Search PubMed⌕ Search

Biomedical subjects

M Kuramochi

Publications and source records attributed to M Kuramochi.

At least 109 records · Page 6Linked to original sources
PubMed1989

Aspirin lowers blood pressure in patients with renovascular hypertension.

To clarify the role of renal prostanoid in hyperreninemia and high blood pressure in human renovascular hypertension, we measured prostaglandin E2 and renin activity in renal venous and abdominal aortic plasma before and after the intravenous administration of the cyclooxygenase inhibitor, aspirin DL-lysine. Subjects were six patients with unilateral renovascular hypertension and six with essential hypertension. In patients with renovascular hypertension, prostaglandin E2 concentration in renal venous plasma from the stenotic kidney was 9.25 +/- 1.48 pg/ml, which was significantly higher (p less than 0.01) than the concentration in the renal venous plasma from the normal kidney (4.97 +/- 1.02 pg/ml) or in the aortic plasma (2.59 +/- 0.15 pg/ml). Plasma renin activity was also higher in the renal vein of the stenotic kidney than in the other two sites. The stenotic side/normal side ratio of the renal venous prostaglandin E2 correlated significantly with a renin ratio greater than 1.5 (r = 0.8211, p less than 0.05). Intravenous injection of aspirin DL-lysine (18 mg/kg) 30 minutes later markedly suppressed prostaglandin E2 and renin levels at all sites and clearly lowered arterial blood pressure (mean: from 120 +/- 6 to 110 +/- 5 mm Hg, p less than 0.01). The reduction in blood pressure correlated significantly with the suppression of plasma renin activity in the aorta (p less than 0.05) and in the renal vein of the stenotic kidney (p less than 0.01). Conversely, in patients with essential hypertension, aspirin had little effect on renin levels and increased mean blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effects of the intracerebroventricular atrial natriuretic factor on angiotensin II or sodium-induced blood pressure elevation and natriuresis.

We examined the effects of intracerebroventricular (i.c.v.) administration of atrial natriuretic factor (ANF) on pressor and natriuretic responses induced by i.c.v. angiotensin II (Ang II) or hypertonic NaCl in conscious male Wistar rats. The i.c.v. artificial cerebrospinal fluid (CSF) or ANF alone did not cause recognizable changes in mean blood pressure (MBP), urinary volume (UV), or sodium excretion (UNaV). The i.c.v. Ang II or 0.6 M NaCl raised MBP, decreased UV, and increased UNaV. When ANF was administered with Ang II, the Ang II-induced changes in MBP, UV, and UNaV were diminished significantly. ANF also opposed the effects of 0.6 m NaCl, though the effect was significant only in the case of blood pressure. Our results indicate that brain ANF may have antipressor and anti-natriuretic roles.

Angiotensin II↗
PubMed1989

[Long-term results of percutaneous transluminal angioplasty in patients with renovascular hypertension--a follow-up study on renal function and renal size].

Twenty patients with renovascular hypertension were followed for at least 1 year (mean 3.3 years) after successful percutaneous transluminal angioplasty (PTA). Renal arteries were patent in 13 (65%) patients and were re-stenosed in 7 (35%). In 12 patients with unilaterally stenosed renal artery which were patent at the end of the follow up period, 6 patients were normotensive, the other 6 patients had less degree of hypertension. Determinations of renal vein renin were only of limited prognostic value. Renal blood flow pattern by doppler echography improved after PTA in the 12 patients. Radioisotope renogram showed tendency of improved Tmax ratio (stenotic kidney/nonstenotic kidney) from 1.5 +/- 0.8 to 1.0 +/- 0.2 (mean +/- SD, p less than 0.1). Serum creatinine levels decreased significantly from 1.2 +/- 0.5 mg/dl to 1.0 +/- 0.2 mg/dl (p less than 0.05) and creatinine clearance increased from 72.1 +/- 18.5 ml/min to 99.6 +/- 31.7 ml/min (p less than 0.02). The size of the stenosed kidneys increased from 11.2 +/- 0.7 cm to 12.0 +/- 0.8 cm (p less than 0.01), while the size of the contralateral kidneys did not change. These results indicate that PTA has favorable long-term effects on blood pressure and renal function with restoration of renal size in cases with patent renal arteries after this procedure.

Adult↗
PubMed1988

Left ventricular structural characteristics in unilateral renovascular hypertension and primary aldosteronism.

To assess the importance of the renin-angiotensin system and plasma volume as determinants of hypertensive left ventricular hypertrophy and its anatomy, patients with unilateral renovascular hypertension and primary aldosteronism were studied by echocardiography. Blood pressure, age and sex were matched as closely as possible. The 19 patients with unilateral renovascular hypertension and the 19 patients with primary aldosteronism were similar in age, sex and blood pressure (168 +/- 19/97 +/- 11 and 163 +/- 17/99 +/- 10 mm Hg, respectively), but plasma volume was increased in the patients with primary aldosteronism. Interventricular septal thickness, left ventricular posterior wall thickness, left ventricular mass index and relative wall thickness did not differ between the 2 groups of patients. There was a significant correlation between the level of systolic blood pressure and either left ventricular mass index (r = 0.34, p less than 0.05) or relative wall thickness (r = 0.58, p less than 0.001) in both groups of patients. Left ventricular end-diastolic dimension index was increased in the patients with primary aldosteronism compared with those with unilateral renovascular hypertension (3.2 +/- 0.4 vs 2.9 +/- 0.3 cm/m2, p less than 0.02). When confined to the patients with systolic pressure greater than or equal to 150 mm Hg, relative wall thickness was significantly increased in the patients with unilateral renovascular hypertension. Patients with primary aldosteronism and unilateral renovascular hypertension of similar blood pressure levels, age and sex have almost identical degrees of left ventricular hypertrophy and anatomy. In contrast, the patients with primary oldosteronism had increased left ventricular dimension index.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Physiologic changes during supraventricular tachycardia and release of atrial natriuretic peptide.

Plasma levels of atrial natriuretic peptide (ANP) increase markedly during supraventricular tachycardia (SVT). Although natriuresis associated with SVT may be secondary to the augmented secretion of ANP, whether or not physiologic changes other than natriuresis can be attributed to the release of ANP has not been determined. In the present study, plasma ANP levels in 10 patients with SVT were found to be significantly (p less than 0.05) increased, from 37 +/- 11 pg/ml (mean +/- standard error of the mean) during the control period to 160 +/- 54 pg/ml at 60 minutes after the induction of SVT. Urinary sodium excretion, although insignificant, tended to increase during the 30-minute period after SVT termination. The filtration fraction determined by the ratio of creatinine to para-aminohippurate clearance significantly increased during SVT. An increase in capillary permeability seemed to have occurred as there was a rise of hematocrit, the changes of which showed a different time course from that of the urine volume. The ratio of plasma aldosterone concentration to plasma renin activity significantly decreased during SVT. As the same effects are observed after ANP infusion, these changes were attributed to ANP activity.

Adult↗
PubMed1988

A novel human plasma factor(s) capable of mobilizing intracellular Ca2+ in cultured rat vascular smooth muscle cells.

Using fura-2-loaded rat vascular smooth muscle cells (VSMCs) in culture, we have attempted to partially purify and characterize yet unidentified factor(s) from normal human plasma that stimulates cytoplasmic free Ca2+ concentration ([Ca2+]i). The plasma extract caused an immediate and transient increase of [Ca2+]i in a dose-dependent manner, of which effect was not prevented by pretreatment with either any of receptor antagonists for -adrenergic agonist, angiotensin II, arginine vasopressin, serotonin, thromboxane A2, or with EGTA and nifedipine. This novel plasma factor(s) was heat-stable and completely inactivated by pronase E, suggesting its protein nature. Furthermore, plasma extracts dose-dependently stimulated the accumulation of [3H] inositol phosphates in rat VSMCs. Sephadex G-50 gel chromatography of plasma extracts resolved one major component (mol wt 13,000) and two minor components with larger (greater than 30,000) and smaller (3,000) mol wt. Present study demonstrates the presence of hitherto unidentified plasma factor(s) with size heterogeneity capable of stimulating both mobilization of [Ca2+]i and breakdown of phosphatidylinositol-4,5-biphosphates in rat VSMCs.

Animals↗
PubMed1988

Measurement of left atrial systolic time intervals in hypertensive patients using Doppler echocardiography: relation to fourth heart sound and left ventricular wall thickness.

The concept of left atrial systolic time intervals and Doppler echocardiography were used in a quantitative assessment of left atrial function in relation to the presence or absence of a fourth heart sound and to left ventricular hypertrophy in 47 patients with hypertension. Left atrial systolic time interval indexes included atrial pre-ejection period (the time between the onset of an electrocardiographic P wave and the onset of left ventricular inflow during atrial systole [A wave]), corrected atrial pre-ejection period (the atrial pre-ejection period divided by the duration of the P wave), and atrial ejection time (the time between the onset and cessation of the A wave). Twenty-one patients with a fourth heart sound on the phonocardiogram had a shorter atrial pre-ejection period (81 +/- 10 versus 89 +/- 14 ms p less than 0.05) and a corrected atrial pre-ejection period (66 +/- 17 versus 83 +/- 18 ms, p less than 0.01), as well as a longer atrial ejection time (147 +/- 15 versus 126 +/- 13 ms, p less than 0.001) than did 26 patients without a fourth heart sound. The ratio of atrial pre-ejection period to atrial ejection time and that of corrected atrial pre-ejection period to atrial ejection time was smaller in patients with than in patients without a fourth heart sound (0.56 +/- 0.08 versus 0.71 +/- 0.11, p less than 0.001; 0.46 +/- 0.16 ms-1 versus 0.67 +/- 0.17 ms-1, p less than 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Influence of sodium concentration in cerebrospinal fluid on plasma atrial natriuretic peptide in conscious rats.

1. To test the influence of a sodium (Na+) stimulus within the central nervous system on the release of atrial natriuretic peptide (ANP), we examined the effects of intracerebroventricular infusion of high Na+ artificial cerebrospinal fluid (CSF) on blood pressure, urinary Na+ excretion and plasma ANP levels in conscious Wistar rats. 2. Infusion of high Na+ (0.6 mol/l) CSF into the lateral ventricle at a rate of 1 microliter/min for 60 min significantly increased mean blood pressure and urinary Na+ excretion, while normal Na+ (0.15 mol/l) CSF had no effects. Plasma ANP levels were higher in the high Na+ CSF group than in the normal Na+ group (154 +/- 39 vs 52 +/- 19 pmol/l, P less than 0.05). 3. Interruption of the sympathetic nervous system and the vascular action of vasopressin with intravenous hexamethonium and d(CH2)5Tyr(Me)arginine vasopressin attenuated the pressor and natriuretic responses to intracerebroventricular high Na+ CSF. Plasma ANP levels in these rats did not differ significantly from those in rats which were similarly treated but were given normal Na+ CSF. 4. These results indicate that elevation of the CSF Na+ concentration without peripheral volume loading can stimulate ANP release into the circulation. ANP release due to central Na+ stimulus appears to be mediated by the sympathetic nervous system, vasopressin, and/or haemodynamic change caused by these factors.

Animals↗
PubMed1988

Cerebrospinal fluid angiotensin II in patients with essential hypertension.

We measured components of the cerebrospinal fluid renin-angiotensin system from patients with essential hypertension under different dietary sodium intakes. The cerebrospinal fluid concentration of angiotensin II (Ang II) from the patients on a normal-sodium diet was 1.36 +/- 0.41 fmol/ml (n = 5). Neither the inactive nor the active form of renin was detected by the enzymatic activity or by the immunoreactivity, whereas angiotensinogen was detected (38.6 +/- 3.1 pmol/ml, n = 5). The Ang II level remained unchanged even after incubation of the cerebrospinal fluid at 37 degrees C for 3 h. Further, when authentic Ang II was added to the cerebrospinal fluid followed by incubation for 3 h at 37 degrees C, more than 90% of the added Ang II remained unchanged. Thus, the cerebrospinal fluid Ang II level may be reflected by the activity of the brain Ang II-forming system, as it was not affected by the cerebrospinal fluid constituents. The circulating renin-angiotensin system was stimulated by sodium depletion, and the cerebrospinal fluid concentration of Ang II also increased significantly. Sodium depletion may stimulate the brain Ang-II forming system, as it does the circulating renin-angiotensin system.

Angiotensin II↗
PubMed1988

Renal actions of atrial natriuretic peptide on the postischemic kidney.

The objective of this study was to evaluate the renal actions of atrial natriuretic peptide (ANP) in the unilateral postischemic kidney of anesthetized dogs with a severe reduction in glomerular filtration rate. The dose of atrial natriuretic peptide (50 ng.kg-1.min-1) we gave did not alter the mean systemic arterial pressure, renal blood flow, and glomerular filtration rate in the normal kidney, as determined in foregoing studies. ANP was infused into the intrarenal artery continuously for 60 min after the release from 45 min of complete renal artery occlusion. In the vehicle-infused group, the glomerular filtration rate fell dramatically (6% of control), the renal blood flow decreased (60% of control), and the mean systemic arterial pressure tended to increase (136% of control). The urine flow rate and urinary excretion of sodium decreased significantly (25 and 25%, respectively) at 30 min after reflow in the postischemic period. Continuous renal artery infusion of ANP resulted in a marked increase in urine flow rate (246% of control) and the urinary excretion of sodium (286% of control). The administration of ANP led to an improvement in renal blood flow (99% of control) and glomerular filtration rate (40% of control), and attenuated the rise in mean systemic arterial pressure (109% of control), compared with findings in the vehicle-infused group. Plasma renin activity and prostaglandin E2 concentration in the renal venous blood were elevated after the release from complete renal artery occlusion in both groups. These results indicate that the vascular effects of ANP on the postischemic kidney were enhanced and that the peptide maintained the natriuretic effect.

Animals↗
PubMed1988

Increases in renal angiotensin II content and tubular angiotensin II receptors in prehypertensive spontaneously hypertensive rats.

To examine the role of the intrarenal renin-angiotensin system in the development of hypertension in spontaneously hypertensive rats (SHR), we measured angiotensin II contents and tubular 125I-angiotensin II binding sites in the kidney of SHR and age-matched Wistar-Kyoto rats (WKY). In prehypertensive (4-week-old) SHR, not only the kidney angiotensin II content but also the angiotensin II receptor density in brush border membranes were significantly higher than in the WKY. In contrast, angiotensin II levels in the 20-week-old SHR kidneys were significantly lower than in the WKY. Acceleration of the intrarenal renin-angiotensin system and the increased density of tubular angiotensin II receptors in young SHR may therefore play an important role in the development of high blood pressure in SHR.

Angiotensin II↗
PubMed1988

Quantitative estimation of dietary intake in patients on hemodialysis.

A simple method to calculate the amount of dietary (protein, sodium and potassium) intake in hemodialyzed patients was developed. In 8 nutritionally stable patients, the amount of dietary intake was monitored conventionally by a dietary record method. In contrast, assuming that the amount of dietary intake was equal to the amount of accumulation in the body, the former was calculated as the change in the product of serum concentrations and total body fluid volume, which was estimated based on the sex and body build of each patient. The urea accumulation was converted to the protein intake. The interdialytic dietary protein and sodium intake calculated by this method, 120 +/- 10 g and 240 +/- 40 mEq, respectively, was not significantly different from that obtained by the dietary record, while the interdialytic potassium accumulation, 60 +/- 7 mEq, was significantly smaller than the dietary intake, 110 +/- 9 mEq, obtained by the record method, though the correlation was significant. Thus, the amount of protein and sodium intake can be calculated simply without diet research or body fluid volume measurements. Although potassium intake can not be calculated exactly because of intestinal loss, this simple method gives us a rough estimate. In addition, multiple regression analysis showed that the amount of energy intake obtained by the record method may be explained by the protein and sodium intake estimated by simple calculation.

Blood Urea Nitrogen↗
PubMed1987

Renal function curve in patients with secondary forms of hypertension.

The causative mechanisms of hypertension were investigated by studying the renal function (pressure-natriuresis) curve in patients with primary aldosteronism (n = 6) and renovascular hypertension (n = 6). Before and after radical operation (removal of adenoma in primary aldosteronism and percutaneous transluminal angioplasty in renovascular hypertension), dietary NaCl intake was altered from 10 to 13 g/day in Week 1 to 1 to 3 g/day in Week 2. Mean arterial pressure (MAP) and urinary sodium excretion were measured on the last 3 days of each week. By restricting sodium intake before operation, MAP was reduced from 122 +/- 7 to 113 +/- 7 mm Hg (p less than 0.025) in primary aldosteronism but not in renovascular hypertension (130 +/- 6 to 128 +/- 5 mm Hg). The renal function curve was drawn by plotting urinary sodium excretion on the ordinate and MAP on the abscissa before and after operation. The slope of the curve was analyzed between the plotted points, and each curve was extrapolated to zero sodium excretion as an estimate of the degree of shift of the curve along the MAP axis. Before, as compared with after operation, the extrapolated x-intercept of the curve was shifted rightward in both primary aldosteronism (111 +/- 7 vs 87 +/- 4 mm Hg; p less than 0.025) and renovascular hypertension (128 +/- 5 vs 95 +/- 2 mm Hg; p less than 0.025) and the slope was depressed in primary aldosteronism (16 +/- 1 vs 40 +/- 17 [mEq/day]/mm Hg; p less than 0.025) but not in renovascular hypertension (130 +/- 75 vs 40 +/- 13 [mEq/day]/mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Regulation of plasma atrial natriuretic peptide and the cardiopulmonary baroreflex in the rat.

To study the physiological regulation of atrial natriuretic peptide (ANP), we examined the effects of volume expansion and depletion and the influence of cardiopulmonary baroreflex on plasma ANP levels in pentobarbital-anesthetized male Wistar rats. The volume expansion by acute intravenous saline infusion (2% of body weight) increased central venous pressure (CVP) and decreased heart rate (HR) in rats with intact baroreflex. The plasma ANP level in the volume expanded group was significantly higher than that in the control rats (453 +/- 100 vs 170 +/- 40 pg/ml, p less than 0.01). Conversely the plasma ANP level decreased from 214 +/- 15 to 125 +/- 13 pg/ml (p less than 0.01) accompanied by a fall in CVP and an increase in HR after nonhypotensive hemorrhage (0.8% of body weight). Hypotensive hemorrhage (2% of body weight) caused a progressive decrease in CVP while plasma ANP did not decrease further (141 +/- 25 pg/ml). Bilateral vagotomy did not modify either the basal plasma ANP level or the plasma ANP responses to volume expansion and depletion, though it inhibited HR response. These results indicate that in the rat, plasma ANP responds not only to volume expansion but also to moderate volume depletion suggesting that ANP may have a physiological role in body fluid homeostasis. The ANP response to changes in blood volume appears to be independent of the cardiopulmonary baroreflex with vagal afferent.

Animals↗
PubMed1987

Effect of propranolol and indomethacin on the depressor action of captopril in patients with essential hypertension.

The contribution of the renin-angiotensin system (RA) and of prostaglandins (PG) to the acute depressor effect of captopril (Capt) was studied in 13 hypertensive patients suppressing either RA by propranolol (Prop) or PG by indomethacin (Indo). Four patients showed abolition of the depressor effect of Capt by pretreatment with both Prop and Indo (Group 1). Indo, but not Prop, cancelled the depressor effect in another 4 patients (Group 2). In the remaining 5 patients, either Prop or Indo did not alter the depressor response to Capt (Group 3). Patients in Group 3 were older than patients in Group 1 and 2 and showed lower plasma volume value. Several mechanisms might contribute to the acute depressor effect of Cap, including not only the suppression of RA and the enhancement of PG, but perhaps other undetermined factor(s), especially in older patients.

Adult↗