Key result
Inhibition of nitric oxide synthesis with L-NMMA or L-NAME attenuated the vasodepressor response by ~40% and potentiated the pressor response to ET-1 by 100-180% in conscious rats.
Why the study?
Does inhibition of nitric oxide synthesis alter the effects of endothelin-1 on blood pressure and microvascular permeability in conscious rats?
Population
Conscious rats
Comparison
Intravenous administration of NO synthesis… vs Noradrenaline infusion followed by endothelin-1…
Design
Preclinical
Authors
Loading...
Endogenous NO modulates ET-1 hemodynamic effects in rats; hypothesis-generating for human endothelial regulation.
Does inhibition of nitric oxide synthesis alter the effects of endothelin-1 on blood pressure and microvascular permeability in conscious rats?
Endogenous nitric oxide partially mediates the vasodepressor effect, attenuates the vasopressor action, and modulates the microvascular permeability effects of endothelin-1 in conscious rats.
Filep et al. (1993) studied Healthy conscious rats. NO synthesis inhibitors (L-NMMA or L-NAME) and ET-1 vs. Noradrenaline infusion was evaluated on Mean arterial blood pressure and microvascular permeability. Inhibition of nitric oxide synthesis with L-NMMA or L-NAME attenuated the vasodepressor response by ~40% and potentiated the pressor response to ET-1 by 100-180% in conscious rats.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: