SUMMARY We investigated the hemodynamics of the greater and lesser circulation in 35 patients with primary hypertension, as well as the effects of calcium-channel blockade, to test whether a common factor may account for the excessive vascular resistance in the two circuits and whether intracellular calcium concentration ([Ca++]i) may be involved. We proved that (1) elevated pulmonary arteriolar resistance (PAR) is not related to pulmonary blood flow and volume, pleural pressure, arterial oxygen or carbon dioxide tension and pH, left ventricular filling pressure and function; (2) systemic vascular resistance (SVR) significantly correlates with PAR; (3) calcium-channel blockade with nifedipine reduces systemic and pulmonary arterial pressures toward normal and significantly lowers both SVR and PAR; (4) the percent decrease in vascular resistance after nifedipine is related to the baseline level of resistance in both the greater and the lesser circulations.Failure of the mechanisms currently indicated as responsible for pulmonary vasoconstriction to explain convincingly the increased PAR, the correlation between SVR and PAR, as well as the qualitatively similar response to calcium-channel blockade suggest that a common factor produces vasoconstriction in the two circuits. A pathogenetic role of a primary disorder in [Ca++]i cannot be excluded, but remains to be proved.BLOOD PRESSURE elevation in most patients with chronic hypertension is associated with increased peripheral vascular resistance, which is due in part to abnormal constriction of the resistance vessels.' For a time, the autoregulatory theory4 was popular. Interest has now focused on the hypothesis that an excessive intracellular calcium-ion concentration ([Ca++] hypertension, these disorders are spread throughout the body and involve arteriolar smooth muscle, which is the actual culprit. Unfortunately, blood cells, which can be easily studied, are not related at all to the muscles of the vessel wall, and the theory of abnormal membrane cation transport, although attractive, will remain speculative, until more is known about the metabolism of this tissue in essential hypertension. Based on previous observations'8 -20 that pressure and arteriolar resistance in the pulmonary circulation are increased in systemic high blood pressure, we decided to investigate the hemodynamics of the lesser circulation in hypertension to determine whether there is a common factor that accounts for the vasoconstriction that involves the two circuits and whether intracellular calcium is involved.