What is the clinical evidence from this study?

Study design: Other. Intervention: L-monomethylarginine vs. Control conditions. Primary outcome: Peak increase in mean arterial pressure after administration of L-monomethylarginine.

What question did this study set out to answer?

This study aims to determine whether autonomic influences contribute to nitric oxide-mediated vasodilatation in rats.

January 1, 1998Journal of Hypertension

Lack of autonomic contributions to tonic nitric oxide-mediated vasodilatation in unanesthetized free-moving rats

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Key result

Tonic NO-dependent vasodilatation can normally be maintained in the unanesthetized unrestrained rat irrespective of autonomic or humoral adrenergic influences.

Why the study?

Does autonomic blockade or denervation alter the pressor response to nitric oxide synthesis inhibition in unanesthetized rats?

Population

Wistar-Kyoto rats (n = 65) with implanted chronic venous and arterial catheters

Comparison

Intravenous L-monomethylarginine under… vs Control conditions

Design

Preclinical

Authors

ARAlberto RadaelliAzienda Ospedaliera San Gerardo LMLuca MircoliFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico SPStefano PerliniHeart Failure & Transplant

Discussion

Member takes

Implication

Should not change clinical NO modulation; leaves open autonomic independence of tonic vasodilatation in humans.

Key Points

This study aims to determine whether autonomic influences contribute to nitric oxide-mediated vasodilatation in rats.
Implanted chronic venous and arterial catheters in Wistar-Kyoto rats (n=65) for measurements and drug administration.
Evaluated vasodilatation through blood pressure changes after NO synthesis inhibition with L-monomethylarginine.
Administered interventions including chemical sympathectomy, ganglionic blockade, and sino-aortic baroreceptor denervation.
Baseline mean arterial pressure was 100±4 mmHg in control rats and varied in other groups (73±3, 62±5, 105±10 mmHg).
Peak increase in arterial pressure post-L-monomethylarginine was 38±3 mmHg in control rats and varied in other groups (51±3, 50±6, 63±10 mmHg).
Significant reduction in catecholamines was observed in ganglion-blocked rats.

Structured PICO

Does autonomic blockade or denervation alter the pressor response to nitric oxide synthesis inhibition in unanesthetized rats?

Population

65 Wistar-Kyoto rats evaluated for tonic NO-dependent vasodilatation under control conditions, chemical sympathectomy, ganglionic blockade, and surgical denervation.

Intervention

Intravenous L-monomethylarginine (100 mg/kg bolus plus 0.5 mg/kg per min infusion for 30 min) under conditions of chemical sympathectomy by 6-hydroxy-dopamine, ganglionic blockade by hexamethonium, or surgical denervation of sino-aortic baroreceptors

Comparator

Control conditions (no autonomic blockade or denervation)

Outcome

Pressor response (peak increase in mean arterial pressure) to inhibition of NO synthesissurrogate

Tonic nitric oxide-dependent vasodilatation is maintained in unanesthetized rats independently of autonomic or humoral adrenergic influences.

Cite This Study

Radaelli et al. (1998) studied this question. L-monomethylarginine vs. Control conditions was evaluated on Peak increase in mean arterial pressure after administration of L-monomethylarginine. Tonic NO-dependent vasodilatation can normally be maintained in the unanesthetized unrestrained rat irrespective of autonomic or humoral adrenergic influences.

synapsesocial.com/papers/6a208e4388cfa9de494d1664 https://doi.org/10.1097/00004872-199816010-00010

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Lack of autonomic contributions to tonic nitric oxide-mediated vasodilatation in unanesthetized free-moving rats

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Lack of autonomic contributions to tonic nitric oxide-mediated vasodilatation in unanesthetized free-moving rats

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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