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Angiology
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Changes in Systemic and Pulmonary Vascular Reactivity in Hypertension Following Nifedipine and Verapamil

Mariangela Bailo

Institute of Cardiology, University of Milan, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "I. Monzino," Istituto Ricerche Cardiovascolari "G. Sisini," Milan, Italy

Cesare Fiorentini

Institute of Cardiology, University of Milan, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "I. Monzino," Istituto Ricerche Cardiovascolari "G. Sisini," Milan, Italy

Andreina Folli

Institute of Cardiology, University of Milan, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "I. Monzino," Istituto Ricerche Cardiovascolari "G. Sisini," Milan, Italy

Claudia Galli

Institute of Cardiology, University of Milan, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "I. Monzino," Istituto Ricerche Cardiovascolari "G. Sisini," Milan, Italy

Alessandro Loaldi

Institute of Cardiology, University of Milan, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "I. Monzino," Istituto Ricerche Cardiovascolari "G. Sisini," Milan, Italy

Anna Maltagliati

Institute of Cardiology, University of Milan, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "I. Monzino," Istituto Ricerche Cardiovascolari "G. Sisini," Milan, Italy

Elena Tosi

Institute of Cardiology, University of Milan, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "I. Monzino," Istituto Ricerche Cardiovascolari "G. Sisini," Milan, Italy

Gloria Tamborini

Institute of Cardiology, University of Milan, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "I. Monzino," Istituto Ricerche Cardiovascolari "G. Sisini," Milan, Italy

Maurizio D. Guazzi

Institute of Cardiology, University of Milan, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione "I. Monzino," Istituto Ricerche Cardiovascolari "G. Sisini," Milan, Italy

Excessive vascular tone and overresponsiveness to adrenergic stimuli char acterize the hemodynamics of the greater and the lesser circulation in hyperten sion. We tested whether calcium entry blockade with verapamil (11 cases) or nifedipine (11 cases) may improve the vascular regulation in high blood pres sure. Mental arithmetic and cold were used as adrenergic activators. The former stimulus produced obvious elevation of epinephrine plasma concentra tion, increase of cardiac output (CO), slight systemic vasodilatation, pulmonary vasoconstriction, and rise of blood pressure in both circuits. After calcium an tagonists, the epinephrine reaction to the arithmetic test was significantly attenuated, variations in CO and systemic blood pressure were unchanged, pul monary vasoconstriction was abolished, and the pressure rise in the lesser cir cuit was halved. The cold pressor test increased norepinephrine plasma concen tration (NE pc), systemic and pulmonary blood pressure, and vascular resist ance and did not alter CO. The attained NE pc during cold was unvaried after verapamil and significantly enhanced after nifedipine; pressure and resistance responses of the two circuits were almost unchanged after the former, whereas systemic and pulmonary vascular resistance rises were importantly attenuated after the latter compound, resulting in much lower pressure reactivity.

A modulation of the sympathoadrenal reaction, per se, can explain changes in the systemic and in the pulmonary vasomotion with calcium blockade during arithmetic. It would seem that after verapamil the sympathetic system was still activated during cold to such an extent as to maintain the same vasoconstrictor potency. NE pc suggests that the sympathetic discharge was not reduced by nifedipine. The impressive attenuation of the constrictor reaction in the two circuits would imply the existence of a shared vascular disorder in which cal cium ions are involved, which is more sensitive to nifedipine.

Angiology, Vol. 38, No. 9, 672-679 (1987)
DOI: 10.1177/000331978703800904
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