Arcading arterioles (average diam 68 microns ID) connecting adjacent triangular vascular sectors in the rat mesentery were examined in vivo for the presence of flow-dependent vasodilation. When a feed artery to one of these sectors was occluded, the affected sector was supplied by collateral flow through the arcading arteriole, and red cell velocity in the arteriole increased by 10-66 mm/s. The velocity increase was followed (with an average delay of 7.7 s) by dilation of the arcading arteriole, which averaged 68%. The dilation was closely correlated with red cell velocity (r = 0.96), volume flow (r = 0.96), and wall shear rate (r = 0.89). The dilation was sustained for the duration of increased velocity (1-10 min) and was not affected when direction of flow in the arteriole was reversed. The flow-induced dilation was equal to the maximal dilation attained with topically applied papaverine. Dilation of the arcading arteriole could be almost completely abolished if the arteriole was also occluded during occlusion of a feed artery. These observations indicate that a potent flow-dependent dilator mechanism is present in arcading arterioles of rat mesentery and may play an important role in local regulation.

Using liquid ion-exchanger semimicroelectrodes with a side pore, we measured changes of extracellular potassium concentration (Ke+) in adult rabbit and cat gastrocnemius muscles and in venous effluent blood flowing from the cat gastrocnemius muscle during various bouts of activity induced by sciatic nerve stimulation. 1. Isometric tetanic contractions (at 50 Hz) of various durations caused transient accumulation of Ke+ which was non-linearly related to the duration of muscle activity. The peak values of Ke+ in response to muscle stimulation were analogous in rabbits and cats, attaining values, e.g. after a 20-sisometric tetanus, between 8-9 mEq/1K+ in both species. 2. Potassium concentration in venous effleunt blood (K+ven) was transiently increased after isometric tetani. Since blood flow was measured at the same time, it was possible to calculate the amount of K+ lost by the muscle after tetani of various durations. A 32 g gastrocnemius muscle of the cat, for example, loses 9.36 +/- 1.52 muEqK+ after a 20-s isometric tetanus, which corresponds roughly to 0.5% of the total muscle potassium content. The loss of K+ in this muscle was 29.3 pEq K+ /impulse/100 g fresh muscle tissue. 3. There was no evident difference between the amount of K+ released during isometric tetani, or tetanic contractions performed under isotonic conditions. Single twitches evoked by indirect stimulation at 1 HZ for several minutes also induced a small rise in K+ven. 4. If the loss of K+ from the muscle into the blood stream is transiently prevented by arterio-venous occlusion installed immediately before a 10-s isometric tetanus, most K+ is released subsequently when blood flow is renewed, if the occlusion lasts for 20-25 s. It is not until blood flow is occuded for 40-60 s that most K+ is apparently resorbed and only a minor portion is released and is to be found in the venous blood. 5. The transient accumulation of muscle extra-cellular potassium may locally affect nerve endings, skeletal and smooth muscle cells.

An increase in blood flow velocity through both arteries and arterioles induces a dilation that is mediated by the endothelium. This is a significant mechanism of flow regulation at normal flow rates and is critically important during high flow conditions.

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