NO donors induce vascular relaxation by different cellular mechanisms in hypertensive and normotensive rats

Nitric Oxide as a Central Molecule in Hypertension: Focus on the Vasorelaxant Activity of New Nitric Oxide Donors

“…NO is highly reactive and its relatively short half-life means that it is responsible for mediating many processes, such as endothelium-dependent vasorelaxation, platelet adhesion and aggregation, relaxation of the corpus cavernosum of the human penis, and regulation of baseline BP [41][42][43]. It also modulates inflammatory or anti-inflammatory reactions that help to regulate the numerous processes of immunological and cardiovascular systems [44,45].…”

“…Regarding the properties of NO, a large number of NO donor compounds have emerged as potential agents for the treatment of the aforementioned diseases, able to exploit the wide variety of biological functions. Thus, pharmacological aspects of NO are constantly under study [45,[123][124][125][126][127]. Furthermore, administration of drugs that mimic the effect of NO on the organism is an attractive proposal, since this is a pharmacological alternative that could reverse and/or prevent cardiovascular disorders [125].…”

“…In view of the promotion of such actions by NO and the side-effects of NO donor drugs, such as nitrate-tolerance in clinical settings, some research groups, including ours, have been studying metal-based NO donor drugs that act on the cardiovascular system, with a potential action to induce vasorelaxant activity and BP and decrease oxidative stress, among other effects [45,[243][244][245][246][247][248].…”

Artemisinin Improves Acetylcholine-Induced Vasodilatation in Rats with Primary Hypertension

“…5 Sodium nitroprusside, an NO donor that directly induces vascular smooth muscle cell relaxation, is commonly used to evaluate endothelium-independent relaxation. 6 In our previous studies, we demonstrated that ACh-induced vasodilatation of three important small arteries, the mesenteric artery, pulmonary artery and coronary artery, of spontaneously hypertensive rats (SHRs) was significantly attenuated. 7,8 Subsequently, elevated peripheral and pulmonary vascular resistance increases the risk of insufficient blood supply to the myocardium and the risk of systemic and pulmonary hypertension.…”

RuBPY decreases intracellular calcium by decreasing influx and increasing storage

“…[2][3][4][5][6] One of them, cis-[Ru(bpy)2 (py)NO2](PF6) (RuBPY), presents a nitrite in its moiety and has been shown to induce vascular relaxation in aorta, 4 coronary, basilar and mesenteric resistance arteries. 7,8 The administration of RuBPY in hypertensive rats evoked a hypotensive effect with no increase in heart rate. 8 These effects were mediated by the release of NO and activation of soluble guanylyl cyclase (sGC), potassium channels sensitive to tetraethylammonium (TEA), and membrane hyperpolarization.…”