Article

Hemodynamic effects of calcium channel blockers at rest and during exercise in essential hypertension.

The American Journal of Medicine (Impact Factor: 5.3). 11/1985; 79(4A):11-8. DOI: 10.1016/0002-9343(85)90495-4
Source: PubMed

ABSTRACT The main hemodynamic disturbance occurring in patients with essential hypertension is an increase in the total peripheral resistance. In young patients with hypertension, this disturbance is clearly seen during muscular exercise, even though the calculated resistance might be normal during rest. This article reports results of studies on the long-term hemodynamic effects of two calcium channel blockers, verapamil and nifedipine, in patients with mild to moderate hypertension. Twenty-five men, aged 20 to 64 years, with diastolic blood pressures between 100 and 120 mm Hg before treatment were studied at rest and during exercise on ergometer bicycles. Blood pressure was recorded intra-arterially, and cardiac output was measured. After this initial study, 10 patients were treated with verapamil (from 40 to 80 mg, three times daily) and 15 patients with nifedipine (long-acting form, from 40 to 80 mg daily). After one year, the hemodynamic study was repeated. Both drugs induced a reduction in blood pressure and in the total peripheral resistance without any reduction in the cardiac index. Verapamil reduced heart rate, particularly during exercise, but this effect was compensated by an increase in the stroke volume. The hemodynamic profile of these two calcium channel blockers clearly differs from the hemodynamic effects of beta blockers.

0 Bookmarks
 · 
14 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: The sympathetic nervous system is important in regulating cardiovascular function. It is therefore of interest to study the influence of antihypertensive drugs on sympathetic nerve activity. For this purpose, measurements of noradrenaline concentrations in forearm venous plasma have often been used. For several reasons, this provides limited information: i) the sympathetic nervous system is highly differentiated, i.e. activity may be high in some organs and low in others; ii) noradrenaline in forearm venous plasma is largely derived from sympathetic activity to the forearm skeletal muscle; iii) plasma noradrenaline concentrations are determined not only by noradrenaline spillover from sympathetic nerve endings, which is related to sympathetic nerve activity, but also by noradrenaline clearance. Under most circumstances plasma noradrenaline concentrations are not high enough to produce hormonal effects. Many types of antihypertensive drugs may cause acute and long-term increases in forearm venous noradrenaline concentrations. The mechanisms underlying these increases are not fully understood but seem to differ between drug classes: Diuretics increase renal noradrenaline spillover; beta-blockers do not affect spillover but reduce total noradrenaline clearance; calcium antagonists and alpha-blockers probably increase noradrenaline spillover, but it is not known which organs are involved, particularly during long-term treatment. ACE inhibitors seem to have a sympatholytic action, which counteract reflex increases in sympathetic nerve activity during blood pressure reduction, and plasma noradrenaline concentrations are generally not affected. To be able to judge the possible clinical consequences of changes in plasma noradrenaline concentrations during chronic antihypertensive treatment, assessments of noradrenaline spillover from individual organs are needed.
    Blood Pressure 12/1994; 3(6):356-63. · 1.39 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In 10 patients with moderate to severe hypertension, the hemodynamic effects of ergometric exercise and nicardipine, a dihydropyridine calcium channel antagonist, were characterized under basal conditions and after 1 week of therapy. The responses of plasma renin activity and catecholamines were also assessed. Nicardipine induced significant reductions of systolic, diastolic and mean blood pressure under conditions of rest and peak exercise (p less than 0.001), mediated by reversal of vasoconstriction (p less than 0.001). Overall, cardiac index and stroke volume index responses were not significantly altered by nicardipine. Although rest pulmonary wedge pressure was unchanged (6 +/- 3 to 5 +/- 4 mm Hg), peak exercise pulmonary wedge pressure decreased from 24 +/- 22 to 7 +/- 5 mm Hg (p less than 0.001) with nicardipine therapy. This effect of nicardipine on pulmonary wedge pressure was present across all work loads studied, and was accompanied by reduction of peak exercise pulmonary artery pressure from 43 +/- 10 to 25 +/- 7 mm Hg (p less than 0.001). Oxygen consumption was unchanged, associated with reduction of arteriovenous oxygen difference (p less than 0.02). Both plasma renin activity (p less than 0.05) and norepinephrine (p less than 0.005) were significantly increased with nicardipine therapy. Thus, nicardipine produced significant blood pressure reduction by reversal of vasoconstriction in patients with essential hypertension. The preservation of cardiac output, with markedly reduced pulmonary wedge pressure, indicated that nicardipine improved ventricular performance in response to reversal of vasoconstriction.
    Journal of the American College of Cardiology 10/1987; 10(3):647-54. · 14.09 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The effect of verapamil (240 mg) on exercise capacity was studied during a short graded and a single-level endurance exercise test in 12 normal volunteers; it was compared to the effects of atenolol (100 mg x day-1). Intake of verapamil, atenolol and placebo, administered according to a randomized, double-blind cross-over design, was started 3 days before the exercise tests. Compared to placebo, verapamil did not affect peak oxygen uptake in the graded test or exercise duration in the endurance test. Heart rate, systolic blood pressure, rating of perceived exertion and respiratory data at submaximal and peak exercise were unaffected in either test. On the other hand atenolol reduced maximal oxygen uptake by 5% (p less than 0.001) and endurance exercise duration by 17% (p less than 0.05). Besides marked decreases in heart rate and systolic blood pressure during the two types of exercise, atenolol also reduced oxygen uptake at submaximal exercise levels and it increased the rating of perceived exertion (p less than 0.05), the latter only during the endurance exercise test.
    European Journal of Applied Physiology and Occupational Physiology 02/1988; 58(1-2):87-91.