The pulmonary arteries have no vasoconstrictor nerves, but maintain an intrinsic muscular tone of moderate degree. They transmit just as much blood as the systemic arteries, for since the system is essentially a closed one, just as much blood must be pumped by the right ventricle as by the left ventricle, minus a slight loss from the lung capillaries. But the thin walls and feebler muscle of the right ventricle and the inability of the tricuspid valve to withstand high pressures, show that less power is required in the transmission of the blood, and it is evident that the pulmonary arteries give little resistance to the blood-flow. It is estimated that the normal pulmonary arterial pressure is only one-seventh to one-third that in the aorta.

In certain cardiac affections, however, where there is back pressure on the pulmonary circulation, as in obstruction at the mitral valve, the right ventricle becomes thick and strong and its cavity larger, and the pulmonary pressure may rise so high as to rupture one or more of the smaller arteries of the lungs. Such a pressure is mechanical, depending upon two factors, viz., increased output of the right ventricle and obstruction to the onward flow of blood in the left heart.

So far as we know, all drugs which affect the left ventricle will proportionately affect the right ventricle; and no difference has been noted except in those rare cases in which, through organic narrowing or impairment of contractility in one coronary, the other only is affected by the drug. The degree of filling of the right ventricle depends upon the amount of venous pressure versus the tone of the heart muscle. The rapidity of filling increases with the venous pressure (Hirschfelder).