In contrast to our present findings in vivo, previous in vitro studies done in the fructose-hypertensive model have suggested a role for nitric oxide dysfunction in these rats . This discrepancy suggests that the in vitro outcomes cannot be extrapolated to in vivo studies in this model. Indeed, compensatory homeostatic mechanisms that exist in vivo, such as the baroreceptor reflex, cannot be mimicked ex vivo. As well, the in vitro model lacks the neurohumoral influences that are present in vivo.As mentioned previously, if neither nitric oxide nor noradrenaline is responsible for the in vivo development of hypertension in the fructose-hypertensive model, a third, distinct factor may be involved. In this regard, we previously demonstrated that arteries from fructose-hypertensive rats exhibit increased levels and altered reactivity to the potent vasoconstrictor endothelin-1 (ET-1) . Furthermore, chronic ET-1 receptor blockade (with Bosentan, F Hoffmann LaRoche Ltd, Basel, Switzerland) causes marked and sustained decreases in blood pressure in these rats . This suggests that an alteration in the ET-1 pathway may be important in the development of fructose-induced hypertension in vivo. Additional studies from our group have demonstrated that hyperinsulinemia in fructose-hypertensive rats may exaggerate pressor responses via increased release or synthesis of ET-1 (personal communication). Best quality drugs are available at the best pharmacy that you can start shopping with right now whenever you need Buy Antidepressants Online, never having to doubt the choice made or the quality of the drug you get.
In summary, data from this study suggest that alterations in the nitric oxide pathway may not be important in the development of fructose-induced hypertension in vivo.