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Growth-related changes in the influence of nitric oxide on arteriolar tone
1Department of Physiology, West Virginia University School of Medicine, Morgantown, West Virginia 26506-9229, USA.
Insights
Juvenile growth in rats involves significant changes in arteriolar tone, influenced by nitric oxide (NO) and prostaglandins. While vasodilator prostaglandins consistently affect tone, NO
Area of Science:
- Physiology
- Vascular Biology
- Developmental Biology
Background:
- Arteriolar tone regulation is crucial for blood flow distribution.
- The roles of nitric oxide (NO) and prostaglandins in vascular tone during growth are not fully understood.
Purpose of the Study:
- To investigate age-related changes in the influence of NO and prostaglandins on arteriolar tone during juvenile growth in rats.
- To determine how basal and stimulated release of vasodilators affects arteriolar function across different developmental stages.
Main Methods:
- In vivo microscopy was used to examine proximal arterioles in the spinotrapezius muscle of rats at three age groups: weanling (4-5 wk), juvenile (7-8 wk), and mature (11-12 wk).
- Pharmacological inhibition of NO synthase (using N(G)-monomethyl-L-arginine, L-NMMA) and cyclooxygenase (using meclofenamate) was employed to assess the contribution of these pathways to arteriolar tone.
- Responses to exogenous vasodilators (sodium nitroprusside, prostaglandin E(2)) and acetylcholine (ACh) were evaluated, along with the effects of flow-related shear stress.
Main Results:
- Arteriolar diameter and volume flow increased, while wall shear rate decreased with age from weaning to maturity.
- Basal nitric oxide (NO) activity influenced arteriolar tone in juvenile and mature rats, but not in weanling rats.
- Vasodilator prostaglandins exerted a constant influence on arteriolar tone across all age groups.
- Agonist-stimulated NO release was prominent in weanling and juvenile rats, decreasing in mature rats, where cyclooxygenase products also contributed to ACh-induced dilation.
Conclusions:
- Arteriolar smooth muscle responsiveness to NO and prostaglandins does not change during juvenile growth.
- Basally released vasodilator prostaglandins consistently modulate arteriolar tone throughout juvenile development.
- Basal NO activity becomes important for arteriolar tone regulation in juvenile and mature rats, while agonist-stimulated NO release declines with maturation.
Abstract:
This study was designed to determine whether juvenile growth is accompanied by changes in the local influence of nitric oxide (NO) or prostaglandins on arteriolar tone. In vivo microscopy was used to study proximal arterioles in the spinotrapezius muscle of rats 4-5 wk (weanling), 7-8 wk (juvenile), and 11-12 wk (mature) of age. From 4 to 12 wk of age, arterioles underwent an increase in resting diameter (from 31 +/- 2 to 49 +/- 2 micrometer) and volume flow (from 7 +/- 1 to 10 +/- 1 nl/s) but a decrease in resting wall shear rate (from 1,901 +/- 150 to 748 +/- 50 s(-1)). NO synthase inhibition with N(G)-monomethyl-L-arginine (L-NMMA) had no effect on arteriolar diameters in weanling rats but reduced diameters by 14 +/- 4% in juvenile rats and by 13 +/- 4% in mature rats. Cyclooxygenase inhibition with meclofenamate reduced arteriolar diameters by a similar amount (13 +/- 4 to 18 +/- 3%) in all age groups. There were no age-related differences in arteriolar responsiveness to locally applied sodium nitroprusside or prostaglandin E(2). Arteriolar responsiveness to ACh was also similar in all groups, but the L-NMMA-sensitive portion of this response was smaller in mature rats than in weanling rats. Elevation of flow-related shear stress caused arteriolar dilation in juvenile rats but not in weanling rats. These findings suggest that arteriolar smooth muscle responsiveness to NO or prostaglandins does not change during juvenile growth and that basally released vasodilator prostaglandins exert a constant influence on arteriolar tone throughout this period. Basal NO activity also modulates arteriolar tone in juvenile and mature rats but not in weanling rats. In contrast, agonist-stimulated NO release is prominent in weanling and juvenile rats but somewhat decreased in mature rats, where cyclooxygenase products also contribute to ACh induced dilation.