INVITED EDITORIAL
Invited Editorial on "Vasomotor responses of soleus feed arteries from sedentary and exercise-trained rats"

Department of Physiology and Biophysics, Indiana University Medical School, Indianapolis, Indiana 46202

	ARTICLE

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THE STUDY BY JASPERSE AND LAUGHLIN (6) continues the growing body of evidence that arteries are capable of significant contributions to regulation of vascular resistance. Their study determined whether exercise conditioning would alter the regulatory properties of feed arteries to the soleus muscle. These feed vessels exhibited a remarkable myogenic response to increased pressurization and well-developed flow-dependent vasodilation. Quite surprisingly, exercise training did not appreciably alter the pharmacological, myogenic, and flow-dependent mechanisms of the feed arteries. All of these measurements were made in vitro by using isolated arteries from sedentary and trained rats. The removal of external influences in the in vitro setting demonstrated that the fundamental regulatory properties of the endothelial and vascular smooth muscle cells were not influenced by exercise training. This point is important because in vitro (7) and in vivo (8, 9) studies of skeletal muscle arterioles from exercise-trained animals have shown changes in endothelial and vascular smooth muscle regulation. Why should the cells of arterioles, but not arteries, change their regulation during exercise training? Perhaps the simplest explanation is that arteries to the soleus muscle were completely competent to deal with demands of exercise hyperemia and need not adapt. However, the lack of a significant alteration need not imply that these or other feed arteries do not adapt to physiological and pathological circumstances. Studies of mesenteric arteries chronically forced to endure constant high blood flow have demonstrated that enlargement of the arterial lumen (12, 13) with endothelial and smooth muscle cell hyperplasia occurred within 7 days (12). The differences between the results of Jasperse and Laughlin (6) and the earlier studies of skeletal muscle arterioles from trained animals (7-9) and mesenteric arteries (12, 13) point out that the issue of how resistance arteries are regulated and respond to a given perturbation over time needs much additional study.

With the advent of pressure-dissipation measurements in the microvasculature, it became apparent that arteries, particularly small arteries, had a substantial vascular resistance. For example, in the skeletal muscle and in cerebral and intestinal vasculatures (1, 4, 11), the feed arteries preceding the arterioles account for 20-40% of the total organ vascular resistance. This percentage is deceptively small. About 30% of the total vascular resistance is generated by the capillary bed and venules. Whereas these vessels are vital to exchange and capacitance functions of the microvasculature, their resistance changes by minor amounts compared with the precapillary resistance. Of the remaining 60-70% of the total resistance, which can be extensively modified by precapillary vessels, the large-to-small arteries control 30-50% of this resistance. What is equally important is that the resistance of arteries does change in concert with microvascular responses. This participation is readily demonstrated in the cerebral circulation. The arteries of the cat (11) and rat (4) brain are known to change their relative resistance almost as much as the arteriolar resistance changes during autoregulation of blood flow. If the cerebral arteries had a fixed resistance, cerebral autoregulation would only function over a pressure range of +20-30 mmHg about the resting arterial pressure, rather than the typical 50-60 mmHg on either side of the resting arterial pressure. The mesenteric arteries of the small intestine also serve as important contributors to organ vascular regulation. During absorptive hyperemia, the resistance of the small arteries in the mesentery actually decreased proportionately more than that of the overall microvasculature (3). In this same context, during exercise hyperemia of skeletal muscle vasculatures studied in vivo, most of the decrease in total vascular resistance is explained by dilation of just the feed arteries and the larger arterioles (2, 8).

If arteries are as important to vascular regulation as the available data indicate, then understanding the mechanisms regulating their responses is essential. The flow-mediated stimulation of nitric oxide (NO) and vasodilatory prostaglandin formation may be a major means to coordinate blood flow requirements of the organ with arterial regulation. The basic premise is that, as arterioles dilate within a host organ, their decreased resistance allows flow to increase in the arteries. The increased flow shear is a physical signal for release of endothelium-dependent vasodilators. In addition, cell-to-cell communication of constrictor and dilator information from arterioles to arteries along the vessel wall is a well-established mechanism that was first demonstrated for a skeletal muscle vasculature (10). The data presented by Jasperse and Laughlin (6) indicated that the soleus feed arteries responded with vasodilation as flow was increased, and it is reasonable to assume that cell-to-cell communication would occur. It would be interesting to determine in in vivo studies to what extent these arteries dilated during muscle hyperemia and what mechanisms dominated the vasodilation. A limited amount of data on such issues is available for in vivo mesenteric arteries responding to the flow needs of the intestinal microvasculature. If mesenteric arteries were forced to increase their blood flow because other arteries in the vicinity were closed, vasodilation occurred in conjunction with an increase in the vessel wall NO concentration, as measured with NO-sensitive electrodes (5). Suppression of NO production attenuated both the vasodilation and increase in NO concentration during forced hyperemia. Under normal conditions, mesenteric arteries experience an increased blood flow each time the intestine absorbs food. Depending on the magnitude of absorptive hyperemia, the NO concentration in mesenteric arteries is increased up to 50-100% (3). However, flow velocity was not an important issue in NO formation during nutrient absorption. Shear rates declined because the arteries dilated proportionally more than flow velocity increased. The increased NO formation by the arteries was due to diffusion of endothelium-dependent vasodilators from the blood of the nearby paired vein. In addition, about one-half of the vasodilation was attributed to cell-to-cell communication from dilated arterioles to arteries. The point to be made from these various studies is that different mechanisms can be used by an artery in its important support of the flow demands of the microvasculature. The study by Jasperse and Laughlin (6) extends our knowledge of small arteries by demonstrating that skeletal muscle feed arteries have both well-developed flow-mediated and myogenic regulatory mechanisms. Furthermore, neither mechanism, when studied under in vitro conditions, is significantly modified by exercise training. These observations tentatively indicate that even the sedentary regulatory mechanisms of small arteries are so competent that they need little modification to serve the high blood flow requirements of exercise training.

	REFERENCES

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