Nitric oxide and carbon monoxide, collaborative and competitive regulators of hypertension

Blood pressure is one of the vital parameters of the body that is normally maintained in homeostasis by a complex multifactorial mechanism mediating constriction or dilation of vessels. Hypertension ensues when the responses to vasorelaxant signals become inefficient or vascular tissues are injured by inflammatory insults, leading to a decrease in arterial compliance and patency. This pathologic condition is best exemplified in atherosclerosis, one of the most common diseases afflicting humans worldwide. It is now generally recognized that nitric oxide (NO) and carbon monoxide (CO), two gaso-transmitters synthesized by inducible NO synthase (iNOS) and heme-oxygenase-1 (HO-1) respectively, play important roles in the compensatory regulation of the blood pressure during the development of hypertension. Nonetheless, much remains elusive regarding how these two stress systems interact with each other. Knowledge about their crosstalk will prove essential in the better understanding of the mechanisms underlying the disease process as well as in the design of potential therapeutic strategies. In this review, we provide an overview of the functions of NO and CO related to cardiovascular health. By dissecting the current findings in the literature, we discuss possible theories about the dynamics and interplay of their actions.