Protective Effect of Tubotaiwine on Cadmium-Induced Hypertension in Rats through Reduction in Arterial Stiffness and Vascular Remodeling

Humans are adversely affected by exposure to cadmium (Cd) as it induces oxidative stress which damages kidneys, bones pulmonary tissues, liver, cardiovascular, immune, reproductive systems and influences endocrine secretions. In the present study tubotaiwine treatment regulated systolic, diastolic and mean arterial blood pressure of the Cd exposed rats. Tubotaiwine significantly promoted vascular responsiveness to Phe, ACh and SNP and reversed Cd mediated decrease in eNOS and increase in iNOS expression. Treatment of the Cd exposed rats with tubotaiwine reduced number of smooth muscle cells, decreased collagen content and promoted content of elastin in aortic artery walls. Tubotaiwine treatment significantly suppressed Cd-induced increase in MMP-2 and MMP-9 in rat aortic artery tissues. Increase in O^2-, urinary nitrate/nitrite, MDA, carbonyl level and decrease in GSH production in rat blood and thoracic aorta tissues were effectively reversed by tubotaiwine treatment. Tubotaiwine treatment of the rats significantly reduced Cd-induced increase in blood, liver, heart and kidney tissue Cd content in dose dependent manner. Thus, tubotaiwine suppresses Cd induced hypertension in rats by reducing arterial stiffness, inhibition of oxidative stress and increasing vascular remodeling. Therefore, tubotaiwine has beneficial effect on Cd induced hypertension in rats and may be developed as a potential candidate for treatment of hypertension.

atherosclerosis; hypertension; metal poisoning; vascular remodeling.