Evidence of a shared mechanism of vasoconstriction in pulmonary and systemic circulation in hypertension: a possible role of intracellular calcium

• Published in: Circulation (New York, N.Y.) Vol. 66; no. 4; pp. 881 - 886
• Main Authors: Guazzi, M D, Polese, A, Bartorelli, A, Loaldi, A, Fiorentini, C
• Format: Journal Article
• Language: English
• Published: United States 01.10.1982
• Subjects: Blood Pressure - drug effects; Calcium Channel Blockers - pharmacology; Cardiac Output - drug effects; Humans; Hypertension - drug therapy; Hypertension - physiopathology; Male; Nifedipine - pharmacology; Pulmonary Circulation - drug effects; Pulmonary Wedge Pressure - drug effects; Vascular Resistance - drug effects; Vasoconstriction - drug effects
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.CIR.66.4.881

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.