Cell-to-cell communication coordinates blood flow control.

Abstract

The control of tissue blood flow is a dynamic process exemplified by the interaction among physical, chemical, and electrical events occurring within the vessel wall and between the vasculature and tissue parenchyma. The range of blood flow control achieved in vivo is illustrated by functional hyperemia in exercising skeletal muscle: maximal flow can exceed resting values by more than 50-fold. Blood flow control is integrated among many vessel segments, beginning with resistance arteries external to the muscle and encompassing the arteriolar network within the muscle. As metabolic demand increases, the locus of blood flow control shifts from distal arterioles, which control capillary perfusion and blood flow distribution within the tissue, to the proximal arterioles and resistance arteries, which control the total volume of flow into the muscle. A fundamental question centers on how this vasomotor activity is actually coordinated throughout the resistance network. The interaction within and among vascular segments can be explained by chemical and electrical signals to smooth muscle cells (SMCs) and endothelial cells (ECs) in response to changes in transmural pressure as well as luminal B lood flow control in the resistance vasculature is a dynamic process exemplified by the interaction among physical, chemical, and electrical events occurring within the vessel wall and originating from the tissue parenchyma. Resistance vessels begin with small (diameter, 100 to 500 /xm) "feed" arteries external to the tissue and encompass the arteriolar network (10 to 100 /im) embedded within the tissue. 1 Feed arteries and proximal arterioles (1A, 60 to 100 /xm) control flow magnitude into the tissue; intermediate arterioles (2A and 3A, 15 to 60 /xm) control flow distribution within the tissue; and terminal arterioles (4A, 8 to 15 /xm) control capillary perfusion, 2 ie, the surface area for exchange between parenchymal cells and the cardiovascular system (Fig 1).The wall of resistance vessels consists primarily of smooth muscle cells (SMCs) wrapped around the vessel lumen, which is lined by a monolayer of endothelial cells (ECs) in contact with the blood.34 Vasoactive substances are produced by ECs, SMCs, and parenchymal cells and are released by autonomic nerve endings on the adventitial surface of SMCs. In addition, vessels are continually exposed to such physical forces as transmural pressure and luminal shear stress (Fig 2). These multiple stimuli interact to control the contractile activity of SMCs (either directly, or indirectly via the ECs) and thereby to change vessel diameter and regulate flow. At each level of the resistance network, the SMCs and ECs must act together to meet the changing requirements of the tissue parenchymal cells. The purpose of this review is to discuss the mechanisms whereby communication among SMCs and ECs, as well as autonomic nerves and parenchymal cells, results in the coordination of blood flow control within and among vascular segments. The influence of hypertension on these relatio...

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“…In microvessels, conducted vasodilation reflects cell-to-cell coupling by gap junctions between smooth muscle and endothelium. 36,37 Conduction is readily induced by activating muscarinic receptors on arterioles; however, a physiological source for stimulating these receptors has not been defined. In hamster skeletal muscle, the stimulation of motor nerves gives rise to dilation of arterioles within the muscle, which is conducted into the feed arteries external to the muscle.…”

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“…In other words, on entry into rG, the diameter of the arterioles in the temporal muscle was larger than that of the 1-G condition because the vascular resistance is dominated by the diameter of blood vessels within a few seconds under physiological conditions (9). With this arteriolar dilatation, a larger number of capillaries are open and perfused (18). An increase in perfusion pressure not only increases the driving force required for perfusion but also leads to passive dilatation of the capillary bed within a second (7).…”

“…The anatomical reason that muscles on the head are not restricted by the hard skull might help to lower the vascular resistance (19). Furthermore, the decrease in sympathetic nerve activity, which is observed during rG (10,16), and the release of nitric oxide induced by increased flow (8,18) might be also involved for the vasodilatation in the temporal muscle.…”