Induction of heme oxygenase produces load-independent cardioprotective effects in hypertensive rats

Although heme oxygenase (HO) has been suggested to be involved in the regul ation of cardiovascular function through production of carbon monoxide (CO) , the pathophysiological significance of HO in hypertensive organ damage re mains unknown. We examined the effects of inducing HO-1 mRNA by stannous ch loride (SnCl2) on cardiac hypertrophy in stroke-prone spontaneously hyperte nsive rats (SHR-SP/Izm). Chronic administration of SnCl2 resulted in a sign ificant decrease in left ventricular (LV) weight/body weight ratio and LV b rain natriuretic peptide (BNP) mRNA levels as a marker of cardiac hypertrop hy and a significant increase in LV HO-1 mRNA levels and LV cGMP contents i n SHR-SP/Izm, while there was no significant change in systemic blood press ure. These results provide the first evidence that induction of HO in the h eart attenuates cardiac hypertrophy in load-independent mechanism in geneti cally hypertensive rats.