Shuichi Sasaki

Altered circadian blood pressure rhythm in patients with Cushing's syndrome.

The circadian blood pressure rhythm was compared in patients with Cushings syndrome, essential hypertension, and primary aldosteronism. In patients with essential hypertension or primary aldosteronism, a clear nocturnal fall in systolic and diastolic blood pressure and heart rate was observed. This fall was seen in untreated subjects as well as in patients receiving combined treatment with a calcium antagonist, diuretic, converting enzyme inhibitor, alpha-blocker and beta-blocker, or sympatholytic drug. In these groups, there was a positive correlation between heart rate and systolic or diastolic blood pressure. On the other hand, in patients with Cushings syndrome, there was no nocturnal fall in blood pressure but in some patients a rise was observed. In all patients there was a nocturnal fall in heart rate. Thus, there was no significant correlation between heart rate and blood pressure in these patients. Exogenous glucocorticoid eliminated the normal nocturnal fall of blood pressure in patients with chronic glomerulonephritis or systemic lupus erythematosus. These results suggest that the changed circadian blood pressure pattern in patients with Cushings syndrome is not due to antihypertensive treatment or to the mineralocorticoid excess accompanying this disease, but it is attributable to excess glucocorticoid or the associated disturbance in the adrenocorticotropic hormone-glucocorticoid system (or both). This conclusion also implies that the normal circadian rhythm of blood pressure may be regulated at least in part by the adrenocorticotropic hormone-glucocorticoid system.

Clinical evaluation of semiautomatic and automatic devices for home blood pressure measurement: comparison between cuff-oscillometric and microphone methods.

The accuracy and reliability of blood pressure (BP) values were evaluated by comparing values obtained with eight automatic or semiautomatic devices designed for home BP measurement (four microphone devices based on the Korotkoff-sound technique and four cuff-oscillometric devices) with those obtained by the auscultatory method, using a standard mercury sphygmomanometer. Systolic blood pressure (SBP) values obtained using the microphone devices coincided well with those obtained by the auscultatory method. However, these devices produced a certain proportion of errors in the measurement of diastolic blood pressure (DBP), sometimes resulting in recordings at least 25mmHg higher than those obtained by the standard method. The most frequent causes of this phenomenon were an auscultatory (silent) gap and a weak Korotkoff sound after phase IV. A microphone device using a condenser microphone built into the manometer displayed comparatively good acoustic characteristics for determining DBP. All cuff-oscillometric devices demonstrated minimal mean differences and a constant s.d. of mean difference for DBP, with no great differences from the auscultatory method. However, mean differences and s.d.s in SBP measurements using cuff-oscillometric devices were relatively greater than those obtained using some of the microphone devices. Furthermore, the direction of the mean differences in measurements from those obtained with the auscultatory method differed. The error in relation to the auscultatory method tended to be reproducible in the same subjects with both the microphone and the cuff-oscillometric devices. These results indicate that practitioners should select the most appropriate method and/or device by taking into account the factors which may cause measurement error in relation to the auscultatory method in each subject, and should then evaluate, at least once, the difference in BP values obtained using the auscultatory method and using the device. In future, home blood pressure measurement devices for determination of SBP should employ a microphone method, while a method which combines a microphone with a cuff-oscillometric device, thereby compensating for the disadvantage of the Korotkoff-sound signal with the pulse wave signal, should be recommended for measurement of DBP.

Exogenous glucocorticoid eliminates or reverses circadian blood pressure variations.

The effect of glucocorticoid on circadian variations of blood pressure was examined. In untreated patients with essential hypertension, a clear nocturnal fall in blood pressure and heart rate was observed and this was unaffected by combined treatment with antihypertensive drugs. The circadian blood pressure variation in patients with chronic glomerulonephritis (CGN) not receiving glucocorticoid treatment was essentially the same as that in patients with essential hypertension. In both groups there was a positive correlation between blood pressure and heart rate. On the other hand, in patients with CGN and systemic lupus erythematosus (SLE) who were treated with glucocorticoid, there was no nocturnal fall in blood pressure, and often a significant rise. In these patients the blood pressure was lowest in the afternoon and began to rise from then, and during the night, attaining a peak level in the morning. Despite this changed pattern of blood pressure variations, the heart rate in these patients was clearly reduced at night. In 10 patients with CGN and SLE, circadian rhythm of blood pressure and heart rate was examined before and during treatment with prednisolone (40.2 ± 17.0mg/day for 58.0 ± 19.4 days, mean ± s.d.). Prednisolone abolished the nocturnal fall of blood pressure, while the nocturnal fall of heart rate remained. There was no correlation between blood pressure and heart rate in patients with glucocorticoid treatment. These results suggest that the circadian blood pressure variation is influenced by the hypothalmo-pituitary-adrenal axis, probably through its action on the autonomic nervous system.

A Finger Volume-Oscillometric Device for Monitoring Ambulatory Blood Pressure: Laboratory and Clinical Evaluations

A new portable device for the indirect measurement of ambulatory blood pressure in the finger was successfully applied to normotensive and hypertensive subjects in and outside a ward setting. The device uses the volume-oscillometric technique and, equipped with a microprocessor, permits long-term ambulatory monitoring of indirect systolic and mean blood pressure at desired intervals (once every 1-10 min). Systolic and mean blood pressures obtained by this method were well correlated with those measured by the direct (Oxford) and arm-cuff methods. Systolic and diastolic blood pressure obtained by the volume-oscillometric device were almost identical with those recorded by an arm-cuff. Systolic blood pressure obtained by the volume oscillometric method was, however, significantly lower than that measured by the direct method. The new device has also been used to measure blood pressure during treadmill exercise and ice-water immersion. Mean values of blood pressure and the SD of these averaged for 24 hours, or for every hour, were reproducible when the measurements were repeated under the same condition. The present device is portable, causes minimal noise, can detect rapid change in blood pressure and causes less discomfort when compared to the conventional arm-cuff method. Regular measurements can be made with minimal sleep disturbance. This fully automatic volume-oscillometric device allows reliable 24-hour monitoring of ambulatory blood pressure not only in but also outside a ward setting, and as such is useful for studies of hypertension.

Suppression by glucocorticoid of the immunoreactivity of corticotropin-releasing factor and vasopressin in the paraventricular nucleus of rat hypothalamus

The effect of glucocorticoid on the production of corticotropin-releasing factor (CRF) and vasopressin in the paraventricular nucleus of the hypothalamus (PVH) was examined immunocytochemically. Intraperitoneal administration of dexamethasone sulfate in a dose of 0.1 mg/day suppressed the immunoreactivity of CRF and vasopressin in the medial parvocellular divisions of the PVH of the rat subsequent to bilateral adrenalectomy. In the magnocellular divisions, suppression of vasopressin-immunoreactivity was not observed. These results suggest that the vasopressin in the medial parvocellular divisions plays a distinct role from that in the magnocellular divisions, the former having functional significance in the hypothalamo-hypophysio-adrenal axis.

Role of vasopressin in cardiovascular response to central cholinergic stimulation in rats.

The cardiovascular effects of centrally administered cholinomimetics were examined in conscious Long-Evans and Brattleboro rats. Carbachol (1 μg/kg) or physostigmine (50 μg/kg) induced a long-lasting increase in blood pressure and a decrease in heart rate in Long-Evans rats whereas no bradycardia was observed in Brattleboro rats, and the pressor response was significantly less than that in Long-Evans rats. The cardiovascular responses to nicotine (30 μg/ kg) in Brattleboro rats were not different from those in Long-Evans rats. Intravenous vasopressin antagonist, d(CH2)5Tyr(Me) arginine vasopressin, significantly attenuated the pressor response and eliminated the bradycardic response to carbachol hi Long-Evans rats. However, the pressor response to carbachol in Brattleboro rats was still significantly less than that in Long-Evans rats treated with vasopressin antagonist. Intravenous phentolamine partially inhibited the pressor response to carbachol in Long-Evans rats and completely eliminated it in Brattleboro rats. Combined intravenous treatment with phentolamine and vasopressin antagonist completely eliminated the pressor response to carbachol in Long-Evans rats. Centrally administered methylatropine eliminated either the hypertensive or bradycardic response to carbachol in Long-Evans rats. These results indicate that the pressor and bradycardic response to carbachol or physostigmine is mediated by the central muscarinic receptor mechanism. Hypertensive response to intracerebroventriculaiiy administered carbachol in normal rats is mediated both by an increase in central sympathetic outflow and in circulating vasopressin. The bradycardia seems to be mediated mainly by vasopressin.

Assessment of age-dependent changes in circadian blood pressure rhythm in patients with essential hypertension

The effects of age on the circadian blood pressure rhythm of patients with untreated essential hypertension (n = 133, World Health Organization stage I or II) were compared with those of normotensive subjects (n = 91). Subjects were classified into three groups by age: young (less than 40 years old), adult (40-59 years old) and old (greater than or equal to 60 years old). Blood pressure was monitored every 5 min for 24 h, using a finger volume oscillometric device under fixed external conditions. The single cosinor method was used to evaluate circadian rhythm. There was no difference in the amplitude of circadian systolic or diastolic blood pressure rhythm among the different normotensive and essentially hypertensive age groups although a wide distribution of amplitude was noted within each group. The distribution of amplitude was wider in the hypertensive than in the normotensive groups. The amplitude of circadian blood pressure rhythm was independent of the mesor level. On the other hand, the amplitude of circadian heart rate rhythm decreased with increasing age both in normotensive subjects (P less than 0.05, young versus adult or old) and hypertensive patients (P less than 0.01, young and old versus adult). The acrophase of circadian systolic blood pressure rhythm in young hypertensives was greater than that in adult or old hypertensives (P less than 0.05, for both). Such age-dependent changes were not observed in the normotensive groups. Consequently, the acrophase of circadian systolic or diastolic blood pressure rhythm in young hypertensives was larger than that in young normotensives (P less than 0.05, for both systolic and diastolic blood pressure).(ABSTRACT TRUNCATED AT 250 WORDS)

Circadian blood pressure variation in patients with renovascular hypertension or primary aldosteronism.

Circadian blood pressure (BP) variation were studied in patients with renovascular hypertension (RVH) and primary aldosteronism (PA). Ambulatory BP (ABP) was monitored every 5 min for 24 hrs in a ward setting in 23 patients with PA and 17 patients with RVH (13 patients with unilateral renal arterial stenosis and 4 with bilateral stenosis). In patients with RVH, ABP was monitored before and after treatment with a converting enzyme inhibitor or percutaneous transluminal angioplasty. Plasma renin activity (PRA) was high before percutaneous transluminal angioplasty in almost all patients with RVH and low in those with PA. Ordinary circadian BP variation, i.e. nocturnal fall and diurnal rise in BP, was confirmed in the patients with unilateral or bilateral renal artery stenosis. Percutaneous transluminal angioplasty successfully normalized both BP and PRA in those with RVH. Normal circadian BP variation was observed in those with RVH before the treatment with a converting enzyme inhibitor or percutaneous transluminal angioplasty as well as during treatment with the former and after treatment with the latter. Circadian BP variation in the patients with RVH was affected by the pathogenesis of renal artery stenosis alone, i.e, fibromuscular hyperplasia and atherosclerosis; with fibromuscular hyperplasia normal circadian BP variation was observed, while with atherosclerosis, nocturnal BP fall was restricted or eliminated. Circadian BP variation in those with PA before and after excision of adrenal adenoma was essentially similar to that in normal subjects and essential hypertensive patients. From these it seems that in patients with RVH or PA, circadian BP variation is not affected by hypertension per se or by pathogenesis of hypertension.

Effect of weight loss on blood pressure and drug consumption in normal weight patients.

The effect of weight loss on blood pressure and on antihypertensive drug consumption was examined in 81 nonobese subjects with essential hypertension who had been chronically treated with antihypertensive drugs. A hypocaloric diet was prescribed for 5 months. A weight loss greater than 2 kg in 5 months was considered significant. Quality and quantity of antihypertensive medications were scored according to a formula. In the subjects whose medication and weight did not change, mean arterial pressure remained unchanged, whereas it decreased significantly (-7.1 +/- 1.9 mm Hg) in those who showed significant weight loss (-3.28 +/- 0.34 kg) with no change in medication. Among the subjects whose antihypertensive medication remained constant during the diet program there was a significant correlation between the change in weight and mean arterial pressure (r = 0.45, p less than 0.01). Mean arterial pressure increased significantly (+5.1 +/- 1.7 mm Hg) in subjects whose weight remained unchanged with a decrease in medication, whereas it remained significantly lower than the control (by -3.1 +/- 2.0 mm Hg) in those whose weight decreased significantly (-4.57 +/- 0.69 kg) with the decrease in medication. The weight loss-induced decrease in blood pressure occurred independently of the initial degree of obesity and the initial level of mean arterial pressure. Urinary sodium excretion in the control period and at the end of the diet program did not differ significantly between subgroups. These results indicate that, even in subjects of normal weight with essential hypertension, weight loss can induce a fall in blood pressure that leads to a reduction of antihypertensive medication.(ABSTRACT TRUNCATED AT 250 WORDS)

AGE-RELATED CHANGES IN BLOOD PRESSURE, HEART RATE AND BAROREFLEX SENSITIVITY IN SHR

1 The age‐related changes in mean arterial pressure (MAP), heart rate (HR), and baroreflex sensitivity (BRS) were studied in spontaneously hypertensive rats (SHR) and Wistar‐Kyoto (WKY) rats from 4 to 20 weeks of age. 2 Intra‐arterial blood pressure (BP) was continuously recorded for 24 h in conscious, freely moving rats. Twenty‐four hour MAP and HR were calculated by an online computer. Baroreflex sensitivity was measured by phenylephrine infusion. 3 In SHR, BRS was significantly lower than in WKY as early as 4‐5 weeks, at which time MAP in SHR was only slightly raised. During subsequent weeks, rapid increase in MAP occurred in SHR, in association with progressive bradycardia. 4 It was concluded that a reduced BRS may be detected in young prehypertensive SHR and this impairment of BRS may be central in origin.