TITLE

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

AUTHOR(S)
Bailo, Mariangela; Fiorentini, Cesare; Folli, Andreina; Galli, Claudia; Loaldi, Alessandro; Maltagliati, Anna; Tosi, Elena; Tamborini, Gloria; Guazzi, Maurizio D.
PUB. DATE
September 1987
SOURCE
Angiology;Sep1987, Vol. 38 Issue 9, p672
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Excessive vascular tone and overresponsiveness to adrenergic stimuli characterize the hemodynamics of the greater and the lesser circulation in hypertension. We tested whether calcium entry blockade with verapamil (11 cases) or nifedipine (11 cases) may improve the vascular regulation in high blood pressure. Mental arithmetic and cold were used as adrenergic activators. The former stimulus produced obvious elevation of epinephrine plasma concentration, increase of cardiac output (CO), slight systemic vasodilatation, pulmonary vasoconstriction, and rise of blood pressure in both circuits. After calcium antagonists, the epinephrine reaction to the arithmetic test was significantly attenuated, variations in CO and systemic blood pressure were unchanged, pulmonary vasoconstriction was abolished, and the pressure rise in the lesser circuit was halved. The cold pressor test increased norepinephrine plasma concentration (NE pc), systemic and pulmonary blood pressure, and vascular resistance 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 calcium ions are involved, which is more sensitive to nifedipine.
ACCESSION #
16352203

 

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