Abstract
Blood flow through a vascular bed is usually determined by the pressure gradient across it and the diameter of the precapillary resistance vessels. Special circulations have additional specific features of blood flow control. Several organs control their blood supply by autoregulation. Coronary blood flow is linked to myocardial oxygen consumption, primarily by a metabolic mechanism. Increases in demand or decreases in supply of oxygen cause the release of vasodilator metabolites, which act on vascular smooth muscle to cause vessel relaxation and hence increase blood flow. Cerebral blood flow is primarily regulated by a myogenic mechanism whereby increases in transmural pressure stretch the vascular smooth muscle, which responds by contracting. Renal blood flow is regulated by both extrinsic and intrinsic mechanisms; sympathetic vasoconstriction of the afferent arterioles reduces renal blood flow in response to a decrease in effective circulating volume, myogenic mechanisms and tubuloglomerular feedback, as well as the release of vasoactive metabolites from the vascular endothelium regulate renal blood flow intrinsically. Hepatic blood flow is delivered via the portal vein and hepatic artery, and the amount of flow varies in these vessels reciprocally to maintain constant total blood flow. The pulmonary circulation receives the entire cardiac output, and blood flow is regulated both passively and actively. Pulmonary vessels are highly distensible and can accommodate increases in blood flow without significant increases in pressure.
After reading this article, you should be able to:
- •
describe the main factors that control blood flow through a vascular bed
- •
describe the special features of these factors as they relate to the coronary, cerebral, renal, hepatic and pulmonary circulations
- •
relate these special features to the particular role played by each circulation
In ‘special circulations’, additional factors govern the control of blood flow beyond the ‘standard’ mechanisms that prevail in most organ systems. In this article ‘special’ circumstances in coronary, cerebral, renal, hepatic and pulmonary circulations are considered.
Blood flow through the cardiovascular system is dependent on the force that drives the blood along the vessel (the pressure gradient), and is restricted by the resistance of the vessels. The resistance to blood flow is dependent on the radius and length of the blood vessel and the viscosity of the blood flowing through it. In practice, the radius of the arterioles has the greatest effect on blood flow. An approximate relation between vessel dimensions and blood viscosity is shown by the equation below (Poiseuille’s law).
Poiseuille’s law is an approximation for the cardiovascular system. Strictly, it applies only to Newtonian fluids flowing through a straight unbranched, non-distensible tube (conditions that do not prevail in the cardiovascular system). However, the equation below does give a useful approximation of blood flow in the cardiovascular system.
Q=π(P1−P2)r48ηl
In Poiseuille’s law, the radius of the vessel is raised to the power of 4, thus if the radius were to double, flow would increase 16-fold. The most important vessels regulating blood flow in this way are the small arteries and arterioles because they contain an abundance of vascular smooth muscle arranged in a circular manner along the length of the vessel, the tone of which is regulated by both extrinsic (neural and humoural) and intrinsic (myogenic and metabolic) factors.
Extrinsic control
The major vasomotor nerves are vasoconstrictor sympathetic fibres, which have tonic activity, accounting for the basal tone in resistance vessels. The primary neurotransmitter released from sympathetic nerve terminals is noradrenaline, which acts on the α- and β-adrenoreceptors. In many vascular beds the sympathetic system is associated with activation of α-adrenoreceptors to mediate a vasoconstriction. Only a small proportion of the resistance vessels in the body receives a parasympathetic (vasodilator) nerve supply (e.g. the cerebral and meningeal blood vessels, parts of the viscera, genitalia, large bowel and bladder, but not skeletal muscle or skin). The vasodilation of cutaneous blood vessels in association with sweating may be partly due to the production of a vasodilator polypeptide, bradykinin, within exocrine glands.
Adrenaline has many effects on vessel diameter and hence blood flow. In skeletal muscle, low concentrations of adrenaline act on the β-adrenoreceptors to induce vasodilation, whereas high concentrations act on the α-adrenoreceptors to induce vasoconstriction. However, noradrenaline always acts as a vasoconstrictor. Other vasoconstrictor hormones include angiotensin II and vasopressin.
Intrinsic control
Intrinsic control relates to local control within a vascular bed rather than a centrally mediated reflex control. Local control of the circulation can be divided into direct effects on vascular smooth muscle and indirect effects via the vascular endothelium.
Properties of vascular smooth muscle
A number of vascular beds can maintain a constant blood flow despite variations in arterial blood pressure (within limits). This process is termed autoregulation. In addition, many organs adjust blood flow to match metabolic activity. This type of local regulation occurs independently of the endothelium and nervous input, and is the result of direct changes in vascular tone. There are currently two main theories that may explain autoregulation of blood flow.
Myogenic mechanism: increased tension in the blood vessel wall, due to increased blood flow, stretches the vascular sarcolemma. The vascular muscle responds by contracting, and increasing resistance to maintain pressure and hence blood flow.
Metabolic mechanism: in certain organs blood flow is regulated to match the metabolic activity of the tissue. A decrease in blood supply or an increase in demand of oxygen causes the tissue to release vasodilator metabolites such as:
- •
potassium ions
- •
hydrogen ions (lactic acid)
- •
phosphate ions
- •
carbon dioxide
- •
prostaglandins
- •
adenosine.
These metabolites act locally, acting directly on vascular smooth muscle, causing relaxation and an increase in blood flow. This process is called functional hyperaemia. A decrease in metabolic activity will decrease the formation of vasodilator metabolites, and hence lead to vasoconstriction. There is normally a background level of metabolites in the tissue and so this mechanism can also form the basis of autoregulation. An increase in blood pressure can increase blood flow (see equation above), which causes a ‘wash-out’ of vasodilator metabolites, leading to a loss of vasodilator influence and hence a vasoconstriction, reducing blood flow back to the original level.
Properties of the endothelium
The vascular endothelium can also influence local blood flow. Endothelial cells produce and release both vasodilator and vasoconstrictor metabolites in response to many stimuli such as shear stress due to increased blood flow, and hypoxia. Nitric oxide (NO) is perhaps the most important of the vasodilator substances.
Coronary circulation
The myocardium receives its entire nutritional blood supply from the coronary arteries. The right coronary artery mainly supplies the right atrium and ventricle, the left coronary artery divides into the anterior descending and circumflex branches, and mainly supplies the left atrium and ventricle.
Control of myocardial blood flow
The primary factor responsible for perfusion of the myocardium is aortic pressure. However, a ‘special’ consideration in the coronary vascular bed is that the moment-to-moment coronary blood flow (CBF) is strongly influenced by mechanical activity of the heart. The coronary blood vessels course through the myocardium and are compressed during systole. Thus, CBF, in contrast to blood flow through most other vascular beds in the body, is at its highest during early diastole (when extravascular compression is minimal and aortic pressure is still high) and at its lowest during isovolumic contraction (when extravascular compression can interrupt or even reverse blood flow in the left ventricular coronary vessels) ( Figure 1 ). Tachycardia (reduced diastolic time), elevations in ventricular end-diastolic pressure and reduced arterial pressure result in a reduction in CBF. Compression of the coronary arteries is greatest near the endocardial surface and diminishes nearer the epicardial surface. Thus, the vessels in the left ventricular inner wall are most susceptible to ischaemic damage in coronary artery disease.
