What question did this study set out to answer?

To determine the contribution of the renin-angiotensin system, endothelin, adrenergic receptors, and eicosanoids to the acute hypertensive response caused by nitric oxide synthase inhibition.

May 1, 1994Journal of Cardiovascular Pharmacology

Endogenous Vasoactive Systems and the Pressor Effect of Acute N ω-Nitro-L-Arginine Methyl Ester Administration

Q: What is the clinical evidence from this study?

Study design: Other. Intervention: N omega-nitro-L-arginine methyl ester (L-NAME) vs. Various pretreatments (losartan, enalapril, DOCA-salt, binephrectomy, low-sodium diet, prazosin, phosphoramidon, indomethacin, SQ 29548, nicardipine). Primary outcome: Increase in mean arterial pressure (MAP).

Q: What does this research mean for the field?

The acute pressor effect of L-NAME is mediated in part by cyclooxygenase-dependent products and endothelin, but not by the renin-angiotensin system. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Key result

The acute pressor effect of L-NAME (38 +/- 4 mm Hg increase in MAP) is mediated in part by cyclooxygenase-dependent products and endothelin, but not by the renin-angiotensin system.

Why the study?

What endogenous vasoactive systems mediate the pressor effect of acute L-NAME administration in anesthetized Wistar rats?

Population

Anesthetized Wistar rats

Comparison

Acute N omega-nitro-L-arginine methyl ester… vs Nonpretreated animals

Design

Preclinical

Follow-up

acute

Authors

NNNafrialdi NafrialdiUniversity of Indonesia BJBernard JoverCentre National de la Recherche Scientifique AMA MimranGeneral / Preventive / Lipids

Discussion

Member takes

Implication

May guide targeted research on endothelin and prostaglandins in endothelial dysfunction; leaves open applicability to clinical hypertension.

Key Points

To determine the contribution of the renin-angiotensin system, endothelin, adrenergic receptors, and eicosanoids to the acute hypertensive response caused by nitric oxide synthase inhibition.
Administered acute L-NAME infusions (200 µg/kg/min) to anesthetized Wistar rats to measure changes in mean arterial pressure.
Evaluated regulatory pathways through chronic suppression of the renin-angiotensin system (via losartan, enalapril, DOCA-salt, binephrectomy, or low-sodium diet) or targeted blockade of adrenergic, endothelin, eicosanoid, and calcium channels.
Baseline L-NAME infusion produced an increase in mean arterial pressure of 38 ± 4 mm Hg in nonpretreated rats.
Chronic renin-angiotensin system suppression by losartan, enalapril, or DOCA did not alter the pressor response to L-NAME, though binephrectomy caused moderate blunting.
Pretreatment with a low-sodium diet, phosphoramidon, SQ 29548, or indomethacin attenuated the pressor response by approximately 25%, whereas nicardipine blunted the response by 74%.

Structured PICO

What endogenous vasoactive systems mediate the pressor effect of acute L-NAME administration in anesthetized Wistar rats?

Population

Anesthetized Wistar rats used to assess the pressor response to acute L-NAME administration.

Intervention

Acute N omega-nitro-L-arginine methyl ester (L-NAME) administration (200 micrograms/kg/min) with various pretreatments (losartan, enalapril, DOCA-salt, binephrectomy, low-sodium diet, prazosin, phosphoramidon, indomethacin, SQ 29548, nicardipine)

Comparator

Nonpretreated animals

Outcome

Increase in mean arterial pressure (MAP)surrogate

The acute pressor effect of L-NAME in rats is mediated partly by cyclooxygenase-dependent products and endothelin, but not by the renin-angiotensin system.

Cite This Study

Nafrialdi et al. (1994) studied this question. N omega-nitro-L-arginine methyl ester (L-NAME) vs. Various pretreatments (losartan, enalapril, DOCA-salt, binephrectomy, low-sodium diet, prazosin, phosphoramidon, indomethacin, SQ 29548, nicardipine) was evaluated on Increase in mean arterial pressure (MAP). The acute pressor effect of L-NAME (38 +/- 4 mm Hg increase in MAP) is mediated in part by cyclooxygenase-dependent products and endothelin, but not by the renin-angiotensin system.

synapsesocial.com/papers/6a1ec40dbf2a5d44faaf4abe https://doi.org/10.1097/00005344-199405000-00011

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Implication

May guide targeted research on endothelin and prostaglandins in endothelial dysfunction; leaves open applicability to clinical hypertension.

Endogenous Vasoactive Systems and the Pressor Effect of Acute N ω-Nitro-L-Arginine Methyl Ester Administration

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Endogenous Vasoactive Systems and the Pressor Effect of Acute N ω-Nitro-L-Arginine Methyl Ester Administration

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Also Consider