Key result
Metabolic syndrome in obese Zucker rats was associated with a ~20% reduction in skeletal muscle post-capillary venular density and blunted venular dilatation compared to lean controls.
In a rat model of metabolic syndrome, post-capillary and collecting venular dilator reactivity in skeletal muscle is impaired due to loss of nitric oxide bioavailability and increased oxidant stress.
Suggests microvascular venous dysfunction may contribute to metabolic syndrome complications; leaves open whether targeting nitric oxide.
Key points With the development of the metabolic syndrome, both post‐capillary and collecting venular dilator reactivity within the skeletal muscle of obese Zucker rats (OZR) is impaired. The impaired dilator reactivity in OZR reflects a loss in venular nitric oxide and PGI2bioavailability, associated with the chronic elevation in oxidant stress. Additionally, with the impaired dilator responses, a modest increase in adrenergic constriction combined with an elevated thromboxane A2production may contribute to impaired functional dilator and hyperaemic responses at the venular level. For the shift in skeletal muscle venular function with development of the metabolic syndrome, issues such as aggregate microvascular perfusion resistance, mass transport and exchange within with capillary networks, and fluid handling across the microcirculation are compelling avenues for future investigation. Abstract While research into vascular outcomes of the metabolic syndrome has focused on arterial/arteriolar and capillary levels, investigation into venular function and how this impacts responses has received little attention. Using thein situcremaster muscle of obese Zucker rats (OZR; with lean Zucker rats (LZR) as controls), we determined indices of venular function. At ∼17 weeks of age, skeletal muscle post‐capillary venular density was reduced by ∼20% in LZRvs. OZR, although there was no evidence of remodelling of the venular wall. Venular tone at ∼25 μm (post‐capillary) and ∼75 μm (collecting) diameter was elevated in OZRvs. LZR. Venular dilatation to acetylcholine was blunted in OZRvs. LZR due to increased oxidant stress‐based loss of nitric oxide bioavailability (post‐capillary) and increased α1‐ (and α2‐) mediated constrictor tone (collecting). Venular constrictor responses in OZR were comparable to LZR for most stimuli, although constriction to α1‐adrenoreceptor stimulation was elevated. In response to field stimulation of the cremaster muscle (0.5, 1, 3 Hz), venular dilator and hyperaemic responses to lower frequencies were blunted in OZR, but responses at 3 Hz were similar between strains. Venous production of TxA2was higher in OZR than LZR and significantly higher than PGI2production in either following arachidonic acid challenge. These results suggest that multi‐faceted alterations to skeletal muscle venular function in OZR may contribute to alterations in upstream capillary pressure profiles and the transcapillary exchange of solutes and water under conditions of metabolic syndrome.
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Lemaster et al. (2017) studied Metabolic syndrome. Metabolic syndrome (Obese Zucker phenotype) vs. Lean Zucker rats was evaluated on Skeletal muscle post-capillary venular density and reactivity. Metabolic syndrome in obese Zucker rats was associated with a ~20% reduction in skeletal muscle post-capillary venular density and blunted venular dilatation compared to lean controls.
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