Key result
ETA/ETB antagonist PD 145 065 abolishes ~85% of the L-NAME-induced pressor response.
Why the study?
Does endothelin receptor blockade prevent acute hypertension induced by nitric oxide synthase inhibition in conscious rats?
Population
Conscious male Sprague-Dawley rats, previously instrumented with aortic and venous catheters
Comparison
ETA/ETB receptor antagonist PD145 065… vs Control conditions, or blockade of…
Design
Preclinical
Follow-up
Acute
Authors
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Endothelin blockade largely prevents acute L-NAME hypertension in rats; hypothesis-generating for human NOS inhibition mechanisms.
Does endothelin receptor blockade prevent acute hypertension induced by nitric oxide synthase inhibition in conscious rats?
Effect estimate: approximately 85% reduction
Acute hypertension following nitric oxide synthase inhibition is primarily mediated by increased endothelin vasoconstriction rather than the renin-angiotensin system, α1-adrenoceptors, or vasopressin.
Banting et al. (1996) studied Acute hypertension after nitric oxide synthase inhibition. ETA/ETB receptor antagonist PD145 065 vs. Control conditions / other antagonists was evaluated on Pressor response to L-NAME (approximately 85% reduction). Treatment with the ETA/ETB receptor antagonist PD 145 065 before and during acute nitric oxide synthase blockade abolished approximately 85% of the L-NAME-induced pressor response.
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