Endothelium-derived nitric oxide is not altered in vivo in fructose-hypertensive rats (part 7). DISCUSSION

fructose-hypertensive rats (part 7). DISCUSSION

The primary finding of this study is that neither impairment of nitric oxide-mediated relaxation nor enhanced sensitivity to noradrenaline-induced contraction can be identified as the cause of elevated blood pressure in fructose-hypertensive rats in vivo. No significant difference was noted in the hypotensive response to ACh between the control and fructose-hypertensive groups either before or after administration of L-NAME. These findings, however, do not negate the role of nitric oxide in mediating ACh vasodilatory responses. A study by Rees et al demonstrated that a bipha-sic hypotensive response to ACh exists, whereby there is an initial, rapidly occurring vasodilation, resistant to nitric oxide synthesis blockade, followed by a delayed response that is susceptible to N -monomethyl-L-arginine. Similar findings have been reported by other groups , and it is postulated that the delayed vasodilation may be the nitric oxide-mediated component of the ACh response.The present study observed similar results in that a two-phase vasodilator response to ACh is present in doses given before L-NAME, while post-L-NAME injections resulted in only the initial, rapid depressor response. Strikingly, we have found that the delayed response is replaced with a transient vasoconstriction, an observation that is in agreement with findings from human studies as well. You can be sure this pharmacy will offer the finest quality drugs you need, so buying prozac antidepressant will always be safe and very pleasant for you as a customer and patient.



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