What is the clinical evidence from this study?

Study design: Other. Intervention: N(G)-nitro-L-arginine. Primary outcome: Contractions induced by KCl.

What question did this study set out to answer?

To determine whether vascular smooth muscle in rat aorta constitutively expresses brain-type or muscle-type isoforms of nitric oxide synthase I.

November 1, 1999Arteriosclerosis Thrombosis and Vascular BiologyOpen Access

Potential Functional Significance of Brain-Type and Muscle-Type Nitric Oxide Synthase I Expressed in Adventitia and Media of Rat Aorta

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Key result

In endothelium-denuded rat aortic rings, contractions induced by KCl were markedly increased in the presence of the NOS inhibitor N(G)-nitro-L-arginine.

Population

Rat aorta (endothelium-denuded and adventitia-removed)

Comparison

N(G)-nitro-L-arginine (NOS inhibitor) vs Control (absence of NOS inhibitor)

Design

Preclinical

Authors

PSPetra SchwarzUniversity of Zurich HKHartmut KleinertUniversity Health Network UFUlrich FörstermannVascular Medicine

Discussion

Member takes

Implication

Highlights non-endothelial NOS contribution to rat vascular tone; leaves open relevance to human vessels.

Key Points

To determine whether vascular smooth muscle in rat aorta constitutively expresses brain-type or muscle-type isoforms of nitric oxide synthase I.
Assessed mRNA and protein expression using RT-PCR, RNase protection assays, Western blotting, and immunohistochemistry in intact, endothelium-denuded, and adventitia-denuded rat aorta.
Evaluated vascular tone by measuring KCl-induced contractions in endothelium-denuded rat aortic rings in the presence and absence of the nitric oxide synthase inhibitor N(G)-nitro-L-arginine.
Endothelium-denuded rat aorta expressed brain-type NOS I (160 kd) alongside lower levels of the muscle-type splice variant microNOS I (164 kd), localized within the adventitia and medial smooth muscle.
Removal of the adventitia markedly reduced but did not eliminate NOS I and microNOS I mRNA in the aortic medial layer.
Inhibition of NOS activity with N(G)-nitro-L-arginine significantly augmented KCl-induced contractions in aortic rings lacking an endothelial layer.

Structured PICO

Population

Rat aorta (endothelium-denuded and adventitia-removed)

Intervention

N(G)-nitro-L-arginine (NOS inhibitor)

Comparator

Control (absence of NOS inhibitor)

Outcome

Expression of NOS I and microNOS I mRNA and protein; functional contractile response to KClsurrogate

Brain-type NOS I and microNOS I are expressed in the adventitia and media of rat aorta, potentially serving as a functional backup to endothelial NOS III.

Cite This Study

Schwarz et al. (1999) studied this question. N(G)-nitro-L-arginine was evaluated on Contractions induced by KCl. In endothelium-denuded rat aortic rings, contractions induced by KCl were markedly increased in the presence of the NOS inhibitor N(G)-nitro-L-arginine.

synapsesocial.com/papers/6a9747b14ae776b3202700cc https://doi.org/10.1161/01.atv.19.11.2584

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Potential Functional Significance of Brain-Type and Muscle-Type Nitric Oxide Synthase I Expressed in Adventitia and Media of Rat Aorta

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Potential Functional Significance of Brain-Type and Muscle-Type Nitric Oxide Synthase I Expressed in Adventitia and Media of Rat Aorta

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider