title: Changes in systemic and pulmonary vascular reactivity in hypertension following nifedipine and verapamil.
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.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Institute of Cardiology, University of Milan, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Bailo
authors.forename: C
authors.initials: C
authors.lastname: Fiorentini
authors.forename: A
authors.initials: A
authors.lastname: Folli
authors.forename: C
authors.initials: C
authors.lastname: Galli
authors.forename: A
authors.initials: A
authors.lastname: Loaldi
authors.forename: A
authors.initials: A
authors.lastname: Maltagliati
authors.forename: E
authors.initials: E
authors.lastname: Tosi
authors.forename: G
authors.initials: G
authors.lastname: Tamborini
authors.forename: M D
authors.initials: MD
authors.lastname: Guazzi
mesh_terms: D000328:Adult; D001775:Blood Circulation / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects; D002986:Clinical Trials as Topic; D003071:Cognition / Q000187:drug effects; D003080:Cold Temperature; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000494:pharmacology* / Q000627:therapeutic use; D009638:Norepinephrine / Q000097:blood; D011446:Prospective Studies; D011652:Pulmonary Circulation / Q000187:drug effects*; D011897:Random Allocation; D014655:Vascular Resistance / Q000187:drug effects*; D014700:Verapamil / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D014700:Verapamil; D009543:Nifedipine; D009638:Norepinephrine