Objective: To investigate the effect and mechanism of valsartan and felodipine extended release tablets (Plendil) on a novel salt-sensitive hypertensive rat induced by sensory denervation.
Methods: Newborn Wistar rats were given 50 mg/kg capsaicin subcutaneously on the 1st and 2nd day of life. Control rats were treated with vehicle solution (10%ethanol, 10%Tween 80 in saline). After weanling period (3 weeks), male rats were divided into 5 groups and subject to the following treatment for 4 weeks: control + high salt diet (4%, CON-HS), capsaicin + normal salt diet (0.5%, CAP-NS), capsaicin + high salt diet (CAP-HS), capsaicin + high salt diet + Valsartan (30 mg/kg per day, by orally) (CAP-HS-VAL), capsaicin + high salt diet + Plendil (30 mg/kg per day, by orally) (CAP-HS-PLE). Tail-cuff systolic blood pressure, body weight, intralymphocytic [Ca(2+)](i), plasma calcitonin gene-related peptide concentration ([CGRP]), angiotensin II concentration ([AngII]) and 24 hour water intake, urinary volume, urinary Na(+) and K(+) concentrations were examined.
Results: Tail-cuff systolic blood pressure and intralymphocytic [Ca(2+)](i) were lower in CAP-HS-VAL or CAP-HS-PLE group than those in CAP-HS group. Plasma [AngII] were higher in CAP-HS-VAL group than that in other groups. Tail-cuff systolic blood pressure were lower in CAP-HS-VAL group than that in CAP-HS-PLE group. Intralymphocytic [Ca(2+)](i) were lower in CAP-HS-PLE group than that in CAP-HS-VAL group. The 24 hour urine sodium excretion was higher in CAP-HS-PLE group than that in CAP-HS or CAP-HS-VAL group.
Conclusion: Valsartan or Plendil could prevent the development of salt-sensitive hypertension induced by sensory denervation and the overloading of intracellular [Ca(2+)](i), which indicated that salt-sensitive hypertension induced by sensory nerve degeneration might be related to renin-angiotensin-aldosterone system (RAAS) and the over loading intracellular [Ca(2+)](i), and might be more closely to RAAS.