Role of Nitric Oxide in the Cardiovascular and Renal Systems

Abstract

The gasotransmitters are a family of gaseous signaling molecules which are produced endogenously and act at specific receptors to play imperative roles in physiologic and pathophysiologic processes. As a well-known gasotransmitter along with hydrogen sulfide and carbon monoxide, nitric oxide (NO) has earned repute as a potent vasodilator also known as endothelium-derived vasorelaxant factor (EDRF). NO has been studied in greater detail, from its synthesis and mechanism of action to its physiologic, pathologic, and pharmacologic roles in different disease states. Different animal models have been applied to investigate the beneficial effects of NO as an antihypertensive, renoprotective, and antihypertrophic agent. NO and its interaction with different systems like the renin–angiotensin system, sympathetic nervous system, and other gaseous transmitters like hydrogen sulfide are also well studied. However, links that appear to exist between the endocannabinoid (EC) and NO systems remain to be fully explored. Experimental approaches using modulators of its synthesis including substrate, donors, and inhibitors of the synthesis of NO will be useful for establishing the relationship between the NO and EC systems in the cardiovascular and renal systems. Being a potent vasodilator, NO may be unique among therapeutic options for management of hypertension and resulting renal disease and left ventricular hypertrophy. Inclusion of NO modulators in clinical practice may be useful not only as curatives for particular diseases but also for arresting disease prognoses through its interactions with other systems.

Physiological regulation of reactive oxygen species in organisms based on their physicochemical properties

“…Research on the convoluted physicochemical properties of free radicals and NO is helpful in revealing the dual roles of RNS in redox signalling and oxidative stress. NO, a vital signalling molecule, has been well reviewed in previous reports, but it is striking to clarify how NO communicates information to achieve signal transduction. In organisms, NO is generated through a nitric oxide synthase (NOS) catalyzed reaction of L‐arginine.…”

Ethyl Rosmarinate Prevents the Impairment of Vascular Function and Morphological Changes in L-NAME-Induced Hypertensive Rats

“…Endothelial dysfunction is one of the critical factors associated with the progression of hypertension. It is characterized by the decrease in NO-induced vasodilation and the lowering of the expression of eNOS in the endothelial cytoplasm [1,3,19]. The use of L-NAME is well established in animal models to mimic hypertension in humans.…”

Diseases Related to Types of Free Radicals

“…The specific markers of ROS are altered to inflammation that enhanced the risk of atherosclerosis by diabetes [72]. The vasodilator activity of NO may be unique among therapeutic options for management of hypertension, renal disease, and left ventricular hypertrophy [73].…”