Pulmonary Vascular Overreactivity in Systemic Hypertension: A Pathophysiological Link Between the Greater and the Lesser Circulation

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 7; no. 6, Part 1; pp. 995 - 1002
• Main Authors: FIORENTINI, CESARE, BARBIER, PAOLO, GALLI, CLAUDIA, LOALDI, ALESSANDRO, TAMBORINI, GLORIA, TOSI, ELENA, GUAZZI, MAURIZIO D
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Heart Association, Inc 01.11.1985; Hagerstown, MD Lippincott
• Subjects: Adult; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure; Cardiac Output; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Cold Temperature; Female; Humans; Hypertension - physiopathology; Male; Medical sciences; Mental Processes - physiology; Middle Aged; Pulmonary Artery - physiopathology; Pulmonary Circulation; Vascular Resistance; Hypertension; Exploration; Hemodynamics; Pulmonary vessel
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.HYP.7.6.995

This study was undertaken to test whether the emphasized systemic vasomotion during sympathetic activation in hypertension is shared by the pulmonary circulation. To this end, 10 normotensive and 29 primary hypertensive subjects were investigated during adrenergic stimulation by mental arithmetic and cold pressor test. Both stimuli induced a systemic pressor reaction in both groups, which was mediated through an increase in cardiac output and a mild reduction in vascular resistance during arithmetic and through a predominant rise in systemic vascular resistance during cold. Each of these changes was emphasized in the hypertensive population as compared with the normotensive one. Pressure in the pulmonary artery remained unchanged during cold and was slightly raised (systolic) during arithmetic in normotensive subjects. On the contrary, in hypertensive subjects systolic and diastolic pulmonary pressures were consistently augmented by both stimuli, and pulmonary arteriolar resistance (dyn sec cm−) rose from 92 in the baseline to 125 (p <0.01) during arithmetic and to 124 (p < 0.01) during the cold test. This reaction is interpreted as reflecting a neurally mediated vasoconstriction and not as the consequence of mechanical or chemical changes, since no difference was observed in pulmonary wedge pressure, pleural pressure, arterial blood gas levels, and pH between controls and hypertensive subjects in the steady state and during either stressful stimulation. Baseline pulmonary arteriolar resistance was also found to correlate positively with systemic vascular resistance in the hypertensive group. When pressure changes occurred, the time course was similar in the two circuits; resistance increased to a proportionally similar degree in the two districts during the cold stimulus. All these observations support the concept that systemic and pulmonary vasculatures become oversensitive to neural activation and that the two vascular beds are exposed to the same type of dysregulation in systemic hypertension.