This review highlights the early research establishing nitric oxide as a key signaling molecule in cardiovascular function and discusses drugs that interfere with the NO signaling cascade.
In retrospect, basic research in the fields of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) during the past two decades appears to have followed a logical course, beginning with the findings that NO and cGMP are vascular smooth muscle relaxants, that nitroglycerin relaxes smooth muscle by metabolism to NO, progressing to the discovery that mammalian cells synthesize NO, and finally the revelation that NO is a neurotransmitter mediating vasodilation in specialized vascular beds. A great deal of basic and clinical research on the physiologic and pathophysiologic roles of NO in cardiovascular function has been conducted since the discovery that endothelium-derived relaxing factor (EDRF) is NO. The new knowledge on NO should enable investigators in this field to develop novel and more effective therapeutic strategies for the prevention, diagnosis, and treatment of numerous cardiovascular disorders. The goal of this review was to highlight the early research that led to our current understanding of the pathophysiologic role of NO in cardiovascular medicine. Furthermore, we discussed the possible mechanism of some drugs interfering with NO signaling cascade.
Ignarro et al. (Wed,) conducted a review in Cardiovascular disorders. Nitric oxide and drugs interfering with NO signaling cascade was evaluated. This review highlights the early research establishing nitric oxide as a key signaling molecule in cardiovascular function and discusses drugs that interfere with the NO signaling cascade.
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