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Biomedical subjects

F Marumo

Publications and source records attributed to F Marumo.

At least 649 records · Page 36Linked to original sources
PubMed1987

Presence of the atrial natriuretic peptide in human cerebrospinal fluid.

Using a highly sensitive and specific radioimmunoassay (RIA) for detection of the atrial natriuretic peptide (ANP), the presence of alpha-human ANP (alpha-hANP) in human cerebrospinal fluid (CSF) was confirmed. Its concentration in CSF, 3.6 +/- 2.3 pg/ml, n = 16, mean +/- SD, was remarkably lower than that in the plasma (161.8 +/- 157.4, p less than 0.0001). The regression coefficient between these concentrations was 0.320 (p = ns). Gel permeation chromatography conducted in conjunction with RIA indicated ANP in CSF to be eluted at the position of a low molecular weight form corresponding to alpha-hANP. No high molecular weight form could be detected. But in the plasma, both low and high molecular forms were found to be present. It is thus evident that ANP is present in human CSF and its origin may possibly be the brain and not the atrium.

Adult↗
PubMed1987

Decreased VLDL apoprotein CII/apoprotein CIII ratio may be seen in both normotriglyceridemic and hypertriglyceridemic patients on chronic hemodialysis treatment.

Pathogenetic factors that may be related to uremic hypertriglyceridemia were studied in 27 patients who had been undergoing chronic hemodialysis treatment for over two years. They were divided into two groups consisting of 14 hypertriglyceridemic (HTG) patients with fasting serum triglycerides (TG) of 170 mg/dL or higher, aged 45 +/- 11 yr (mean +/- SD) and 13 normotriglyceridemics (NTG) with serum TG less than 170 mg/dL aged 42 +/- 9 yr. Serum lipid, lipoprotein [low density lipoprotein (LDL) and very low density lipoprotein (VLDL)] and apoprotein (Apo) levels, as well as ultracentrifugally obtained VLDL apo subfractions and serum carnitine were compared between the two groups, which enabled us to rule out various factors inherent to uremic state and present in both groups. The HTG group of patients, who showed (by definition) significantly elevated TG (300 +/- 167 mg/dL v 123 +/- 30 mg/dL in NTG) and VLDL levels, concomitantly showed significantly increased serum total cholesterol (P less than .001) and LDL (P less than .001), and significantly decreased apo AI/apo B, or an index of risk of atherogenesis (P less than .05). Serum apo CII (7.3 +/- 3.3 mg/dL v 3.6 +/- 1.0 mg/dL in NTG), apo E (4.8 +/- 2.8 mg/dL v 2.9 +/- 1.3 mg/dL) and VLDL/serum apo CII (38 +/- 18 v 22 +/- 12), ie, the amount of VLDL covered by a unit of apo CII, were elevated in the HTG compared with the NTG group of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Mechanisms for the inhibition of vasopressin-stimulated water flow by captopril in the toad bladder.

The mechanisms by which captopril inhibits vasopressin-stimulated osmotic water flow in the toad bladder have been investigated in vitro. Captopril has two possible mechanisms for the inhibitory action on the water flow, one is its stimulative effect on prostaglandin E2 (PGE2) biosynthesis by inhibition of kininase II activity, the other, is a direct effect on water flow independent of PGE2. Captopril inhibited the vasopressin-, cyclic adenosine monophosphate- and 3-isobutyl-1-methyl-xanthine-stimulated water flow. The inhibition of water flow by bradykinin was enhanced by captopril. These data indicate that captopril increased the amount of bradykinin in toad bladder cells resulting in the production of PGE2 which inhibited the increase in water flow induced by vasopressin. The inhibitory effect of captopril, however, also occurred in the presence of indomethacin, when the production of PGE2 was attenuated. Thus, it was concluded that captopril inhibits the vasopressin-stimulated water flow indirectly by inhibiting the degradation of bradykinin and thereby enhancing the production of PGE2, and directly at a site following the production of cyclic adenosine monophosphate by vasopressin.

1-Methyl-3-isobutylxanthine↗
PubMed1987

Transverse fractures of the spinous process of the 7th cervical vertebra in RDT patients: an Al related disease?

Transverse fractures of the spinous process of the 7th cervical vertebra were noted in 2 patients and of the 1st thoracic vertebra in 1 patient on maintenance hemodialysis. Two patients with aluminum (Al)- and/or iron-related bone disease complained of bone pain, relieved by deferoxamine therapy. In all three cases, the bone fractures had occurred suddenly while the patients were going about their daily work. These observations indicate that Al- or iron-related bone disease with secondary hyperparathyroidism can induce bone fracture by only slight stress in patients maintained on hemodialysis.

Adult↗
PubMed1986

Enhancing effects of angiotensin I on the vasopressin-stimulated water flow of toad bladder through increased cyclic AMP in mucosal cells.

The effects of angiotensins I and II on 10 mU/ml vasopressin-stimulated water flow across toad bladder were examined. Angiotensin I at concentrations of 10(-6) and 10(-7) M enhanced the water flow, but angiotensin II failed to do so at these concentrations. Angiotensin I had no effect on 5 mM cyclic AMP-stimulated water flow. After being preincubated for 30 min with angiotensin II, angiotensin I failed to have any stimulatory effect on vasopressin-stimulated water flow. At 10(-6) M angiotensin I significantly enhanced vasopressin-stimulated cyclic AMP content in bladder mucosal cells. These results indicate that angiotensin I enhances vasopressin-stimulated water flow by increasing cyclic AMP production in bladder cells and that angiotensin II may possibly interfere with angiotensin I in a competitive manner.

Angiotensin I↗
PubMed1986

A highly sensitive radioimmunoassay of atrial natriuretic peptide (ANP) in human plasma and urine.

A highly sensitive radioimmunoassay has been established for measurement of human plasma and urine concentrations of atrial natriuretic peptide (ANP) and requires no extraction or concentration process such as Sep-Pak C-18 cartridge treatment. An antiserum was prepared from rabbits immunized with alpha-human ANP (alpha-hANP) coupled with bovine-thyroglobulin. The sensitivity of this method was 0.3 pg/tube of synthetic alpha-hANP utilized as authentic standard. Recovery of alpha-hANP spiked to plasma and urine was 97.7 +/- 15.4% and 97.1 +/- 9.5% (mean +/- SD), respectively. Plasma and urinary ANP concentrations versus assay data showed satisfactory linearity. In 124 healthy subjects, the plasma ANP-concentration was 31.7 +/- 12.0 pg/ml. Two different molecular forms of ANP in plasma and a single form in urine were found by gel permeation chromatography.

Atrial Natriuretic Factor↗
PubMed1986

Hyperchloremia in patients with chronic renal failure.

The electrolyte and acid base composition of steady state chronic renal failure patients were studied. A particular comparison was made between the group of hyperchloremic and normochloremic patients, matched for sex, age, serum creatinine concentration and the etiology of the disease. Hyperchloremia was constantly seen in any stage of the disease in hyperchloremic patients, and they were found to be more acidemic, with lower anion gap, than normochloremic patients. A greater degree of tubular dysfunction than glomerular dysfunction was considered as the cause of acidosis and hyperchloremia in any stage of the disease. Hyperchloremia could be an indication to initiate alkali therapy to protect against further loss of bone mineral and the progression of the disease itself.

Acid-Base Equilibrium↗
PubMed1986

Two cases of saline-responsive metabolic alkalosis associated with high urinary chloride concentrations.

Two particular cases of saline-responsive metabolic alkalosis associated with high urinary chloride concentrations were documented. In the first case, pseudoaldosteronism with long term glycylrrhetinic acid ingestion, and in the second case, probably salt losing nephropathy with extracellular fluid volume contraction were the putative causes of metabolic alkalosis, respectively. Sodium chloride loading with saline (0.9% NaCl) infusion to these patients corrected the accompanying hypopotassemic metabolic alkalosis. Recent trends in the pathophysiology of both saline-responsive and saline-resistant metabolic alkalosis were discussed.

Aged↗
PubMed1986

Role of inhibitory and stimulative effects of prostaglandins on vasopressin-stimulated osmotic water flow in the toad bladder.

Vasopressin-prostaglandin (PG) interaction, especially the role of the inhibitory effects of PGE2 on vasopressin action, was studied using toad urinary bladders. The PGH2, at 1 X 10(-7) M, inhibited vasopressin-stimulated water flow (Marumo, 1982); PGE2 inhibited the water flow at 10(-8) M, but PGD2, PGF2 alpha, and PGI2 did not do so even at 10(-7) M. Thus, PGE2 has a physiological effect in contrast to other PGs converted from PGH2. Indomethacin enhanced both the vasopressin- and cyclic AMP-stimulated water flow across the toad bladder. However, the half maximum activation dose for vasopressin was 2 X 10(-10) M, but for cyclic AMP, as much as 3 X 10(-8) M. The PGE2 inhibited both vasopressin- and cyclic AMP-stimulated water flow. However, PGE2 inhibited vasopressin action in a dose-dependent manner which was not noted as a PGE2 effect on cyclic AMP action. The W-7, which is a specific inhibitor of calmodulin, suppressed cyclic AMP-stimulated water flow in a dose-dependent manner. Thus, PGE2 may suppress vasopressin-stimulated water flow at a site of cyclic AMP generation under physiological conditions. Thromboxane B2 (TXB2) enhanced vasopressin-stimulated water flow but not cyclic AMP-stimulated one. Thus PGE2 and TXB2 may be concluded as negative or positive modulators of vasopressin action in the toad bladder on the step(s) as the site of cyclic AMP generation under physiological conditions.

Animals↗