The relative volumes of arteries and veins, considered as percentages of total blood volume, constitute a total of around 72% (10). Arteries constitute 12% and veins 60% of total vascular capacity. (Elsewhere venous volume is said to constitute 70% (14). 

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... return) amounts to total tissue blood flow and as the heart puts out what it receives cardiac output is therefore determined at the tissues. Hence, regulation of arterial blood pressure is independent of the distributed independent regulation of individual tissues. It is proposed here that mechanical features of arterial blood pressure regulation will depend rather on the balance between blood volume and venous wall tension, determinants of venous pressure. The potential for this explanation is treated in some detail. Blood flow regulation is subordinate to the oxygen requirements of individual tissues. For the majority of individual tissues the rate of oxygen delivery (DO 2 ) is normally sustained at a specific, individual, ratio relationship to oxygen consumption (VO 2 ) (1-4). For skeletal muscle the ratio is close to 1.5, for brain 3 and heart 1.6. These ratios are sustained over a moderate physiological range of metabolic rate changes by proportional changes in blood flow. Where arterial oxygen content (CaO 2 ) is reduced, blood flow increases such that the DO 2 to VO 2 ratio is sustained. For example, for moderate levels of activity, normal skeletal muscle oxygen delivery (1.5 times VO 2 ) is sustained in the face of reduced oxygen content (CaO 2 , either anaemia, hypoxia or both combined), down to levels only 60% of normal CaO 2 (5). Compensation for low CaO 2 is also sustained for the cardiac blood supply down to 60% of normal CaO 2 (3) whereas, for the brain, the lower limit for CaO 2 is around 90% of normal (6). The regulation of blood flow, sustaining appropriate rates of oxygen delivery, resides at the tissues. Blood flow regulation at the tissues has been shown to be independent of the nervous system (2). Guyton’s group showed that there is the same ‘correlation between local blood flow and arterial oxygen saturation in animals under total spinal anesthesia as seen in normal animals’ (7,8). An example of the determination of cardiac output and oxygen delivery by the metabolic requirements of tissues is found in the study of exercise by Donald and Shepherd (9); illustrated in Figure 1. Here the tissue demand from exercise is met, whether or not cardiac innervation is present. The difference is that there is a much larger stroke volume for the denervated heart, since the heart rate fails to increase normally. Since there is independent control of blood flow at the tissues, the idea that sympathetic vaso-constrictor nerves are the principal regulator of blood flow by acting on the arterioles or on myocardial contractility (10,11) requires revision. There is a related problem in view of known arteriolar constriction which occurs with stimulation of the sympathetic nerve supply to arterioles. The main problem, however, is the need for hypotheses addressing means by which blood pressure regulation occurs independently of the regulation of blood flow. A wealth of evidence attests to the role of the autonomic nervous system, especially the sympathetic division, in the regulation of arterial blood pressure (11). There is the well-known short-term regulation, via afferent information from the arterial baro-receptors, with brain stem processing and both parasympathetic and sympathetic efferent output. Where arterial blood pressure rises, or the arterial baro- receptor mechanism is stimulated by some other means, the inhibitory response results in reflex lowering of arterial pressure. There is also the longer term renal mediation, partly via sympathetic efferent innervation, with additional humoral involvement. The renal involvement affects blood volume, which in turn affects arterial blood pressure (12). There are also effects mediated by volume receptors on the venous side of the circulation. There is a mass of detail available in the literature concerning, in particular, central connections involving major sites, such as the nucleus of the tractus solitarius (NTS), the rostral ventro-lateral medulla (RVLM) and the hypothalamus (11). It is known that there is sympathetic innervation of the arterioles, causing the theoretical difficulty mentioned above, since the resistance offered by arterioles is adjusted precisely such that DO bears the correct relationship to VO . This problem will be considered later. A second known innervation is of the peripheral veins, where sympathetic stimulation raises venous pressure (11,13). Furthermore, “small veins and venules are more sensitive to sympathetic activation than arterioles” (14,15). The role of changes in venous pressure will be discussed in relation to means by which arterial blood pressure may be regulated independently of blood flow changes. (i) Altered venous capacity The dominant role of peripheral venous pressure in determining arterial BP is discussed in Guyton et al. (2). In relation to the interdependence of arteries and veins it is worth considering the relative volumes of the whole arterial tree and that of both the venous and arterial systems. Figure 2 illustrates the approximately five- to six-fold difference in venous and arterial volumes. Assuming the venous system volume is five times the arterial volume, knowing the venous and arterial percentages, we can calculate the effect of small changes in venous volume. Starting with the idea of a total blood volume of 5 litres, the arterial volume, at 12%, is 600 ml, whereas the venous volume, at 60%, will be 3000 ml. If we reduce the venous volume by 150 ml, and this is transferred into the arteries, it will have increased arterial volume by 25% (to 750 ml) and thus arterial blood pressure might be expected to increase by more than 25% since arterial compliance decreases as its volume increases. The initial action, reducing venous volume, would require reduction of venous wall compliance (or increase in wall tension or ‘tone’). Hottenstein and Kreulen (15) emphasize the particular role of the sympathetic activation here. Although this is a very simple model it shows how we would expect a small change in venous volume to generate a large change in arterial blood pressure. (ii) Altered blood volume If the venous wall initial ‘tone’ remains unaltered but blood volume increases, for whatever reason, this will stretch the vein walls and the pressure on the venous side of the circulation will increase. This will also cause a re-distribution, with a sharing of the extra volume between arteries and veins, according to their relative compliance. While mean arterial compliance is much lower than venous any extra fluid will raise arterial pressure. It is known that there is sympathetic innervation of both arteriolar and peripheral venous wall smooth muscle and, as pointed out above, this raises the question as to how the tissues sustain precisely appropriate blood flows in the face of alterations in sympathetic drive to arterioles. It is possible that, under particular circumstances, there is local modulation of arteriolar and venous tone, such that the tissue concerned still achieves the appropriate input resistance. Overall sympathetically mediated increases in arteriolar tone could be compatible with facilitating appropriate blood flow in individual tissues, under conditions of altered systemic arterial blood pressure. In other words the sympathetic efferent input/output reflex may well function specifically at locations where the situation changes, such as in the leg vasculature with postural change (such as standing up from the sitting position). Postural change alters the head of pressure (16). A second example is the classic effect of the Valsalva maneuver in normal subjects. Here, blood flow is strongly opposed by the raised intra-thoracic pressure since arterial blood pressure falls to low levels. Recovery of blood flow is assumed to result from the restoration of systemic arterial blood pressure towards the end of the maneuver. This is attributed to the well documented sympathetically driven increase in tone in splanchnic and renal veins, with restoration of arterial blood pressure. Recent unpublished work shows that blood flow is also restored as arterial blood pressure recovers in the late stage of the Valsalva manoeuver. Hence we have the possibility that changes in arteriolar resistance mediated by sympathetic innervation can be over-ridden by the tissue concerned and that situations can occur where tissue blood flow control is facilitated. During exercise venous tone is presumably greater than at rest, avoiding dilatation from the increased blood flow. This area remains open to further discussion and investigation. One of the situations where abnormal blood volume re-distribution occurs is with the induction of anaesthesia. There is known reduction of sympathetic outflow (17,18,19) and cardiac output and arterial blood pressure fall together. This is a situation where the fall in arterial blood pressure is entirely due to relaxation of the venous system walls, since there has been no change in blood volume. The relaxed venous system having a larger capacitance (with increased compliance/reduced tone) results in a redistribution of the blood volume. The small loss of arterial volume will have a disproportionate effect in lowering the arterial blood pressure. It also means that the tissue requirement becomes deficient with artificial reduction of cardiac output (slower arrival of tissue output at the heart, and less blood in the arterial system to sustain perfusion). Abnormal blood volume distribution is also recognised in the setting of arteriovenous (AV) fistulae or large AV malformations and is associated with reduction in arterial blood pressure. Here the primary mechanism is the reduction in total systemic vascular resistance resulting in a modicum of arterial blood loss to the veins increasing venous volume, rather than any change in venous wall tone. Here cardiac output is increased. This finding has been exploited to therapeutic benefit in a novel technology to treat hypertension: the ...