Elevating dietary salt exacerbates hyperpnea-induced airway obstruction inguinea pigs

Previous studies have indicated that increased dietary salt consumption wor sens postexercise pulmonary function in humans with exercise-induced asthma (EIA). It has been suggested that EIA and hyperpnea-induced airway obstruc tion (HIAO) in guinea pigs (an animal model of EIA) are mediated by similar mechanisms. Therefore, the purpose of this study was to determine whether altering dietary salt consumption also exacerbated HIAO in guinea pigs. Fur thermore, the potential pathway of action of dietary salt was investigated by blocking leukotriene (LT) production during HIAO in guinea pigs. Thirty- two male Hartley strain guinea pigs were split into two groups. One group ( n = 16) of animals ingested a normal-salt diet (NSD) for 2 wk; the other gr oup (n = 16) ingested a high-salt diet (HSD) for 2 wk. Thereafter, animals were anesthetized, cannulated, tracheotomized, and mechanically ventilated during a baseline period and during two dry gas hyperpnea challenges. After the first challenge, the animals were administered either saline or nordih ydroguaiaretic acid, a LT inhibitor. Bladder urine was analyzed for electro lyte concentrations and urinary LTE4. The HSD elicited higher airway inspir atory pressures (Ptr) than the NSD (P < 0.001) postchallenge. However, afte r infusion of the LT inhibitor and a second hyperpnea challenge, HIAO was b locked in both diet groups (P < 0.001). Nonetheless, the HSD group continue d to demonstrate slightly higher Ptr than the NSD group (P < 0.05). Urinary LTE4 excretion significantly increased in the HSD group compared with the NSD group within treatment groups. This study has demonstrated that dietary salt loading exacerbated the development of HIAO in guinea pigs and that L T release was involved in HIAO and may be moderated by changes in dietary s alt loading.