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Biomedical subjects

T Haruyama

Publications and source records attributed to T Haruyama.

86 records · Page 5Linked to original sources
PubMed1978

Implication of renal prostaglandin E in urinary sodium excretion.

To investigate the role of renal prostaglandin in the regulation of sodium metabolism, ruinary prostaglandin E excretion, an indicator of renal prostaglandin synthesis, urinary sodium excretion, plasma renin activity and urinary aldosterone excretion were measured in 84 normal subjects and 55 patients with essential hypertension on ad lib intake of sodium. The excretion rates of urinary prostaglandin E were 736.8 +/- 32.2 ng/day in normal subjects and 394.3 +/- 28.7 ng/day in essential hypertensives. The excretion rate was significantly decreased in essential hypertensives (P less than 0.001). A significant positive correlation was found between urinary sodium excretion and urinary prostaglandin E excretion in normal subjects (r = 0.39, P less than 0.001), and in essential hypertensives (r = 0.62, P less than 0.001). There was no correlation between the renin-angiotensin-aldosterone system and urinary prostaglandin E excretion in normal subjects as well as in essential hypertensives. The present data show that renal prostaglandin might be involved in the renal handling of sodium, and prove the possibility that the decrease of renal prostaglandin synthesis is one of the etiological factors in essential hypertension.

Adolescent↗
PubMed1978

Elevated plasma renin activity in patients with acute pyelonephritis.

Thirty-three patients with acute pyelonephritis were studied with regard to the changes in plasma renin activity (PRA) along the clinical course of the disease. 1) Abnormally high PRA was found in 64% of patients in the active stage of acute pyelonephritis; they showed a decrease in urinary output of sodium, a reduction in creatinine clearance, and high indices of inflammatory activity. 2) The changes of PRA in the course of acute pyelonephritis were negatively correlated to the urinary sodium excretion and creatinine clearance, but positively to the activity of inflammation, serum sodium concentration and the number of E. coli in the urine. PRA returned to normal with the improvement of pyelonephritis. 3) Concerning the mechanism of hyperreninemia in the active stage of the disease, the following three factors may be considered; renal ischemia, negative sodium balance in the body, and inflammation. Of these, the negative sodium balance seems to be the most important. The patients could not take enough foods to maintain their energy and sodium balance because of fever and pain. 4) The significance of resting PRA in acute pyelonephritis might be to reflect the sodium status in the body, but not to be related to hypertension.

Acute Disease↗
PubMed1977

A patient with recurrent hepatic encephalopathy and chronic renal failure treated successfully with long-term hemodialysis.

A 38-year-old man suffering from chronic recurrent hepatic enchephalopathy due to liver cirrhosis complicated with chronic renal failure had been maintained well by regular hemodialysis treatment for 14 months. Only four episodes of hepatic encephalopathy occurred in that period. Each of four episodes of disturbed consciousness was accompanied by slightly elevated blood ammonia levels. Energetic serial dialysis for 5-7 days was necessary for its recovery. The factors causing hepatic encephalopathy did not appear to be easily dialysable as compared with those of uremic coma. It is concluded that the hemodialysis is quite an effective treatment for the recurrent type of hepatic encephalopathy.

Adult↗
PubMedDate not supplied

Calcium responsive two-dimensional molecular assembling of lipid-conjugated calmodulin.

Calmodulin (CaM), a calcium ion sensitive protein, was conjugated with dioctadecyldimethylammonium bromide and subsequently assembled into a monolayer at the air-water interface using the LB method. The lipid-conjugated calmodulin (LCC) retains its calcium sensitivity, determined from the changes in the area-pressure isotherm of the monolayer obtained at the air-water interface. The functionality of this protein assembly was characterized by the activation of phosphodiesterase (PDE), a CaM responsive enzyme. The enzyme activity of PDE coupled with LCC at the air-water interface was measured by using the enzymatic method. It was found that LCC retained its enzyme activity modulating function of calmodulin, which is triggered by calcium ions. This characteristic plays an important role in fabricating molecular assembly of proteins which have a cooperative interaction at the molecular level.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMedDate not supplied

On-off switching of enzymatic reaction by recombinant calmodulin on a solid-phase matrix.

A fusion protein consisting of human calmodulin (CaM) and glutathione S-transferase (GST) was produced by gene fusion. The fusion protein was overexpressed in Escherichia coli as a soluble form and purified with one-step affinity chromatography using glutathione-Sepharose. The protein had the modulating activity of CaM and the binding capability to glutathione of GST. Phosphodiesterase, which is a CaM dependent enzyme, was activated by the fusion protein, with the Ca2+ level equal to the level equivalent to a native CaM. Furthermore, CaM could be immobilized on a solid-phase matrix through the use of GST moiety while its modulating activity was retained. Phosphodiesterase activity was switched on and off by the immobilized CaM with or without Ca2+, and repeated use of CaM was demonstrated.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMedDate not supplied

Attenuation of pressor responses to norepinephrine and pitressin and potentiation of pressor response to angiotensin II by captopril in human subjects.

The present study was conducted to investigate the influence of captopril on cardiochemodynamic responses in 38 normal volunteers (20- to 35-year-old men) to exogenously administered vasopressor substances. Norepinephrine (NE), 0.05, 0.1, and 0.2 micrograms/kg min-1; angiotensin II (AII), 5, 10, and 20 ng/kg min-1; and pitressin (2 mU/kg min-1) were infused for 10 minutes. Each infusion was reported twice, and the responses were reproducible. Captopril (50 mg by mouth) significantly attenuated the pressor responses to NE and pitressin, but the decrease in heart rate in response to NE and pitressin was almost the same before and after captopril treatment, suggesting that captopril potentiates reflex slowing of the heart. Captopril significantly potentiated the pressor response to AII. Attenuation of pressor response and potentiation of reflex slowing of the heart, in response to NE and pitressin, disappeared when a subdepressor dose of AII (1 ng/kg min-1) was infused in addition to captopril. Infusion of a subdepressor dose of bradykinin (BK), 0.1 microgram/kg min-1, had no influence on the pressor response to NE. In the subjects treated with indomethacin (225 mg/54 hrs), captopril still attenuated the pressor response to NE. These results suggest that captopril attenuates the pressor responses to NE and pitressin primarily by depletion of endogenous AII; decreased AII may desensitize the contraction of arterial smooth muscle and may potentiate the compensatory reflex mechanism.

Adult↗