Lead-induced hypertension is associated with impaired nitric oxide bioactivity

Abstract

This study was designed to discern whether alteration in baroreceptor sensitivity, renin-angiotensin system, calcium coupling mechanism or nitric oxide activity is/are responsible for lead-induced hypertension. The effect of exposure to 100 ppm of lead in tap water for 4 months on mean arterial pressure (MAP) and heart rate (HR) were investigated in male Sprague-Dawley. After the treatment period, femoral artery and vein were cannulated for blood pressure measurement and infusion of drugs respectively. Baroreceptor sensitivity was determined through bilateral carotid occlusion (BCO), while the effect of angiotensin II, calcium channel and nitric oxide were blocked by infusing 1 mg/kg-body weight of captopril, 10 mg/kg-body weight of diltiazem and 30 mg/kg-body weight of L-NAME respectively. Exposure to chronic lead led to an increase (P<0.0002) in mean arterial pressure of lead-treated rats {LR} (117.2 ± 3.5 mmHg, n=6) compared with controls {NR} (92.4 ± 3.5 mmHg, n=6), without any effect on the heart rate. This was associated with an increase (P<0.012) in peak MAP due to BCO but a lower (P<0.0035) change in MAP due to L-NAME infusion in LR compared with NR. However, there was similar baroreflex sensitivity and changes in MAP due to captopril and diltiazem infusions in both groups. Captopril infusion led to increase (P<0.025) in HR of LR compared with controls. Data suggested that depressed nitric oxide bioactivity may play an important role in the pathogenesis of lead-induced hypertension, while no alteration in baroreflex sensitivity was recorded, probably due to depressed action of angiotensin II on HR.

Keywords: Lead-induced hypertension, baroreflex sensitivity, nitric oxide, renin-angiotensin system

Nigerian Journal of Health and Biomedical Sciences Vol. 5 (2) 2006: 1-5