JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
Volume 51, Issue 10
Displaying 1-15 of 15 articles from this issue
  • OSAMU TOCHIKUBO, NAOMICHI MIYAZAKI, YUTAKA YAMADA, MASAKAZU FUKUOKA, Y ...
    1987 Volume 51 Issue 10 Pages 1123-1130
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The characteristics of 24-hour blood pressure variation in hypertensive patients were assessed using new indices of variability. Blood pressure of 43 inpatients with essential hypertension was measured using a portable device without disturbing daily behaviors. Variances in systolic and diastolic pressure values obtained for a day (SDd2), and short-term (SDh2) and long-term (SD242) variances were calculated; their relationship was expressed as SDd2 =SDh2 + SD242. SDh and SD24 were expedient in assessing the relatively fast and slow blood-pressure variations, respectively. The results showed that the ratio SDh2/SDd2 (percentile of the short-term variance in a whole-day variance) increased and therefore SD242/SDd2 decreased as age increased for both systolic and diastolic pressures. It was found, moreover, that systolic SDh was significantly related to age and baroreflex sensitivity, and systolic SD24 to the heart rate during waking hours. The physiological and clinical significance of SDh and SD24 is discussed, briefly, including arterial wall stiffness.
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  • KAZUSHI TSUDA, SEIKO TSUDA, ICHIRO NISHIO, YOSHIAKI MASUYAMA
    1987 Volume 51 Issue 10 Pages 1131-1137
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The present study was carried out to elucidate the role of epinephrine as a neuromodulator in hypertension. The effects of epinephrine on norepinephrine release form the sympathetic nerve endings were examined in isolated perfused mesenteric arteries of spontaneously hypertensive rats (SHR) and age-matched Wistar Kyoto rats (WKY). Norepinephrine overflow during electrical nerve stimulation (5, 15 Hz) was significantly greater in SHR than in WKY. Low concentration of exogenous epinephrine (5.5×10-9 M) potentiated norepinephrine overflow during nerve stimulation in SHR, and this (at 15 Hz stimulation) was antagonized by propranolol (5.0×10-7 M), whereas, the overflow in WKY was reduced y the same concentration of epinephrine. A high concentration of epinephrine (1.4×10-8 M) decreased norepinephrine overflow in both SHR and WKY, and this change (at 15 Hz stimulation) was antagonized by yohimbine (1.0×10-7 M). Further, magnitudes of the suppression were smaller in SHR than in WKY. These results suggest that altered modulations of norepinephrine release by epinephrine through presynaptic β- and α2-adrenoceptors might induce increased sympathetic nerve activity in SHR.
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  • KAZUHIKO YOSHIMURA, TOSHIO KOBAYASHI, SHOZO KUSAMA, AKIO SAKAI, GOU UE ...
    1987 Volume 51 Issue 10 Pages 1138-1146
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    We evaluated the effects of captopril and nifedipine on normoxic and hypoxic pulmonary vascular tone in unanesthetized sheep. Infusion of captopril (10 μg/kg/min) in normoxia revealed a tendency to increase the mean pulmonary arterial pressure (Ppa) and the pulmonary vascular resistance (PVR) following the systemic vasocilation. A statistically significant increase was reached by 20 minutes. Hypoxia of 10% oxygen in nitrogen produced a prominent pulmonary hypertensive response. Captopril significantly decreased the hypoxic values of Ppa and PVR from 20.3±1.3 to 17.1±1.1 mmHg (p<0.01) and from 4.31±0.45 to 3.49±0.45 mmHg/L/min (p<0.01), respectively. Infusion of nifedipine (10 μg/kg/min) in normoxia caused an increase in Ppa from 15.5±0.9 to 18.9±1.0 mmHg (p<0.01), but not in PVR. This elevation in Ppa was considered to be derived from the significant increase in the cardiac output. Nifedipine significantly decreased the hypoxic values of Ppa and PVR from 21.3±1.5 to 19.3±1.5 mmHg (p<0.01), respectively. Captopril and nifedipine produced systemic hypotensive responses during both normoxic and hypoxic ventilation. It is concluded that both captopril and nifedipine are potent pulmonary vasodilating drugs in animal subjects with a hypoxic condition and that they might be useful in the clinical vasodilator therapy of hypoxic pulmonary hypertension in man.
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  • KINJI ISHIKAWA, KEN KANAMASA, SHUICHIRO OSATO, TOSHIHIRO OGAI, AKIO OD ...
    1987 Volume 51 Issue 10 Pages 1147-1156
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    It has been stated that the coronary flow paradoxically falls in response to tachycardia if the coronary artery is stenotic and "compliant". To clarify this, we measured coronary vascular resistance by cannulating the left anterior descending coronary artery in open-chest dogs. In constant flow perfusion of 41±5 ml/min/100 gm, coronary perfusion pressure was decreased by pacing, while at lower flow of 14±3 ml, it was increased by pacing, indicating that coronary vascular response was reversed. In constant pressure perfusion, coronary vascular resistance was reduced by pacing at high perfusion pressure, while it was paradoxically increased by pacing at low perfusion pressure. In the third experiment at constant flow perfusion, perfusing blood was changed from arterial to venous blood to induce myocardial hypoxia. At high flow, venous blood perfusion reduced coronary vascular resistance, while at low flow it increased coronary vascular resistance. All three experiments indicated that at high perfusion, tachycardia and hypoxia caused a reduction in coronary vascular resistance to meet the increased myocardial oxygen demand; however, at low perfusion, those stimuli increased coronary vascular resistance. The present study showed that the coronary vascular response is reversed at low flow and suggested that those stimuli might reduce flow further in patients with stenotic coronary artery and could be one of the mechanisms causing the development of myocardial infarction in those patients.
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  • YORINOBU SONODA, KEISUKE MORI, HIROFUMI YASUE, YUTAKA HORIO
    1987 Volume 51 Issue 10 Pages 1157-1162
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    We have developed a simple quantitative analysis system for coronary cineangiograms using a personal computer and a standard projector-video camera system. The selected frame of cinefilm was projected onto the target area of a CCD video camera. To decrease spatial fluctuations due to quantum noise, the digital data were smoothed spatially by applying a moving averaged filter and a median filter. Following the smoothing process, the digital data with gray level were transformed to binary data by quantifying the threshold property of their gray level. To minimize the geometric influence, mainly pincushion effect, a cinefilm of a 1 cm grid was placed against the input screen of the image intensifier to correct the distortion by using 3rd degree polynomials. The accuracy of the contour detection procedure was validated on the basis of phantom models filled with a contrast medium. Despite the potential influence of many radiographic variables on computerized diameter measurements, the overall accuracy was found to be 0.26-0.33 mm over a wide range of clinically relevant artery diameters and radiographic conditions. Using this system we demonstrated one method of examining the effects of acetylcholine and nitroglycerin on coronary artery diameter in adult humans.
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  • YUKI ISHZUKA, YUKIO MIURA, SHINOBU KIMURA, HIROBUMI OHASHI, TAKASHI SU ...
    1987 Volume 51 Issue 10 Pages 1165-1173
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Baroreflex sensitivity was evaluated in 19 patients with essential hypertension (EH), 8 patients with borderline hypertension (BH) and 12 age-matched normal controls (N), by measuring the reflex-mediated changes in plasma norepinephrine (NE) and heart rate (RR interval) while a phenylephrine hydrochloride or a sodium nitroprusside solution was infused in graded doses for a total of 24 minutes. Changes in RR interval and plasma NE showed a significant linear correlation to those in mean arterial pressure (MAP) in every subject studied. The slopes of RR/MAP and %NE/MAP tended to be reduced in EH and BH patients during both pressor and depressor stimulations. There was a significant (p<0.01) inverse correlation between the basal MAP levels an RR/MAP or %NE/MAP except for %NE/MAP during pressor stimulation. Fifteen minutes after the pressor stimulation was stopped, MAP and RR interval in each group tended to be greater than their baselines. Plasma NE remained significantly (p<0.01) depressed in N and BH subjects while those in EH returned to their baselines. When pressor stimulations were repeated twice at intervals of 15 minutes in hypertensive subjects, the second response curves of MAP-RR interval tended to shift slightly to the right while the slopes of the second response curves of plasma NE were significantly (p<0.05) reduced compared with the first ones. These findings indicate that an inability of the baroreflex to produce a sustained suppression of sympathetic nerve activity associate with an efficient ability to reset at the higher pressure levels in EH patients results in a continued tendency for blood pressure to rise and contributes to the development of hypertension.
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  • OSAMU TOCHIKUBO, HISAO OCHIAI, TAKASHI OOTA, EIJI MIYAJIMA, YOSHIHIRO ...
    1987 Volume 51 Issue 10 Pages 1174-1183
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The intra-arterial blood pressure (BP) was measured during 24 hours on 52 patients with essential hypertension using a portable device. The minimum BP inherent to each subject (base BP) was determined from the systolic and diastolic BP histograms during sleep. In this study the systolic and diastolic BPs were presented as a mean BP ((BP)^^-) and a base (BP)^^-, and the average of (BP)^^-s during waking hours was considered as the sum of the base (BP)^^- and the additional (BP)^^- increment. The crinical significance of the base (BP)^^- and (BP)^^- increment was examined by comparing them with the results of clinical examinations. The comparison showed that the base (BP)^^- was closely related with the left ventricular hypertrophy and severity of hypertension, while the (BP)^^- increment correlated with the baroreflex sensitivity and plasma norepinephrine concentration. In this paper, a new tonometry was developed to indirectly record the BP of the superficial temporal artery. The tonometry correlated well with the intra-arterial BP measurement, and was available for the indirect base BP evaluation at an outpatient-clinic.
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  • TETSUYA OSHIMA, HIDEO MATSUURA, KOJI KIDO, KOJI MATSUMOTO, TOMOFUMI OT ...
    1987 Volume 51 Issue 10 Pages 1184-1190
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    In order to clarify the relation between salt sensitivity and changes in intracellular sodium ([Na]i) and free calcium concentration ([Ca2+]i) after salt loading, [Na]i and [Ca2+]i were determined in lymphocytes of twenty patients with essential hypertension under a low salt diet (3 g/day) and a high salt diet (20 g/day) for seven days, respectively. They were classified as "salt-sensitive" (n=10) or "nonsalt-sensitive" (n=10) on the basis of the changes in blood pressure after salt loading. Both lymphocytic [Na]i and [Ca2+]i were significantly increased with salt loading in salt-sensitive patients (p<0.05 for both), while they were not affected by salt loading in nonsalt-sensitive patients. Lymphocytic [Ca2+]i showed a positive correlation with lymphocytic [Na]i under both low salt diet (r=0.62, p<0.01) and high salt diet (r=0.70, p<0.01) in all patients in both groups. In addition, a close and positive correlation was observed between the changes in lymphocytic [Na]i and those in lymphocytic [Ca2+]i after salt loading in all patients in both groups (r=0.80, p<0.001). These results suggest that the increase in [Ca2+]i, possibly linked with the increase in [Na]i, may be involved in elevation of blood pressure in the salt-sensitive patients after salt loading.
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  • TAKAAKI MOTOYAMA, HIROSHI SANO, HIROSHI SUZUKI, KEIZO KAWAGUCHI, HISAS ...
    1987 Volume 51 Issue 10 Pages 1191-1198
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Selective sodium loading attenuated the development of hypertension in the deoxycorticosterone acetate (DOCA) treated rat. The DOCA treated rat fed a diet equimolar in sodium to a 7% sodium chloride diet and in chloride to a standard diet, differed in various parameters from the DOCA treated rat fed a 7% sodium chloride diet : it had higher sodium concentration in both erythrocytes and muscles, a higher erythrocyte ouabain sensitive 22Na efflux rate constant (Kos), and a lower norepinephrine turnover rate in the heart and the spleen. These results suggest that the suppressed sympathetic nervous system activity and the activated cell membrane sodium pump contribute in part to the mechanism for the suppression of the development of hypertension in the DOCA-selective sodium loaded rat.
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  • HAKUO TAKAHASHI, MAKOTO MATSUZAWA, HIDEOKI OKABAYASHI, KEISUKE SUGA, I ...
    1987 Volume 51 Issue 10 Pages 1199-1207
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The origin and the physiological role of an endogenous digitalis-like substance were investigated by measuring both the digoxin-like substance by a digoxin radioimmunoassay (RIA) and the inhibitory activity on the ouabain sensitive Na+, K+-ATPase in rats. The digitalis-like substance was in high concentration in the pituitary, and in decreasing concentration in the hypothalamus, adrenal and the other organs as measured by RIA using an antibody raised from a goat. However, the adrenal showed the highest content of digitalis-like substance as measured by the antibody raised from a rabbit. The plasma level markedly decreased during a 2-week sodium-loading, and the adrenal content decreased markedly on hypophysectomy as measured with the rabbit-antibody. Therefore, the substance measured with the rabbit-antibody must be one of ACTH-dependent adrenal steroids. The inhibitory activity on the Na+, K+-ATPase was high in he pituitary gland, and was decreased in order of the adrenal, hypothalamus and other organs. The 2-week sodium-loading increased both the content in the pituitary gland and the output in the urine, and decreased the hypothalamic content. Immunohistochemical staining of the hypothalamus with the antibody revealed that the immunoreactivity is restricted to the neurons of the paraventricualr nucleus, supraoptic nucleus, magnocellular accessary nuclei and extended their fibers reaching to the inner layer of the median eminence. To determine the role of the substance in the brain, the crude extract dissolved in artificial cerebrospinal fluid was injected into the lateral ventricle; vasopressor responses, tachycardia and hyperactivity of the splanchinic nerve lasting for more than 30 min were recorded, which resembled the responses to ouabain injected similarly. Electrical lesions of the anteroventral third ventricle significantly attenuated the DOCA-salt hypertension and decreased the urinary output of the digitalis-like activity. These results suggest that the digitalis-like substance could be produced in the hypothalamus and secreted from the pituitary gland in a fashon similar to vasopressin secretion, and that the turnover is increased in the hypothalamus with sodium-loading. The substance could also play a physiological role on the central cardiovascular regulation to increase blood pressure particularly when sodium is loaded.
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  • HIROSHI ITOH, KAZUWA NAKAO, NARITO MARII, AKIRA SUGAWARA, TAKAYUKI YAM ...
    1987 Volume 51 Issue 10 Pages 1208-1215
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The effects of intracerebroventricular (i.c.v.) administration of ANP on blood pressure and intakes of water and salt were examined, using conscious, unrestrained normotensive Wistar rats and spontaneously hypertensive rats (SHR). In normotensive rats, i.c.v. administration of α-rat ANP (α-rANP), α-human ANP (α-hANP), α-rANP (4-28) and α-rANP (5-28) at the dose of 1.5 nmol significantly attenuated water intake induced by i.c.v. injection of 0.1 nmol of angiotensin II (AII). Centrally administered α-hANP (5 μg) also attenuated AII-induced pressor response. Centrally injected α-hANP (1 μg) produced a greater reduction of water intake after 24-hour water deprivation in SHR compared to control WInstar Kyoto rats (WKY). Central infusion of α-hANP for 1 week also reduced the salt appetite of SHR, as shown by two bottle preference test with 0.3 N NaCl solution and tap water, while it had no effect on drinking behavior of WKY. These results suggest the central antagonistic relationship of the ANP and renin-angiotensin systems and the possible involvement of brain ANP in the pathophysiology of genetically hypertensive rats.
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  • AKIRA BABA, KAZUYA FUKUDA, MASATO KUCHII, MASAKO URA, HIROYUKI YOSHIKA ...
    1987 Volume 51 Issue 10 Pages 1216-1222
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    Using fluorescent calcium indicator quin2, we studied intracellular free calcium concentration in platelets that have a number of features similar to vascular smooth muscle cells. Intracellular free calcium concentration in platelets of male SHR was significantly higher at 4, 11 and 28 weeks old compared with age-matched male WKY. However, no significant difference was observed in platelets cytosolic free calcium level of DOCA-salt hypertensive and two-kidney, one clip hypertensive rats in the chronic stage. Cardiac Ca++ channels were estimated by means of radioligand binding method with [3H]-nimodipine. No significant changes were observed in the concentration and affinity of cardiac Ca++ channel in SHR, DOCA-salt hypertensive and two-kidney, one clip hypertensive rats. Calmodulin levels in mesenteric arteries of SHR were significantly decreased in comparison with those of WKY. However no significant differences were observed in DOCA-salt hypertensive rats in the chronic stage. These results indicate that the increase in intracellular free calcium concentration of SHR is not the secondary change caused by high blood pressure. It is impossible to detect the ratio of the three states (open, resting and inactivated) of Ca++ channel. Therefore, there remains a possibility of the changes in the ratio of he states of Ca++ channel. The observed abnormalities of Ca++ regulation may contribute to the pathogenesis of hypertension.
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  • SHINGO SHIBATA, KENJIRO KIKUCHI, IZUMI YAMAJI, AKIHIKO NOZAWA, MITSUHI ...
    1987 Volume 51 Issue 10 Pages 1223-1225
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
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  • MANABU YOSHIMURA, SEIICHI KAMBARA, HIDEOKI OKABAYASHI, IWAO IKEGAIKI, ...
    1987 Volume 51 Issue 10 Pages 1226-1231
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    The aim of the study is to investigate the pathophysiological role of dopamine (DA) in the development of hypertension in DOCA-salt hypertensive rats and spontaneously hypertensive rats (SHRs). The augmentation of dopaminergic activity by chronic administration of bromocriptine, a DA agonist, suppressed the increase of blood pressure in DOCA-salt hypertensive rats. In contrast, suppression of dopaminergic activity by chronic administration of carbidopa, an inhibitor of dopa decarboxylase, accelerated the development of hypertension in SHRs, and this acceleration was also increased by salt loading. Increased urinary excretion of norepinephrine (NE) by DOCA-salt treatment was suppressed by the treatment of bromocriptine. In contrast, administration of carbidopa and salt loading in SHRs resulted in an increase in renal NE content and in urinary NE and epinephrine (E) excretion and a decrease in urinary sodium excretion. These results suggest that dopaminergic activity participate in the development of hypertension and decreased dopaminergic activity accelerates the development of hypertension in hypertensive rats mainly through the enhancement of peripheral sympathetic nerve activity.
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  • OSAMU IIMURA, IZUMI YAMAJI, KENJIRO KIKUCHI, SHINGO SHIBATA, MITSUHIRO ...
    1987 Volume 51 Issue 10 Pages 1232-1240
    Published: October 20, 1987
    Released on J-STAGE: April 14, 2008
    JOURNAL FREE ACCESS
    To evaluate the role of the renal dopaminergic system on renal water-sodium metabolism patients with essential hypertension (EHT), urinary excretion of dopamine, urinary excretion of sodium (UNaV) and fractional excretion of sodium (FENa) were all investigated before and after the administration of dopamine (3 μg/kg/min, intravenous infusion for 60 minutes), dopamine antagonist, metoclopramide (8 mg/m2 BSA, intravenous injection) or mild sodium loading in both normotensive subjects and benign EHT). In the basal values, no significant difference in urinary excretion of free (u-fDA), conjugated (u-cDA) or total dopamine (u-tDA) was found between normotensives and hypertensives. However, low renin EHT showed a pronounced reduction in u-fDA compared with normotensis subject and (NT) normal renin EHT. In this study, a significant reduction of u-cDA and of u-tDA was also found in those patients with low renin essential hypertension. In the normotensive and essential hypertensive groups UNaV or FENa showed a positive correlation with u-fDA (measured simultaneously), but not with u-tDA or u-cDA. The regression line between u-fDA and UNaV or FENa in EHT was shifted towards a lower u-fDA level than in NT. UNaV and FENa were increased by dopamine infusion and were decreased by metoclopramide injection in both NT and EHT. Changes of UNaV and FENa following dopamine or metoclopramide, showed a negative correlation with u-fDA measured immediately before the administration of these drugs. The enhanced natriuretic response to infused dopamine and the attenuated antinatriuretic response to injected metoclopramide were significant in low renin EHT, when compared with NT or normal renin EHT patients. Mild sodium loading brought about significant increases of UNaV, FE Na and u-fDA, while no change took place in u-tDA or u-cDA in EHT. These findings suggest that the renal dopaminergic activity, which might play an important role in sodium handling of the kidney, was attenuated in EHT particularly in low renin EHT. This attenuation may contribute to the water-sodium expansion in the pathophysiological mechanisms of EHT and in particular low renin EHT.
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