The gross factors which go to maintain arterial pressure are four in number, viz., the arteriole or peripheral resistance, the heart's output in a given time, the volume of blood in the arteries, and the viscosity of the blood.

The pressure may be lowered by general dilatation of the arterioles, by decrease in the heart's output, by loss of blood or the fluid of the blood, and slightly by a decrease in viscosity. It may be raised by general contraction of the arterioles, by increase in the output of the heart, by the addition of fluid to the blood, and by an increase in viscosity.

The most important regulators of arterial pressure are the arterioles, but even if the arterioles remain contracted, pressure cannot be maintained if the heart gives out or if there is much loss of blood.

Of the arterioles, those of the splanchnic area have most to do with the regulation of arterial pressure. They are strongly muscular, are abundantly supplied with nerves so that they are readily influenced, and have, when dilated, an enormous capacity. Indeed, when these arteries are much relaxed, so much blood passes into them that the brain may be depleted, with fainting or even death as the result, so that a person may be said to bleed into his own splanchnic arteries. On the contrary, they may be so strongly contracted that the weaker arteries of the limbs and skin are forced to dilate to accommodate the blood.

It is to be noted that, so far as life is concerned, the maintenance of adequate cerebral and coronary circulation is the essential, for upon these depends the activity of the vital centers in the medulla and of the heart. Many times it is in response to the needs of the vital centers that physiologic changes in the caliber of the arteries take place. The needs of other parts of the body, such as the kidneys, may also greatly influence the general arterial pressure. Hence reduction of what seems abnormally high arterial pressure may result in a failure of these organs to functionate. (For a resume of theories relating to high pressure in kidney disease see Janeway's Harvey Society Lecture, 1913.)