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Biomedical subjects

M Kuramochi

Publications and source records attributed to M Kuramochi.

At least 91 records · Page 5Linked to original sources
PubMed1991

Dominance of blood pressure in natriuresis associated with supraventricular tachycardia.

Supraventricular tachycardia was induced in 10 patients by programmed cardiac stimulation through esophageal lead. Blood pressure, heart rate, renal function, and hormonal factors were measured before, during, and after tachycardia. The patients were divided into two groups, depending on whether antinatriuresis occurred during tachycardia; one group (n = 5) with antinatriuresis during tachycardia associated with a decrease in blood pressure and the other group (n = 5) with neither antinatriuresis nor changes in blood pressure. The urinary sodium excretion tended to increase after tachycardia only in the latter group. On the other hand, urine volume and free water clearance increased during or after tachycardia in both groups. Plasma levels of atrial natriuretic peptide significantly increased and the urinary vasopressin excretion significantly decreased during tachycardia in both groups. During tachycardia, natriuresis due to atrial natriuretic peptide secretion seems to be hampered by hypotension, but polyuria is preserved despite the fall in blood pressure probably related to suppression of vasopressin release.

Adult↗
PubMed1991

Changes in sodium-22 turnover and total body potassium in two-kidney, one-clip renovascular hypertension.

Changes in sodium-22 turnover and total body potassium (TBK) were studied during acute (within 2 weeks after clipping) and chronic (12-14 weeks after clipping) phases in two-kidney, one-clip (2k, 1c) hypertensive rabbits by using a whole body counter. Sodium-22 injected intravenously was eliminated more rapidly in hypertensive rabbits than in controls. The biological half-life (BHL) of sodium-22 was shorter in hypertensive rabbits during both acute (p less than 0.05) and chronic phases (p less than 0.001). A significant negative correlation was obtained between the BHL of sodium-22 and blood pressure (r = -0.588, p less than 0.05) in hypertensive rabbits. TBK decreased significantly at the chronic phase in hypertensive rabbits (p less than 0.05), while TBK showed no significant change in controls. Serum sodium and potassium did not change during the observation period. Increased plasma aldosterone concentration was observed during the acute phase in hypertensive rabbits. These results suggested that sodium retention was not a major factor in the acute and chronic phases of 2k, 1c hypertension in rabbits and that pressure natriuresis could explain, at least in part, the lack of sodium retention. Furthermore, there appears to be a derangement in the intracellular potassium metabolism which may be associated with the maintenance rather than the development of hypertension.

Aldosterone↗
PubMed1991

Differential modulation of norepinephrine-induced contractile response by ryanodine and verapamil in the isolated aortic ring of spontaneously hypertensive and Wistar-Kyoto rats.

Using ryanodine and verapamil, we compared the relative contributions of SR Ca2+ release and gated Ca2+ entry in arterial contractions induced by norepinephrine (NE) between spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Aortic rings of 10 SHR and 10 WKY aged 10-12 weeks were superfused in small water-jacketed tissue chambers with physiological salt solution and isometric tension was measured. The inhibition of the NE (3 x 10(-8) M)-induced contraction of aortic rings by ryanodine (10 microM) was significantly greater in WKY (40.1 +/- 6.9%) than in SHR (2.2 +/- 9.0%) (p less than 0.01). The inhibition of the NE-induced contraction by verapamil (10 microM) in the presence or absence of ryanodine (10 microM) was significantly greater in SHR than in WKY. The residual ryanodine and verapamil-insensitive component of NE-induced contraction was significantly greater in WKY than in SHR. Caffeine (5 mM)-induced contraction in the presence of verapamil and phentolamine was significantly smaller in SHR than in WKY. These results suggest that gated Ca2+ entry plays a more important role in Ca2+ control and that ryanodine-sensitive Ca2+ store is smaller, or the ryanodine receptor is altered in these tissues of SHR compared with those of WKY.

Animals↗
PubMed1991

Split intrarenal hemodynamics in renovascular hypertension.

Split intrarenal hemodynamics in stenotic and contralateral kidneys of unilateral renovascular hypertension (RVH) were estimated by Gomez's formulae. Ten patients with RVH were studied. Split para-amino hippurate and inulin clearances were measured by ureteral catheterization as indexes for renal plasma flow and glomerular filtration rates, allowing the estimation of intrarenal hemodynamics such as preglomerular arteriolar resistance, postglomerular arteriolar resistance and glomerular hydrostatic pressure in each kidney. Renal plasma flow and glomerular filtration rates were lower in the stenotic kidney (83 +/- 12, 19 +/- 2 ml/min/m2) than in the contralateral kidney (170 +/- 19, 43 +/- 4). Preglomerular arteriolar resistance was elevated due to the stenotic lesion in the stenotic kidney (30,900 +/- 4,500 dyns.sec.cm-5) while the elevation in the contralateral kidney (11,300 +/- 1,000) was less. Postglomerular arteriolar resistance was high in both kidneys. Glomerular pressure was lowered in the stenotic kidney (54 +/- 1 mmHg), while elevated in the contralateral kidney (71 +/- 3). Although the stenotic kidney of RVH was protected from systemic hypertension (138 +/- 6 mmHg) by stenosis of the renal artery, the increase in preglomerular arteriolar resistance in the contralateral kidney was not sufficient, making glomerular pressure elevated. Thus, glomerular hypertension and hyperfiltration were demonstrated in the contralateral kidney of RVH.

Adult↗
PubMed1991

Aspirin injection test to predict angioplasty outcome in unilateral renovascular hypertension: preliminary report.

We examined the usefulness of aspirin DL-lysine for prediction of the outcome of renal artery angioplasty in renovascular hypertension. The study was carried out in eight hypertensive patients with unilateral renal artery stenosis: six were free from azotemia and two had slight azotemia. Before and 30 min after an intravenous injection of aspirin DL-lysine (18 mg/kg), renal venous and abdominal aortic plasma was sampled and assayed for prostaglandin E2 and plasma renin activity. Blood pressure and heart rate were serially measured at this time. Renal angioplasty was later performed and was technically successful in all patients. In the six patients without azotemia, aspirin inhibited renal prostaglandin E2 synthesis and suppressed renin release from the ischemic kidney, resulting in lowered blood pressure. Renal angioplasty caused plasma renin activity to become normal and lowered high blood pressure. The reduction in blood pressure by angioplasty was correlated with the responses of blood pressure and renin release to aspirin. However, in the two patients with azotemia, aspirin neither suppressed renin release nor lowered blood pressure. Their hypertension was not reduced by the angioplasty. These results indicate that an aspirin injection test could be useful for prediction of the outcome of angioplasty in unilateral renovascular hypertension.

Adult↗
PubMed1990

Possible role of renal prostaglandin E2 in natriuresis associated with supraventricular tachycardia.

We investigated the possible role of renal prostaglandin (PG) E2 in natriuresis associated with supraventricular tachycardia (SVT). In five female patients with paroxysmal tachycardia, SVT was artificially induced and then stopped 60 min later. Before, during, and after SVT, plasma levels of arginine vasopressin and atrial natriuretic peptide (ANP) and the urinary excretion of sodium and PGE2 were measured. Polyuria was observed during SVT. However, natriuresis did not occur until immediately after the termination of SVT. During SVT, the plasma levels of arginine vasopressin tended to decrease. When SVT was terminated, the vasopressin levels increased significantly (p less than 0.01). Urinary excretion of PGE2 tended to decrease during SVT and then increased significantly (p less than 0.01) after SVT ended. Urinary excretion of sodium was correlated (r = 0.699, p less than 0.001) with the urinary excretion of PGE2. Plasma ANP increased during SVT, but there was no correlation with urinary sodium excretion. These results suggest that renal PGE2, the biosynthesis of which may be stimulated by a increase in plasma vasopressin, is an important factor contributing to the natriuresis observed after the end of SVT.

Adult↗
PubMed1990

Normalization of increased sodium sensitivity by maintenance hemodialysis.

Blood pressure (BP) becomes more sodium and body fluid sensitive as renal function deteriorates. Thus, hypertension in chronic renal failure is mostly of the sodium sensitive type. We studied whether the increased sodium sensitivity (SS) can be restored to normal on the maintenance phase of hemodialysis (HD) therapy. Body weight (BW) and BP (specifically, mean arterial pressure [MAP]) were measured after HD and before the next HD, and the body fluid sensitivity (BFS) was calculated as the ratio of changes in these factors on both introduction and maintenance phases in HD patients (n = 56) who were not taking any antihypertensive drugs (BFS = delta MAP/delta BW). In a preliminary study, the amount of interdialytic sodium intake (QNa+) was measured (n = 30), and SS was calculated as the ratio of the change in MAP to QNa+ (SS = delta MAP/QNa+). Interdialytic BW gain (3.1 +/- 0.1 kg) was correlated with the amount of sodium intake (136 +/- 17 mEq), resulting in a positive relationship between BFS and SS (r = 0.79, P less than .0001). Therefore, BFS was used as an index of SS. As a whole, BFS decreased from the introduction to the maintenance phase (6.5 +/- 1.0 to 3.5 +/- 0.6 mm Hg/L, P less than .01). This decrease was marked (6.2 +/- 1.1 to 2.9 +/- 0.6 mm Hg/L, P less than .01) in patients (n = 46) whose BP was normalized in the maintenance phase, while not significant (7.9 +/- 1.9 to 6.3 +/- 1.3 mm Hg/L) in patients (n = 10) whose BP was still high.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

A comparison of lisinopril with enalapril by monitoring plasma angiotensin II levels in humans.

The present study was designed to examine and compare the acute effects of lisinopril (20 mg) and enalapril (10 mg) after a single oral administration on the inhibition of the renin-angiotensin system (RAS) in eight normal subjects. Serum concentration of lisinopril and enalaprilat, an active metabolite of enalapril, reached the respective maximal levels at 6 and 4 hr after administration of the drugs. At 24 hr, the serum concentration of lisinopril was higher than that of enalapril; thus the rate of disappearance of lisinopril was retarded, in comparison to that of enalapril. The reduction of serum angiotensin I converting enzyme (ACE) activity was consistent with the pattern of increase of concentration of the drugs in the serum. However, with these two drugs, the concentration of plasma ANG II was decreased in a similar manner, and it returned to the pretreatment level within 24 hr. Thus, there was no significant difference in ANG II levels throughout the 24 hr-study between the lisinopril and enalapril treatment. The results indicate that a single administration of 20 mg lisinopril and 10 mg enalapril show similar potency for lowering the circulating ANG II level, although lisinopril exerts a more sustained inhibition of serum ACE activity. The measurement of ANG II provides useful informations for evaluating the efficacy of ACE inhibitors for the inhibition of circulatory RAS.

Administration, Oral↗
PubMed1990

[A study of developmental changes of Indian mandibles concerning development of weight, height, thickness and length of the mandible].

A total of 230 mandibles were classified into 7 groups 8 stages according to eruption phase, observing developmental changes from unerupted stage (Group A) to permanent dentition (Group G) 1. Development from Group A to deciduous dentition completion stage (Group C) was classified into 3 types. 1) Regarding height of mandibular ramus, height and weight of mandibular body, the increase from Group B where the deciduous central incisor erupts to Group C is greater that from Group A-B (type a). 2) As to coronoid process height, length of mandibular body, mandibular length and mandibular ramus width, equal increases were seen between Group A-B and B-C (type b). 3) Chin height and thickness of the mandibular body developed suddenly with the eruption of the deciduous central incisors. The increase is greater in Group A-B (type c). 2. They are classified according to size proportion in unerupted stage as compared to entire size. The classification are: 42%-33% (smaller), 50%-45% (medium), 70%-50% (bigger). 1) Type a is small at Group A and developed steadily after Group C. Development is greater, about 2.3-3 times. 3) Type b at Group A is larger than type a. It continuously developed after Group C. The developmental rate is about 2 times except the coronoid process height. 3) Type c is large at Group A. No development occurred after D1 stage when first molars erupt. Developmental rate is 1.4-1.85 times and smallest of the 3 types. 3. Developmental quantity: 1) Regarding total increase; The height of the mandibular ramus, the height of the mandibular ramus and coronoid process showed about 28-32 mm increase Group C accounted for 55%, Group C-D2 14%-17%, Group D2-G 30%-27% of the developmental increase. The mandibular ramus width showed increases of 14.43mm (74% at D1 stage) and subsequent increase was 7% between each group, showing equal increases. 2) Chin and mandibular ramus height showed increases of 14 mm. At Group C, development in chin height accounted for 67%. The mandibular body width increased 4.0mm-6.0mm at the foramen in m2/m2 and 6/6 portions. It reached 82%-100% in D1 stage. 3) An increase in mandibular body length and mandibular length was 50mm and 32mm, reaching 73% of the entire developmental amount by D1 stage.

Adolescent↗
PubMed1989

Removal of intracellular waste products by hemofiltration.

Because the total amount of waste products removed by hemofiltration can be measured exactly, it was divided into two components, that removed from the extracellular compartment and that removed from the intracellular compartment, using inulin as a marker for extracellular fluid in five uremic patients treated with hemofiltration in the postdilution mode. The amount removed from the extracellular compartment as a proportion to the total amount removed from the whole body by hemofiltration was 86.5% +/- 10.6% for guanidinosuccinic acid, 69.1% +/- 15.6% for sodium, 59.4% +/- 3.3% for uric acid, 56.4% +/- 2.1% for inorganic phosphate, 45.6% +/- 5.3% for creatinine, 43.1% +/- 7.2% for potassium, 42.9% +/- 3.1% for guanidinoacetic acid, 42.5% +/- 7.5% for methylguanidine, 37.2% +/- 8.4% for chloride, 36.3% +/- 2.8% for urea, and 6.9% +/- 2.9% for glucose. These results show that extracellular substances such as sodium and guanidinosuccinic acid were removed mainly from the extracellular compartment. On the other hand, glucose was removed only from the intracellular compartment, since blood glucose level is regulated. Although uric acid, inorganic phosphate, creatinine, potassium, guanidinoacetic acid, and methylguanidine are intracellular substances, they accumulated also in the extracellular fluid in renal failure, and were removed from both compartments, intracellular as well as extracellular, by hemofiltration.

Body Fluids↗
PubMed1989

Alterations in cerebrospinal fluid angiotensin II by sodium intake in patients with essential hypertension.

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 +/- 0.38 (SEM) to 1.83 +/- 0.43 fmol/ml (P less than 0.01) and of ANG III from 0.65 +/- 0.11 to 0.86 +/- 0.15 fmol/ml (P less than 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

Adult↗
PubMed1989

Hypotensive mechanisms of antihypertensives based on the water tank model.

Mechanisms of hypotensive action of antihypertensive drugs were theoretically considered using the water tank model on body fluid volume-blood pressure regulation. If a cock is attached to a tank with a base area corresponding to the reciprocal of total peripheral resistance (TPR) and water is poured into this tank at a rate corresponding to the amount of Na+ intake, then equilibrium should be achieved at a certain water level, volume, and output from the cock, which represent mean arterial pressure (MAP), cardiac output (CO), and urinary Na+ excretion rate. The height of the cock from the tank bottom and the size of the cock correspond to the x-intercept and slope of the renal function curve (pressure-natriuresis relationship). Vasodilators lowered the cock height and enlarged the base area (reduced TPR), resulting in an increase in the volume (CO). beta-Blockers not only lowered the height, but also decreased the size of the cock. Because they do not alter TPR (base area), CO (volume) must be reduced. Converting-enzyme inhibitors had the same effects on the height and size of the cock as beta-blockers, but enlarged the base area (reduced TPR), resulting in an increase in the volume (CO). Diuretics increased the cock size without affecting the cock height or the base area, resulting in a decrease in CO. The effects of antihypertensive drugs on the cock (kidney) seemed essential in their hypotensive action, similarly as abnormality of the renal function curve is essential in the genesis of hypertension. These analyses can illustrate schematically the hemodynamic changes induced by antihypertensive drugs.

Antihypertensive Agents↗
PubMed1989

Effect of dietary sodium on the Na-K ATPase inhibitor in patients with essential hypertension.

To study the circulating humoral factor modifying transmembrane sodium transport, plasma was obtained from 12 patients with essential hypertension (EH) fed a high sodium diet (NaCl 15 to 17 g/d) for seven days and thereafter a low sodium diet (NaCl 2 to 3 g/d) for seven days. Ouabain-sensitive 86Rb+ influx into the red blood cells (RBC) obtained from a healthy subject, and incubated with the plasma obtained during the high sodium diet was significantly lower than that incubated with the plasma obtained during the low sodium diet (3.74 +/- 0.26 v 3.97 +/- 0.30 nmol/10(8) cells, P less than .05). The changes in mean blood pressure from the high to low sodium diet showed a significant positive correlation with the changes in the ouabain-sensitive Rb influx into RBC in the plasma from the high to low sodium diet. These results suggest that a humoral factor modifying the sodium pump might be altered by sodium balance in EH, especially in salt-sensitive hypertension.

Aldosterone↗
PubMed1989

The cardiovascular effect of intracerebroventricular endothelin in rats.

To investigate the cardiovascular action of endothelin within the central nervous system, we studied the effect of intracerebroventricular endothelin in conscious Wistar rats. The endothelin increased blood pressure and the heart rate in a dose-related way. The increase in mean blood pressure produced by 100 ng/kg of endothelin (45 +/- 6 mmHg, mean +/- s.e.m., n = 10) was much greater than that produced by the same amount of intravenous endothelin (4 +/- 1 mmHg, n = 7). Pretreatment with intravenous hexamethonium significantly attenuated the rise in blood pressure elicited by intracerebroventricular endothelin. Combined administration of hexamethonium and a vasopressin antagonist abolished the pressor response. These results indicate that centrally administered endothelin raises blood pressure through activation of the sympathetic nervous system and vasopressin. It is suggested that endothelin may play a role in the central regulation of cardiovascular function.

Animals↗
PubMed1989

Effects of 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. Conscious male Wistar rats were given one of the following solutions into the lateral ventricle: artificial cerebrospinal fluid (CSF); rat ANF (99-126) 1.0 microgram/kg per min; Ang II 100 ng/kg per min; 0.6 mol/l NaCl; Ang II plus ANF, and 0.6 mol/l NaCl plus ANF. The i.c.v. infusion of artificial CSF or ANF alone did not cause significant changes in mean blood pressure, urinary volume or sodium excretion (UNaV). The i.c.v. infusion of Ang II or 0.6 mol/l NaCl raised mean blood pressure, decreased urinary volume and increased UNaV. When ANF was administered with Ang II, the Ang II-induced responses were diminished significantly (delta mean blood pressure, +10 +/- 3 versus +20 +/- 4 mmHg; delta urinary volume, -38 +/- 9 versus -78 +/- 5 microliters/min; delta UNaV, +0.49 +/- 0.51 versus +2.28 +/- 0.58 mumol/min). The centrally administered ANF opposed the effects of 0.6 mol/l NaCl, though the effect was significant only in respect of blood pressure. Our results indicate that the brain ANF may have an antinatriuretic role in some conditions.

Angiotensin II↗
PubMed1989

Increased sodium-calcium exchange in arterial smooth muscle of spontaneously hypertensive rats.

We compared sodium-calcium (Na-Ca) exchange in vascular smooth muscle between spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Aortic rings of 11 SHR and 11 WKY rats aged 11-12 weeks were superfused with physiological saline, and isometric tension was measured. Systolic blood pressure was higher in SHR (174 +/- 12 mm Hg) than in WKY rats (132 +/- 4 mm Hg): 1) In the presence of 10 microM phentolamine, 10 microM verapamil, and 5 mM caffeine, reduction of ionized extracellular sodium concentration [( Na+]o) from normal (139.2 mM) to 1.2 mM (replaced by N-methyl-D-glucamine) caused an external Ca2+-dependent increase in tonic tension (calcium entry by Na-Ca exchange). The rate of increase was higher in SHR (35.4 +/- 3.9 mg/min) than in WKY rats (17.9 +/- 1.3 mg/min) (p less than 0.01). 2) In the presence of phentolamine, verapamil, and caffeine, relaxation from low-Na+ contraction was promoted by external calcium removal. The rate of relaxation was directly related to [Na+]o. The rates of relaxation at normal (139.2 mM) [Na+]o were higher in SHR than in WKY rats (p less than 0.05). The rates of relaxation at 1.2 mM [Na+]o (calcium extrusion by adenosine triphosphate-driven calcium pump) were not different between SHR (11.6 +/- 2.8 mg/min) and WKY rats (8.9 +/- 2.5 mg/min). The increase in the rates of relaxation from 1.2 mM to normal (139.2 mM) [Na+]o (calcium extrusion by Na-Ca exchange) was greater in SHR (34.9 +/- 6.6 mg/min) than in WKY rats (17.1 +/- 4.5 mg/min) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗