Abstract
There is a relationship between arterial blood pressure, cardiac output and vascular resistance described mathematically, that helps us to understand short-term control of blood pressure in terms of a hydraulic system. Arterial baroreceptors are specialized sensors mediating a rapid response to changes in pressure through interaction with the autonomic nervous system. This in turn influences heart rate, inotropic state and vascular tone, altering distribution of blood between arterial and venous systems, compensating for acute changes in total blood volume. Total blood volume is controlled predominantly by the kidney, with the renin–angiotensin–aldosterone system acting as both the ‘sensor’ of blood pressure/volume (via the juxtaglomerular apparatus) and the ‘effector’ of blood pressure/volume (via renin and aldosterone secretion). Overall control is shared; the baroreceptors being responsible for mediating short-term changes, and renal mechanisms determining the long-term control of blood pressure. These systems have to be adaptable in order to deal with physiological variation in the delivery of blood to tissues from rest to exercise, and with the large shifts in blood volume seen in acute haemorrhage. Pathophysiological changes in these systems lead to maladaptive responses, with systemic hypertension the most commonly seen.
After reading this article, you should understand:
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how arterial blood pressure is controlled by the baroreceptor reflex
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the sensory, transduction and effector systems in the baroreceptor reflex
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how vascular parameters (pressure, flow, radius, blood volume) are combined to create a hydraulic model of blood pressure
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how the kidney contributes to blood pressure control
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pressure natriuresis and diuresis as mechanisms that control blood volume
Introduction
The cardiovascular system can be envisaged as a pipeline, transporting energy to and from cells throughout the body. Within this hydraulic model, the heart is the prime mover, working in conjunction with blood vessels to create a pressurized system of flow. Systemic blood pressure, cardiac output and circulating blood volume determine tissue blood flow and as such the function of organ system. Regional flow is governed by a combination of pressure generated by the heart and resistance to flow exerted by the blood vessels supplying that region. In order to maintain adequate blood supply to individual organs, a system of feedback loops regulate blood pressure on a short-term (i.e. beat-to-beat) and long-term basis.
Blood pressure
Grodins derived a number of equations to describe flow through blood vessels. They help enhance understanding of the relationship between blood pressure, circulating volume and vascular resistance. Flow is proportional to pressure gradient across a vessel, and indirectly proportional to its resistance. Expressed simply for the whole circulation:
In these equations, Pa = arterial pressure, Pv = venous pressure, R = total peripheral resistance, V = total blood volume, Va = arterial blood volume, Vv = venous blood volume, Ca = arterial compliance, Cv = venous compliance. Also, Cardiac output = Heart rate × Stroke volume, and R α vessel radius −4 .
The equations form a basis of a hydraulic model of blood pressure control. Hydraulics is the science of the movement of fluid under pressure, within a system (usually tubes). In biology this system is capable of absorbing fluid volume fluctuations, thus ensuring flow meets the demands of the vital end organs. The equations assume a fixed total blood volume and thus reflect a ‘closed’ system model. This is useful in understanding acute control mechanisms of blood pressure. The equations described contain only vascular considerations, but over longer periods of time feedback systems allow total blood volume to be controlled independently of these, primarily by the kidney. The kidney achieves this by regulating total blood volume by balancing intake and excretion of fluid.
The arterial system includes the resistance vessels. By varying smooth muscle tone in their walls, vasoconstriction and vasodilation can occur, with a direct effect on total peripheral resistance. Changes in their calibre results in alteration of perfusion pressure across tissue beds and flow rate through these vessels. By varying the arteriolar radius in different tissue beds (and whole circulations), the pressure and flow to those organs can be managed independently, allowing a variety of operating flows to meet demand. In contrast, the venous system comprises capacitance vessels, containing 70–80% of the blood volume. Venoconstriction or venodilation will influence this volume distribution (and will transiently alter venous return and stroke volume), but has little effect on total peripheral resistance.
Mean arterial pressure (MAP) is a term used to describe the average blood pressure in an individual during a single cardiac cycle. MAP is determined by cardiac output (CO), systemic vascular resistance (SVR) and central venous pressure (CVP):
The mean systemic arterial pressure decreases from the aorta at 100 mmHg–35 mmHg at the level of the arteriole, whereas mean systemic venous pressure is 3–8 mmHg ( Figure 1 ). The arterial and venous pressures in the pulmonary circulation are about one-fifth of systemic values.

In a meta-analysis of 61 prospective studies, the risk of cardiovascular disease increased in a log-linear fashion from systolic blood pressure (SBP) levels <115 mmHg to >180 mmHg and from diastolic blood pressure (DBP) levels <75 mmHg to >105 mmHg. It is useful to categorize blood pressure levels for clinical and public health decision making. Blood pressure has been categorized into four levels on the basis of average BP measured in a healthcare setting ( Table 1 ).
BP category | Systolic BP | Diastolic BP | |
---|---|---|---|
Normal | <120 mmHg | and | <80 mmHg |
Elevated | 120–129 mmHg | and | <80 mmHg |
Hypertension | |||
Stage 1 | 130–139 mmHg | or | 80–89 mmHg |
Stage 2 | ≥140 mmHg | or | ≥90 mmHg |

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