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[Changes in the endotheliocyte activity of the coronary vessels under the influence of stress]
Insights
Stress increases coronary blood flow velocity in rats via nitric oxide (NO) released from endothelium. Blocking NO or damaging endothelium abolished this effect, highlighting NO's crucial role.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Nitric Oxide Signaling
Background:
- Stress can impact cardiovascular function, including coronary blood flow.
- The role of endothelial-derived nitric oxide (NO) in mediating stress responses in the coronary vasculature is not fully understood.
Purpose of the Study:
- To investigate the effect of saponin and nitric oxide (NO) blockade on coronary endothelium in rats under stress.
- To determine the contribution of NO to the stress-induced increase in coronary blood flow velocity.
Main Methods:
- Rats were subjected to a 6-hour stress protocol.
- Effects of saponin and NG-monomethyl-L-arginine (a NO synthase inhibitor) on coronary endothelium were assessed.
- Coronary blood flow velocity, index of autoregulation, and its efficiency were measured.
- L-arginine was administered to assess its preventative effect against NO blockade.
Main Results:
- Stress induced an increase in coronary blood flow velocity.
- Endothelial damage and NO blockade abolished the stressor-induced increase in coronary blood flow velocity.
- The index and efficiency of autoregulation remained unchanged.
- L-arginine prevented the inhibitory effect of NG-monomethyl-L-arginine on coronary flow.
Conclusions:
- The post-stressor increase in coronary blood flow is mediated by nitric oxide released from coronary endotheliocytes.
- Nitric oxide plays a significant role in regulating coronary blood flow dynamics during stress.
Abstract:
The effect of saponin and blockade of the nitrogen oxide upon the coronary endothelium was found in rats subjected to a 6-hrs stress. The damage of the endothelium and the blockade abolished the stressor-induced increase in the coronary blood flow velocity. The index of autoregulation and the latter's efficiency, however, remained the same. Preliminary administration of L-arginine prevented the effect of NG-monomethyl-L-arginine upon the coronary flow in the isolated hearts of rats subjected to stress. The post-stressor increase in the coronary blood flow seems to be due to an increase in releasing the nitrogen oxide from the coronary vessels' endotheliocytes.