Endothelium-derived nitric oxide is not altered in vivo in fructose-hypertensive rats (part 8) / generic prozac
In vitro work in mesenteric arteries suggests that this secondary constrictor response may be due to the unmasking of endothelium-derived contracting factors previously hidden by the ACh-mediated nitric oxide release . Therefore, while no change in response amplitude was observed when comparing pre- and post-L-NAME doses of ACh, shifts in phasic response have been noted, implying that nitric oxide is indeed a key mediator of the ACh response. Your drugs could be a lot cheaper and your treatment could be still as safe and efficient as always: all you need to do to get your generic prozac is shop at the best pharmacy offering its services to you right here right now.
It is important to note that following injection of L-NAME, further administration of ACh doses resulted in an increased hypotensive response. Similar results have been documented in a previous study by Bryant et al , and several mechanisms for this response have been postulated. In their study, chronic but not acute L-NAME (10 ^mol/kg) enhanced ACh responses in Wistar rats. The authors suggested that either increased guanylyl cyclase sensitivity or increased release of vasodilators (other than nitric oxide) may be a possible explanation for this phenomenon.Because vasodilator responses to any drug depend on the initial blood pressure, it is possible that this exaggerated response is secondary to an increase in resting pressure occurring upon administration of L-NAME. The above mentioned findings suggest the possibility that factors distinct from nitric oxide play a role in modulating endothelial dysfunction in fructose-hypertensive rats.