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Imbalances in the synthesis or in the bioavailability of nitric oxide (NO), the freely dif‐ fusible vasodilator, in myocardial endothelial cells were demonstrated to be crucial in the development of hypertension. Glucocorticoids (GCs) are widely used as immuno‐ modulators. One of the numerous side effects of GC therapy is hypertension arising from reduced release of the endothelium‐derived NO. GCs can modulate NO synthesis by targeting the genes involved in it, like nitric oxide synthase (NOS) and guanosine tri‐ phosphate (GTP) cyclohydrolase‐1 (GTPCH‐1). This chapter will give an overview on the impact of GCs on NO synthesis and signalling in animal models as well as in in vitro cell culture models. Moreover, strategies for preventing or neutralizing side effects of long‐term GC therapy will be discussed.

Role of Endothelial Nitric Oxide Synthase in Glucocorticoid- Induced Hypertension: An Overview of Experimental Data