Local control of veins: Biomechanical, metabolic, and humoral aspects

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Scientists have recognized only in the last decades that veins are not purely passive conduits of the organism, but they comprise a specific complex multifunctional system; thus the physiological significance of the veins has been reevaluated. The physiological functions related to the veins include conduit (collecting) function with flow-rectifying valves, selective barrier and regulated capacity functions, distribution of the blood volume, maintenance of the filling pressure of the heart, increasing the orthostatic tolerance of the organism, postcapillary resistance function, angiogenesis, synthesis of biologically active substances in the vascular wall (EDRF, endothelium-derived constricting factor, histamine, arachidonic acid metabolites, etc.), immune function, cooperation between the venular endothelium and the polymorphonuclear leukocytes, inhibition of the thromboembolic reactions, and special regional functions (e.g., venous pressure buffer function in the regulation of the intracranial pressure and portal type function of the portal vein and the renal peritubular venous plexus). In humans, ~60-80% of the total blood volume is localized in the highly distensible low pressure venous vessel network of ~450- to 500-km length. Mechanical properties of the passive connective tissue components (collagen, elastin) of the vessel wall, as well as its smooth muscle tone and the axial extension ratio, greatly affect the quasi-static pressure-volume characteristics, while the contribution of the endothelium is negligible. Apart from their neurogenic and other extrinsic tones, certain veins (e.g., human saphenous vein, rat portal vein, bat wing vein) also develop pronounced intrinsic myogenic tone to increased intraluminal pressure, which may contribute to the active capacitance response of the veins that can influence venous return. Blood flow rate can also affect venous tone independently of the pressure. Mechanical properties of the veins were shown to change as a function of age and body size and, probably as a result of adaptive processes, due to chronically increased gravitational load and long-term strenuous exercise and in human and experimental hypertension. At the present state of our knowledge, it is not possible to form a coherent picture of the involvement of the venular side in local metabolic vascular control processes for different tissues in the same way that the events at the arteriolar side have been explored. Despite the limited significance of venular resistance among the serially connected microvessels, such changes can be expected to be physiologically important, since capillary pressure is determined by the ratio of postcapillary to precapillary resistance. Accumulated data show that venules take part in local metabolic control processes; local metabolites can alter venous myogenic tone and modulate the effects of sympathetic outflow on the tone of the veins. The local ionic environment of the venous wall affects venous function significantly. Transport systems regulating the distribution of Na+ across cell membranes in the venous wall are known to be important in modulating membrane potential Coy Na+-K+ pump), intracellular Ca2+ (by Na+/Ca2+ exchange), intracellular pH (by Na+/H+ exchange), and cell volume and/or resting membrane potential (by Na+-K+-Cl- cotransport). The Na+ pump may play a greater physiological role in the maintenance of the resting membrane potential in venous than in arterial smooth muscle cells. Blockade of Na+ pump by exogenous or endogenous compounds in the large veins increases intracellular Na+ content, which in turn would make the Na+/Ca2+ exchange transport system less effective, causing the intracellular Ca2+ and, hence, the vascular contractility to increase. This hypothesis, however, has not been confirmed on smaller peripheral vessels. Venous smooth muscle tone and reactivity may not be influenced only by inhibition of the Na+-K+ pump of smooth muscle cells but also by inhibition of the Na+-K+ pump of adrenergic nerve endings. It should also be noted that vascular smooth muscle cells have an extremely low number of Na+ pump sites per cell when compared with cardiac and skeletal muscle. Increased vascular wall Na+ content remains today the most direct link between Na+ and hypertension, but its pathophysiological significance is still unknown. It was reported in the late 1970s that the accumulation of vascular wall Na+ occurs not only in the high-pressure portion of the aorta in coarctation hypertensive rats but also in the normal pressure portion of the aorta and in the veins. The Na+ concentration was also increased in the vena cava of rats with one-kidney one-clip hypertension, which was reversed in the 'unclipped' rats. These and other results suggest that circulating factor(s) may be responsible for the accumulation of excess Na+ in cardiovascular tissue in hypertension.

Original languageEnglish
Pages (from-to)611-666
Number of pages56
JournalPhysiological reviews
Issue number3
Publication statusPublished - Jul 1995

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Physiology (medical)

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