Endogenous Nitric Oxide Production Inhibits Myogenic Tone in Rat Coronary Arteries

Myogenic tone is the constriction of vascular smooth muscle in response to an elevation of luminal blood pressure, which serves to protect downstream capillaries and allows the regulation of blood flow to match demand. While the level of MT is high at rest in skeletal muscle arterioles (~50%), such high levels of autoregulation are undesirable in other parts of the body, including the brain and heart. However, the characteristics of small coronary arteries and regulation of their resting MT is relatively unexplored.

Rat coronary arteries (mean maximum diameter ~240 µm), were dissected, cannulated and pressurized to 80 mmHg. The diameter of arteries and endothelial cell (EC) Ca²⁺ activity were recorded using confocal microscopy.

Coronary arteries from the rat developed 29±2% MT, which increased to 47±4% when endogenous nitric oxide (NO) production was abolished using L-NAME, a NO synthase inhibitor (P<0.05, n=6). However, L-NAME had no affect against MT in cremaster muscle arterioles (49±1 to 53±1, n=4-5). The activation of NOS appeared secondary to a spontaneous increase in coronary artery EC Ca²⁺, as the frequency in coronary arteries was two-fold higher than cremaster arteriole ECs (3.2±0.1 vs 1.7±0.1 events per minute, P<0.05, n=3-5).

Our data suggest endogenous NO provides a tonic inhibitory effect against MT in rat coronary arteries. This regulation appears to be is absent in arterioles isolated from cremaster muscle. Furthermore, coronary ECs had double the frequency of spontaneous Ca²⁺ events compared to cremaster ECs, which may contribute to the higher level of NO production.