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Biomedical subjects

M Arita

Publications and source records attributed to M Arita.

At least 55 records · Page 3Linked to original sources
PubMed2000

JTV-519, a novel cardioprotective agent, improves the contractile recovery after ischaemia-reperfusion in coronary perfused guinea-pig ventricular muscles.

A newly synthesized benzothiazepine derivative, JTV-519 (JT) has been reported to be cardioprotective. However, the precise mechanism underlying the cardioprotective effect of this drug is unknown. Coronary-perfused guinea-pig ventricular muscles were subjected to 20-min no-flow ischaemia followed by 60-min reperfusion (I/R). I/R significantly decreased the contraction in untreated preparations (control group, 34+/-4% of baseline value, n=6). Brief administration of JT (1.0 microM) prior to ischaemia significantly improved the postischaemic contractile recovery (63+/-5% of baseline value, n=4), as compared to the control group. JT (1.0 microM) slightly prolonged action potential duration before ischaemia and induced conduction disturbance (2 : 1 block) after the initiation of ischaemia. The cardioprotective effect of JT was antagonized by chelerythrine (CH, 5.0 microM), an inhibitor of protein kinase C (PKC) or by 5-hydroxydecanoic acid (5-HD, 400 microM), an inhibitor of mitochondrial ATP-sensitive K(+) (K(ATP)) channels. These results suggest that the protective effect of JT is due to the opening of mitochondrial K(ATP) channels, which, in turn, is linked to PKC activation.

Action Potentials↗
PubMed2000

[Chest radiograph of atypical pneumonia: comparison among Chlamydia pneumoniae. Pneumonia, ornithosis, and Mycoplasma pneumoniae pneumonia].

No report has been found comparing Chlamydia pneumoniae (C. pneumoniae) pneumonia radiographically with other atypical pneumonias, Chlamydia psittaci (C. psittaci) pneumonia and Mycoplasma pneumoniae (M. pneumoniae) pneumonia. We described the chest radiographs of three kinds of pneumonia cases: 46 cases of C. pneumoniae pneumonia, 39 cases of C. psittaci pneumonia, and 131 cases of M. pneumoniae pneumonia. Radiographic shadows were categorized into main shadows and sub-shadows. The main shadows are classified from the viewpoint of the characteristics; air space consolidation(AS), ground-glass opacity(GG), reticular shadow(RS), bronchopneumonia(BP), and small nodular shadows (SN). The size, the site, and the number of the main shadows were also analyzed. In comparison among the three pneumonias, BP was the most frequent in M. pneumoniae pneumonia (0.40/case). AS predominated in C. pneumoniae pneumonia (0.67/case), and GG in C. psittaci pneumonia (0.62/case). The number of main shadows was equal, about 1.4/case in three pneumonias. Large shadows were less frequent in M. pneumoniae pneumonia than C. pneumoniae pneumonia (p = 0.02) and C. psittaci pneumonia (p = 0.01). Main shadows were more frequent in the outer zone in M. pneumoniae pneumonia than C. psittaci pneumonia (p = 0.01), and in the middle zone in C. psittaci pneumonia than in M. pneumoniae pneumonia (p = 0.02). Cases with bilateral main shadows were less common in M. pneumoniae pneumonia (9%) than C. pneumoniae pneumonia(33%, p = 0.001) and C. psittaci pneumonia(30%, p = 0.005). Thickening of bronchovascular bundles as a sub-shadow was most frequently noted in M. pneumoniae pneumonia. Some differences among the three atypical pneumonias were seen in the chest radiograph. However, no specific findings of C. pneumoniae pneumonia were shown radiographically in this study.

Aged↗
PubMed2000

Coronary artery spasm induced by carotid sinus massage.

A 60 year old man with a history of frequent episodes of chest pain and dizziness was referred for evaluation of coronary artery disease. He had no significant coronary artery stenosis at baseline coronary angiography. A carotid sinus massage was performed for evaluation of carotid sinus hypersensitivity in the patient. Both heart rate and blood pressure decreased a little, and returned to baseline level immediately after carotid sinus massage. However, 2.5 minutes after carotid sinus massage, ECG showed ST segment elevation in leads II, III, and aVF. Four minutes after carotid sinus massage, he had chest pain with a progressive elevation in the ST segment in the same leads, when he had 99% focal spasm in the right coronary artery. The vasospasm induced by carotid sinus massage was reproducible over several minutes and resolved spontaneously. Coronary artery spasm may be provoked by the enhanced vagal activation due to carotid sinus massage.

Carotid Sinus↗
PubMed2000

Postmortem study of ataxia with retinitis pigmentosa by mutation of the alpha-tocopherol transfer protein gene.

A new syndrome of ataxia and retinitis pigmentosa with vitamin E deficiency caused by the missense mutation of alpha-tocopherol transfer protein (alpha-TTP) gene was recently proposed. After studying the first postmortem case with this mutation pathologically and biochemically, whether the symptoms can be treated by supplementation of vitamin E or not is discussed. The major pathological findings were retinal atrophy; severe dying back-type degeneration of the posterior column; and massive accumulation of lipofuscin in neurons including dorsal root ganglion (DRG) cells, which were almost identical to those in vitamin E deficient animals and patients with fat malabsorption. Also, mild loss of Purkinje cells was noted. Because robust expression of alpha-TTP was detected in the cerebellum as well as in the liver and the tissue concentration of vitamin E in the cerebellum was still low even after oral supplementation, the mild Purkinje cell loss might be related to the mutant alpha-TTP in the cerebellum. By contrast, in the DRG, thought to be mainly responsible for ataxia, no expression of alpha-TTP was detected, and the tissue concentration of vitamin E increased to normal after supplementation. It is therefore considered that oral supplementation of vitamin E should effectively counteract the progression of ataxia.

Aged↗
PubMed2000

Walking 10,000 steps/day or more reduces blood pressure and sympathetic nerve activity in mild essential hypertension.

We investigated the effects of walking 10,000 steps/day or more on blood pressure and cardiac autonomic nerve activity in mild essential hypertensive patients. All subjects were males aged 47.0+/-1.0 (mean+/-SEM) years old. The original cohort consisted of 730 people in a manufacturing industry who measured the number of steps they walked each day using a pedometer. Eighty-three of these subjects walked 10,000 steps/day or more for 12 weeks. Thirty-two of these were hypertensives with systolic blood pressure (SBP) greater than 140 mmHg and/or diastolic blood pressure (DBP) greater than 90 mmHg. Thirty of these hypertensive subjects (HT) were examined twice, once during the pre- and once during the post-study period, for body mass index (BMI), maximal oxygen intake (Vo2max), blood pressure, heart rate (HR), and autonomic nerve activity by power spectral analysis of SBP and HR variability. In the HT group, walking 13,510+/-837 steps/day for 12 weeks lowered blood pressure (from 149.3+/-2.7/98.5+/-1.4 to 139.1+/-2.9/90.1+/-1.9 mmHg; p<0.01, respectively). In both the 34 normotensive controls and 17 hypertensive sedentary controls, blood pressure did not change. Walking also significantly lowered low-frequency fluctuations in SBP as an index of sympathetic nerve activity, from 1.324+/-0.192 to 0.738+/-0.154 mmHg2/Hz (p<0.05). VO2max rose significantly from 26.1+/-2.4 to 29.5+/-2.5 ml/kg/min (p<0.05). There were no changes in parasympathetic nerve activity, baroreceptor reflex sensitivity, or BMI. Our results indicate that walking 10,000 steps/days or more, irrespective of exercise intensity or duration, is effective in lowering blood pressure, increasing exercise capacity, and reducing sympathetic nerve activity in hypertensive patients.

Blood Pressure↗
PubMed2000

Familial cases of severe measles pneumonia.

We report two cases of severe measles pneumonia. Patient 1, a 17-year-old boy who contracted measles in the acute phase of infectious mononucleosis caused by Epstein-Barr virus (EBV), transmitted the disease to patient 2, his father. Both patients presented severe pneumonia with bilateral diffuse micronodular shadows. Diagnoses were established in both patients by antibody titers for measles and reverse transcriptase-polymerase chain reaction (RT-PCR) of blood and throat swab. Multinucleated giant cells with intranuclear inclusion bodies were revealed in the transbronchial lung biopsy (TBLB) specimen of patient 2. Both patients recovered with pulse steroid therapy.

Adolescent↗
PubMed2000

Selective block of late currents in the DeltaKPQ Na(+) channel mutant by pilsicainide and lidocaine with distinct mechanisms.

The congenital long QT syndrome is an inherited disorder characterized by a delay in cardiac repolarization, leading to lethal cardiac arrhythmias such as torsade de pointes. One form of this disease involves mutations in the voltage-dependent cardiac Na(+) channel, which includes an in-frame deletion of three amino acids (Lys-1505, Pro-1506, and Gln-1507; DeltaKPQ). The potential for selective suppression of the mutant was examined by heterologous expression of DeltaKPQ-Na(+) channels in Chinese hamster fibroblast cells via single-channel recording. In a single-channel cell-attached patch study, DeltaKPQ-Na(+) channels yielded currents that peaked at approximately 1 ms after voltage steps to 0 mV with aberrant late currents, which were composed of burst and isolated openings. The affinity of certain anesthetics (pilsicainide and lidocaine) to the late currents of the mutant channels was examined. It was revealed that 1) pilsicainide (1 microM), an open channel blocker of voltage-dependent Na(+) channels, remarkably decreased the late currents primarily by the shortening of burst duration without suppressing the initial peak current; and 2) lidocaine (1 microM), an inactivated channel blocker, decreased the late currents primarily by the suppression of isolated channel openings. Because the late currents in DeltaKPQ mutants are mainly composed of the burst openings, we conclude that pilsicainide is capable of selectively blocking the late currents in the mutant Na(+) channels that show dominant abnormal burst openings such as in DeltaKPQ mutants.

Animals↗
PubMed1999

Different functional aspects of the group II subfamily (Types IIA and V) and type X secretory phospholipase A(2)s in regulating arachidonic acid release and prostaglandin generation. Implications of cyclooxygenase-2 induction and phospholipid scramblase-mediated cellular membrane perturbation.

We have recently reported that members of the heparin-binding group II subfamily of secretory PLA(2)s (sPLA(2)s) (types IIA and V), when transfected into 293 cells, released [(3)H]arachidonic acid (AA) preferentially in response to interleukin-1 (IL-1) and acted as "signaling" PLA(2)s that were functionally coupled with prostaglandin biosynthesis. Here we show that these group II subfamily sPLA(2)s and the type X sPLA(2) behave in a different manner, the former being more efficiently coupled with the prostaglandin-biosynthetic pathway than the latter, in 293 transfectants. Type X sPLA(2), which bound only minimally to cell surface proteoglycans, augmented the release of both [(3)H]AA and [(3)H]oleic acid in the presence of serum but not IL-1. Both types IIA and V sPLA(2), the AA released by which was efficiently converted to prostaglandin E(2), markedly augmented IL-1-induced expression of cyclooxygenase (COX)-2 in a heparin-sensitive fashion, whereas type X sPLA(2) lacked the ability to augment COX-2 expression, thereby exhibiting the poor prostaglandin E(2)-biosynthetic response unless either of the COX isozymes was forcibly introduced into type X sPLA(2)-expressing cells. Implication of phospholipid scramblase, an enzyme responsible for the perturbation of plasma membrane asymmetry, revealed that the scramblase-transfected cells became more sensitive to types IIA and V, but not X, sPLA(2), releasing both [(3)H]AA and [(3)H]oleic acid in an IL-1-independent manner. Thus, although phospholipid scramblase-mediated alteration in plasma membrane asymmetry actually led to the increased cellular susceptibility to the group II subfamily of sPLA(2)s, several lines of evidence suggest that it does not entirely mimic their actions on cells after IL-1 signaling. Interestingly, coexpression of type IIA or V, but not X, sPLA(2) and phospholipid scramblase resulted in a marked reduction in cell growth, revealing an unexplored antiproliferative aspect of particular classes of sPLA(2).

Annexin A5↗
PubMed1999

Effect of dipyridamole on QT dispersion in vasospastic angina pectoris.

Life-threatening ventricular arrhythmias have frequently been documented in patients with vasospastic angina. Moreover, the incidence of ventricular arrhythmias has been closely associated with increased QT dispersion. However, the underlying mechanism responsible for this arrhythmogenesis has not been clarified. The effects of dipyridamole and subsequent aminophylline administration on QT dispersion were examined in 35 patients with vasospastic angina and 30 patients with atypical chest pain. None of the patients enrolled in this study revealed any significant stenosis in coronary angiography. QT dispersion during dipyridamole followed by aminophylline administration was compared between the 2 groups. The baseline QT dispersion was similar in both groups (vasospastic angina: 27 +/- 8 ms; atypical chest pain: 28 +/- 7 ms). No significant changes in QT dispersion were observed in patients with atypical chest pain by dipyridamole (23 +/- 9 ms) and subsequent aminophylline administration (23 +/- 5 ms). However, the QT dispersion in patients with vasospastic angina increased significantly by dipyridamole administration (53 +/- 14 ms, p <0.0001) and returned to baseline by subsequent aminophylline administration (26 +/- 10 ms). Our data suggest that the disparity of ventricular repolarization in vasospastic angina may be mediated by increased endogenous adenosine.

Adult↗
PubMed1999

Inhibition of Na(+)-K+ pump alleviates the shortening of action potential duration caused by metabolic inhibition via blockade of KATP channels in coronary perfused ventricular muscles of guinea-pigs.

The Na(+)-K+ pump is a consumer of intracellular ATP. We therefore examined whether blockade of the Na(+)-K+ pump by cardiac glycosides could inhibit ATP-sensitive K+ (KATP) channels and prolong the action potential duration (APD) of the guinea-pig ventricular muscles perfused with Tyrode's solution via the coronary artery and stimulated at 3 Hz. The metabolic inhibition (MI) achieved by application of 0.1 microM carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (a mitochondrial uncoupler) shortened the APD in a time-dependent manner. When dihydroouabain (DHO, 5 microM) was introduced 5 min but not 10 min after introduction of MI, the APD shortening was significantly attenuated. Application of glibenclamide (1 microM), a blocker of KATP channels, introduced both 5 and 10 min after MI also alleviated the APD shortening: DHO did not alleviate the APD shortening effect produced by cromakalim (5 microM), a KATP-channel opener. In separate experiments using whole-cell patch-clamp techniques, we found that this concentration of DHO (5 microM) depressed the Na(+)-K+ pump current of the guinea-pig ventricular myocytes from 210 to 100 pA (at 0 mV) or by 49.5%. We conclude that, during early phase (approximately 5 min) of MI, the APD shortening mostly results from the activation of KATP channels, and that even a approximately 50% inhibition of the Na(+)-K+ pump by DHO leads to the blockade of KATP channels and eventual lengthening of the APD.

Action Potentials↗
PubMed1999

Anoxia depresses sodium-calcium exchange currents in guinea-pig ventricular myocytes.

Cardiac Na-Ca exchange is related to the intracellular calcium overload that occurs during ischemia and reperfusion. However, direct observation of the membrane current through Na-Ca exchange during ischemia has not been performed. The purpose of this study was to clarify the effect of simulated ischemia (substrate-free anoxia) and intracellular acidification on the Na-Ca exchange current. The electrogenic Na-Ca exchange current was recorded from isolated guinea-pig ventricular myocytes by using patch-clamp techniques. Exposure to anoxia significantly decreased both the inward and outward directed Na-Ca exchange currents (from -1.21+/-0. 18 to -0.04+/-0.32 pA/pF at -80 mV; from 6.58+/-1.06 to 3.14+/-1.06 pA/pF at +40 mV). The reversal potential of Na-Ca exchange current shifted to negative direction during anoxia. Subsequent reoxygenation rapidly restored the amplitude of exchange currents and the reversal potential. These anoxia/reoxygenation-induced changes were completely inhibited when the intracellular pH was clamped at 7.3 by using 20 m m HEPES-buffer. Furthermore, the anoxia-induced changes of Na-Ca exchange current were mimicked by the intracellular acidosis induced by a brief exposure to ammonium chloride in normoxic conditions. We conclude that the Cardiac Na-Ca exchange is suppressed by anoxia secondary to intracellular acidosis, and that these changes were reversed by reoxygenation.

Acidosis↗
PubMed1999

Multiple pathways for establishment of poliovirus infection.

Poliovirus (PV) infects susceptible cells through poliovirus receptor (PVR), which functions to bind virus and to convert its conformation. To study early infection process of PV, infection systems were employed using in vitro cultured cells and in vivo neural pathway of PVR transgenic (Tg) mice. For in vitro study, mouse L cells were established expressing mouse high affinity Fc gamma receptor molecules, and used them as in vitro PV infection system. PV infection was mediated, albeit inefficiently, by mouse anti-PV monoclonal antibodies (mAbs; IgG2a subtypes) that did not show an activity to convert PV (160S) to 135S particle. The infection efficiency was enhanced when PVR-IgG2a, a chimera molecule consisting of the extracellular moiety of PVR and the Fc portion of mouse IgG2a, was used for anti-PV mAbs. Virion conformational change to 135S particle was induced by PVR-IgG2a. For in vivo study, intramuscular (i.m.) inoculation of PV into the calves of PV-sensitive Tg mice was employed. PV-related materials recovered from the sciatic nerve, after the i.m. inoculation, were mainly composed of intact 160S virion particle, although this neural pathway appeared to be dependent on PVR. These results suggested that some specific interaction(s) of PVR to PV beyond its binding activity was important to enhance infectivity of PV in in vitro cultured cells, and that PV uncoating occurs after retrograde axonal transport of the virus through the sciatic nerve of Tg mice. Thus, PV infection may be established by any of these several pathways. reserved.

Animals↗
PubMed1999

Detection of acute cardiac rejection by analysis of heart rate variability in heterotopically transplanted rats.

BACKGROUND: A less-invasive method for cardiac allograft surveillance than endocardial biopsy is needed. We analyzed heart rate variability of heterotopically transplanted rat hearts as a method of detecting rejection of rat cardiac allografts. METHODS: Two kinds of heterotopic transplants were performed: 1) Brown-Norway rats received Brown-Norway rat isografts, and 2) Lewis rats received Brown-Norway rat allografts. The electrocardiogram (ECG) of the grafts were serially recorded under non-anesthetized and non-restricted conditions using a telemetric ECG transmitter implanted in the recipient's abdomen. Frequency domain analysis of the ECGs was performed using a fast Fourier algorithm. RESULTS: Total power of the heart rate variability in the isograft heart was reduced to 1.1%, compared to normal subjects without transplantation (p < .001). In the allograft heart, it was also reduced to 1.0% on days 1.5 (rejection score 0 to 1), but gradually increased thereafter up to 185% on day 6 (rejection score 3.75+/-0.50). The increase in spectral power was frequency-dependent (i.e., changes in the power in lower frequency range [LF, 0.04 to 0.67 Hz] were significantly higher than other ranges). This increase was reversible when immunosuppressive therapy was performed with the use of cyclosporine A. In the allograft group, peak-to-peak amplitudes of the QRS complex and heart rate were significantly decreased on day 5.5 or later, whereas the power of the LF was significantly increased by day 3.5 or later. CONCLUSIONS: Our data suggest that heart rate variability analysis is a promising noninvasive marker for early detection of cardiac allograft rejection. This method may also provide a sensitive means of assessing the effects of immunosuppressive therapy.

Abdomen↗
PubMed1999

Effects of pimobendan on the L-type Ca2+ current and developed tension in guinea-pig ventricular myocytes and papillary muscle: comparison with IBMX, milrinone, and cilostazol.

In this study, we compared the effects of pimobendan (PIM), a putative Ca(2+)-sensitizer and phosphodiesterase (PDE) inhibitor, on the L-type Ca2+ current (ICa) of guinea-pig ventricular myocytes and contractile tension of ventricular papillary muscles with those of a nonselective PDE inhibitor, isobutylmethylxanthine (IBMX), and selective PDE-III inhibitors, that is, milrinone (MIL) and cilostazol (CIL). The efficacy (maximum attainable effect) of these drugs for increasing ICa or developed tension (DT) ranged in the order of IBMX >> MIL > PIM > CIL. This finding suggests that the positive inotropic effect of each drug is roughly proportional to its increasing effect on ICa. The additional effect of PIM (a Ca(2+)-sensitizing effect) was not identified in "intact" preparations, and the potentiating effects of PIM on the DT and ICa were virtually the same as those observed for MIL. To isolate the Ca(2+)-sensitizing effect of PIM on the DT, we studied the effects of PIM in the presence of H89, an isoquinoline derivative possessing a selective inhibitory effect on cAMP-dependent protein kinase. In the absence of H89, 50 microM PIM increased the DT by 68 +/- 11% (mean +/- SE, n = 6). However, in the presence of 20 microM H89, which completely blocked the PIM-induced increase in ICa, PIM (50 microM) significantly increased the DT by 19 +/- 6% (n = 6), thereby indicating the presence of a positive inotropic effect attributable to a mechanism other than increased intracellular cAMP, that is, a Ca(2+)-sensitizing effect. The latter notion was supported by the finding that in the presence of H89 (20 microM), the PIM-induced augmentation of DT was accompanied by a prolongation of the time to 50% relaxation of contractile tension. In contrast, MIL (50 microM) and forskolin, a direct activator of adenylate cyclase (1-10 nM), did not increase DT in the presence of 20 microM H89. These results suggest that the fraction of positive inotropic effect of PIM attributable to its Ca(2+)-sensitizing effect is masked by its potent PDE-III inhibitory effect in "intact" ventricular preparations.

1-Methyl-3-isobutylxanthine↗
PubMed1999

Mutations in COL11A2 cause non-syndromic hearing loss (DFNA13).

We report that mutation of COL11A2 causes deafness previously mapped to the DFNA13 locus on chromosome 6p. We found two families (one American and one Dutch) with autosomal dominant, non-syndromic hearing loss to have mutations in COL11A2 that are predicted to affect the triple-helix domain of the collagen protein. In both families, deafness is non-progressive and predominantly affects middle frequencies. Mice with a targeted disruption of Col11a2 also were shown to have hearing loss. Electron microscopy of the tectorial membrane of these mice revealed loss of organization of the collagen fibrils. Our findings revealed a unique ultrastructural malformation of inner-ear architecture associated with non-syndromic hearing loss, and suggest that tectorial membrane abnormalities may be one aetiology of sensorineural hearing loss primarily affecting the mid-frequencies.

Amino Acid Sequence↗
PubMed1999

Bepridil differentially inhibits two delayed rectifier K(+) currents, I(Kr) and I(Ks), in guinea-pig ventricular myocytes.

1. We investigated the effects of bepridil on the two components of the delayed rectifier K(+) current, i.e., the rapidly activating (I(Kr)) and the slowly activating (I(Ks)) currents using tight-seal whole-cell patch-clamp techniques in guinea-pig ventricular myocytes, under blockade of L-type Ca(2+) current with nitrendipine (5 microM) or D600 (1 microM). 2. Bepridil decreased I(Ks) under blockade of I(Kr) with E4031 (5 microM), in a concentration-dependent manner. The concentration-dependent inhibition of I(Ks) by bepridil was fitted by a curve, assuming one-to-one interactions between the channel and the drug molecule. The concentration of half-maximal inhibition (IC(50)) was found to be 6.2 microM. 3. The effect of bepridil on I(Kr) was assessed using an envelope-of-tails test. In the control condition, a ratio of the tail current to the time-dependent current measured during depolarization was large (>1) at shorter pulses (<200 ms), and it decreased to a steady state value of approximately 0.4 with increases in the pulse duration. Bepridil at a concentration of 2 microM did not decrease this ratio at shorter pulses. 4. In a short-pulse (duration=50 ms) experiment that largely activates I(Kr), the drug was found to block I(Kr) in a cooperative manner (Hill coefficient=3.03) and the IC(50) was 13.2 microM. 5. These results suggest that bepridil at a clinical therapeutic concentration ( approximately 2 microM) selectively blocks I(Ks) but does not inhibit I(Kr). This may relate to the characteristic frequency-dependent effects of bepridil on the action potential duration (APD), e.g., the non-reverse use-dependent prolongation of APD.

Action Potentials↗
PubMed1999

A new Ca-antagonist, azelnidipine, reduced blood pressure during exercise without augmentation of sympathetic nervous system in essential hypertension: a randomized, double-blind, placebo-controlled trial.

This study was carried out to evaluate the effect of a new long-acting calcium-channel antagonist, azelnidipine, on hemodynamic and neural responses to exercise. Ten patients (age, 36-69 years) with mild essential hypertension were enrolled in this study. A randomized, double-blind, crossover treatment of azelnidipine at a dose of 8.0 mg once daily for 4 weeks was performed. After a 4-week placebo period, the patients exercised in a submaximal test by using an ergometer with azelnidipine or placebo treatment. The changes caused by exercise in arterial blood pressure (BP), heart rate, cardiac output (CO), and systemic vascular resistance were evaluated. In addition, the plasma norepinephrine (NE), epinephrine (E), plasma renin activity, and plasma aldosterone concentration were determined at rest, at peak exercise, and at the recovery period. Both the SBP and diastolic (D) BP were decreased at rest by azelnidipine treatment (from 158 +/- 10/97 +/- 7 to 145 +/- 14/90 +/- 9 mm Hg). Azelnidipine significantly decreased both SBP and DBP during exercise (SBP, F = 6.09, p < 0.05, Fi = 0.612, NS; DBP, F = 17.78, p < 0.001, Fi = 0.298, NS). No significant changes in the resting heart rate and CO were observed, and the exercise-induced increase of these parameters was also not affected by azelnidipine. Azelnidipine produced no significant change of the resting plasma NE and E levels and an exercise-induced increase of plasma NE. In conclusion, these results indicate that azelnidipine, different from another dihydropyridine-type calcium channel antagonists, does not produce any changes in the hemodynamic and neurohumoral response to exercise, and it may be beneficial for patients with mild essential hypertension.

Adult↗