Dietary Pulmonary Hypertension

• The regulation of the pulmonary circulation is inextricably linked to the role of the lungs in gas exchange. Accordingly, it is not surprising that hypoxia and acidosis predominate as stimuli for vasomotor activity or that their main effects are exerted locally on the pulmonary vascular tree. Although pulmonary vasomotor nerves do exist, they operate more to adjust the distensibility of capacitance vessels than to modulate the caliber of resistance vessels (1). Clearly this heavy reliance on local control of the pulmonary circulation is diametric to the situation in the systemic circulation where an elaborate baroregulatory apparatus and the renin-angiotensin system, exerting their influences from afar, dominate circulatory control. Since regulatory devices in the pulmonary circulation are so primitive and the pulmonary vascular bed is so extensive and capacious, it is reasonable to anticipate that pulmonary arterial hypertension would be difficult to generate (2). This expectation has been fulfilled both in experimental animals and in man. Except for those who reside at high altitude, pulmonary hypertension is a rarity in subjects who are free of heart or lung disease (3). Moreover, the pulmonary hypertension of high altitude is generally benign and reversible when hypoxia is relieved. In contrast, pulmonary hypertension at sea level is usually a distressful complication of heart, lung, or vascular disease which, in one way or another, has led to curtailment of the pulmonary vascular bed and to impediment to blood flow through it. In addition, once started, secondary pulmonary hypertension at sea level tends to be self-perpetuating and progressive in its course. Also, contained within the universe of pulmonary hypertension in which the causes are known is a sprinkling of patients with "primary