension recently developed in our laboratory shows that neonatal
degeneration of capsaicin-sensitive sensory nerves renders a rat
responsive to a salt load with a significant rise in blood pressure. To
determine the role of the renin-angiotensin system and the
sympathetic nervous system in the development of hypertension in this
model, newborn Wistar rats were given capsaicin 50 mg/kg SC on the
first and second days of life. Control rats were treated with vehicle.
After they were weaned, male rats were divided into 6 groups and
subjected to the following treatments for 2 weeks: control+high sodium
diet (4%) (CON-HS), capsaicin+normal sodium diet (0.5%) (CAP-NS),
capsaicin+high sodium diet (CAP-HS), capsaicin+high sodium
diet+losartan (10 mg/kg per day) (CAP-HS-LO), capsaicin+high
sodium diet+prazosin (3 mg/kg per day) (CAP-HS-PR), and capsaicin+high
sodium diet+hydralazine (10 mg/kg per day) (CAP-HS-HY). Levels
of calcitonin gene–related peptide in dorsal root ganglia were
decreased by capsaicin treatment (P<0.05). Both
tail-cuff systolic blood pressure and mean arterial
pressure were higher in CAP-HS and CAP-HS-PR than in CON-HS, CAP-NS,
CAP-HS-LO, and CAP-HS-HY (P<0.05). The 24-hour urinary
volume and sodium excretion were increased when a high sodium diet was
given (P<0.05), but they were lower in CAP-HS,
CAP-HS-LO, CAP-HS-PR, and CAP-HS-HY than in CON-HS
(P<0.05). Urinary potassium excretion was not different
among all 6 groups. We conclude that blockade of the
angiotensin type 1 receptor with losartan but not
antagonism of the 
1-adrenoreceptor with
prazosin prevents the development of salt-sensitive hypertension
induced by sensory denervation. Sensory denervation impairs urinary
sodium and water excretion in response to a high sodium intake,
regardless of blood pressure, suggesting that sensory innervation plays
a direct role in regulating the natriuretic response to
sodium loading.
Key Words: capsaicin • sodium, dietary • innervation, sensory • hypertension, salt-sensitive • renal circulation
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