Author + information
- Received March 10, 1986
- Revision received May 19, 1986
- Accepted June 4, 1986
- Published online November 1, 1986.
- Maurizio D. Guazzi, MD*,1,
- Nicoletta De Cesare, MD1,
- Cesare Fiorentini, MD1,
- Claudia Galli, MD1,
- Piero Montorsi, MD1,
- Mauro Pepi, MD1 and
- Gloria Tamborini, MD1
- ↵*Address for reprints: Maurizio D. Guazzi, MD, Istituto di Cardiologia, Via Bonfadini 214, 20138 Milano, Italy.
Pulmonary pressure and arteriolar resistance are elevated in uncomplicated primary systemic hypertension. This study was carried out in 16 men with this form of hypertension and in 9 healthy men to compare 1) their pulmonary vascular reactivity to endogenous catecholamines released during mental arithmetic and cold pressor tests, and 2) the dose-response relation to exogenous epinephrine and norepinephrine. Arithmetic and cold pressor tests were associated, respectively, with a predominant increase in plasma epinephrine and norepinephrine concentration; changes were significantly greater in hypertensive men. During the two tests, pulmonary arteriolar resistance in the normotensive group was reduced by 13% and augmented by 7% of baseline, respectively, whereas it was raised by 31 and 70%, respectively, in the hypertensive group. In normal subjects, the dose (μg)-response (Δ dynes) relation to epinephrine was 1 = −4, 2 = −9, 3 = −9 and 4 = −10; to norepinephrine it was 2 = +3, 4 = +6, 6 = +7 and 8 = +7. In hypertensive patients, the respective relations were 1 = +18, 2 = +44, 3 = +59 and 4 = +77; and 2 = +39, 4 = +54, 6 = +76 and 8= +98. Group differences were highly significant. In each of these circumstances, the driving pressure across the lungs was significantly augmented in the hypertensive but not the normotensive group.
Both epinephrine and norepinephrine have a vasoconstrictor influence on the lesser circulation as a consequence of vascular over reactivity. The opposite changes in resistance between normotensive and hypertensive subjects produced by epinephrine suggest that a constrictor vascular supersensitivity becomes active in the pulmonary circuit with the development of systemic high blood pressure.
- Received March 10, 1986.
- Revision received May 19, 1986.
- Accepted June 4, 1986.
- American College of Cardiology Foundation