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Biomedical subjects

C H Pak

Publications and source records attributed to C H Pak.

At least 19 recordsLinked to original sources
PubMed1992

Bidirectional transbilayer movement of phospholipid analogs in human red blood cells. Evidence for an ATP-dependent and protein-mediated process.

The transbilayer movement of fluorescent and isotopically labeled analogs of phosphatidylserine (PS), phosphatidylethanolamine (PE), and phosphatidylcholine (PC) from the outer to the inner leaflet (flip) and from the inner to the outer leaflet (flop) of human red blood cells (RBC) was examined. The inward movement of 1-oleoyl-2-(N-4-nitrobenzo-2-oxa-1,3-diazole-aminocaproyl)- (C6-NBD-), 1-oleoyl-2-(N-(3-(3-[125I]iodo-4-hydroxyphenyl)propionyl)aminocaproyl)- (C6-125I-), or 1-oleoyl-2-(N-(3-3-[125I]iodo-4-azido-phenyl)propionyl)aminocaproyl- (C6-125I-N3-) analogs of PC and PE were relatively slow. In contrast, all analogs of PS and PE analogs containing aminododecanoic acid (C12 lipids) were rapidly transported to the cell's inner leaflet. Analysis of 125I-N3 lipids cross-linked to membrane proteins revealed labeling of 32-kDa Rh polypeptides that was dependent on the lipid's capacity to be transported to the inner leaflet but was independent of lipid species. To investigate whether lipids could also be transported from the inner to the outer leaflet, lipid probes residing exclusively in the inner leaflet were monitored for their appearance in the outer leaflet. Lipid movement could not be detected at 0 degrees C. At 37 degrees C, however, approximately 70% of the PC, 40% of the PE, and 15% of the PS redistributed to the cells outer leaflet, thereby attaining their normal asymmetric distribution. Continuous incubation in the presence of bovine serum albumin depleted the cells of the analogs (t1/2 approximately 1.5 h) in a manner that was independent of lipid species. Similar to the inward movement of aminophospholipids, the outward movement of PC, PE, and PS was ATP-dependent and could be blocked by oxidation of membrane sulfhydryls and by the histidine reagent bromophenacyl bromide. Evidence is presented which suggests that the outward movement of lipids is an intrinsic property of the cells unrelated to compensatory mechanisms due to an imbalance in lipid distribution.

Amines↗
PubMed1990

Hydrocortisone induction during oligodendroglial differentiation.

Steroid hormones are important for the normal development of brain. The addition of hydrocortisone to oligodendroglia in culture increases the level of mRNA for proteolipid protein, increases the synthesis of cerebrosides, and provides an induction of activities for the ketone body metabolizing enzymes. While proteolipid protein and cerebrosides are major components of myelin membranes, ketone bodies serve as precursors for lipid synthesis during development. Thus, hydrocortisone is important during the differentiation of oligodendroglia and during initial myelin production.

Animals↗
PubMed1990

Induction of cerebroside synthesis in oligodendroglia.

Oligodendroglia function to produce myelin membranes which surround axons, enhancing saltatory conduction. Myelin consists of a multitude of condensed membranes which are rich in lipids with the major glycolipids, cerebrosides, being 25% of the total lipid. Thus a fully differentiated oligodendroglial cell that is producing myelin membranes would be actively synthesizing cerebrosides. Our laboratory has prepared and analyzed oligodendroglia from mature bovine brain, from neonatal rat brain, and from actively myelinating rat brain. Our studies suggest that the rat oligodendroglia in our culture systems are less differentiated than bovine cells in that they produce lower levels of cerebrosides. Addition of glucocorticoids, thyroid hormone, or retinoic acid all increased synthesis of cerebrosides in rat oligodendroglia. Ketone bodies were also somewhat stimulatory. Having no effect or causing dedifferentiation of the cells were 5-azacytidine and phorbol esters. Thus induction of cerebroside synthesis in oligodendroglia is complex and may involve many factors.

Animals↗
PubMed1987

The effects of nifedipine and captopril on renal function in patients with essential hypertension: comparison with sodium nitroprusside.

In comparison with a nonspecific vasodilator, sodium nitroprusside (SNP), we intended to deduce the characteristics of nifedipine (NIF) and captopril (CAP) in the treatment of hypertension. Ten patients with essential hypertension were hospitalized and kept on a constant sodium diet (10 g NaCl/day). Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured before and after the respective administration of SNP (0.9 +/- 0.5 mcg/kg/min), NIF (17 +/- 5 mg), and CAP (85 +/- 24 mg). SNP significantly reduced the mean blood pressure (MBP), the renal vascular resistance index (RVRI), urine volume (UV), urinary excretion of sodium (UNaV), and significantly raised active renin concentration (ARC), plasma norepinephrine (NE), and the heart rate (HR). RBF, GFR, and plasma epinephrine (E) were not changed. Compared with SNP, NIF significantly raised RBF, UV, UNaV, and fractional excretion of sodium (FENa) and significantly reduced RVRI. The differences between the increases in ARC, NE, and HR by NIF and those by SNP were not significant. GFR and E were not changed by NIF. Although CAP did not reduce MBP as much as SNP did, the increase in RBF by CAP was significantly greater than that by SNP. Changes in GFR, UV, UNaV, FENa, and E by CAP were not different than those by SNP. CAP increased ARC and did not raise E, NE, and HR. In conclusion, compared with SNP, NIF significantly raised RBF, UV, UNaV, and FENa and significantly reduced RVRI. On the other hand, the renal response to CAP was not very much different from the response to SNP. The characteristics of CAP were the suppressed sympathetic response to the decrease in blood pressure.

Adult↗
PubMed1986

Dynamic changes in plasma inactive renin levels in Bartter's syndrome after administration of captopril and angiotensin II.

Changes in plasma active and inactive renin concentration (ARC and IRC) after captopril administration and angiotensin II (AII) infusion were studied in six patients with Bartter's syndrome. A single oral dose of captopril (8-25 mg) lowered the blood pressure and increased both ARC and IRC. AII infusion elevated blood pressure, suppressed ARC and increased IRC. In this syndrome of high renin levels, infused AII appeared to increase inactive renin secretion by reducing its conversion to active renin. On the other hand, an acute fall in AII levels and/or renal perfusion pressure by captopril increased both active and inactive renin. This indicates that the increase in the secretion of inactive renin, stimulated by captopril, might exceed any increase in its conversion to active renin in patients with Bartter's syndrome, in whom the production of renin is accelerated, and conversion of inactive renin to active renin probably already operates near its maximum.

Adolescent↗
PubMed1986

Prevention of nephrosclerosis and cardiac hypertrophy by captopril treatment of spontaneously hypertensive rats.

The relationship between hypertension and cardiovascular damage was assessed in three groups of spontaneously hypertensive rats (SHR): 1. stroke prone SHR (SHR-SP) treated orally with an angiotensin I converting enzyme inhibitor (captopril) (100-400 mg/L in the drinking water) from 6 to 35 weeks of age, 2. SHR-SP maintained on tap water until 30 weeks of age, 3. stroke resistant SHR (SHR-SR) maintained on tap water. The controls were Wister Kyoto rats (WKY) maintained on tap water. Captopril-treated SHR-SP showed blood pressure lower than that of untreated SHR-SP, similar to SHR-SR. The ratio of heart weight to body weight was 0.55% in SHR-SP, 0.39% in captopril-treated SHR-SP, 0.46% in SHR-SR, and 0.39% in WKY. The kidneys of SHR-SP showed glomerular sclerosis, glomerular fibrosis, tubular casts, interstitial cell infiltration and vascular wall thickening or hyperplasia of the small arteries and arterioles. The severe glomerular sclerosis was mostly distributed in the inner and middle portions of cortex. Immunohistological study showed IgG, C3 and fibrinogen in the glomeruli and arterioles in SHR-SP. In captopril-treated SHR-SP, similar to SHR-SR, only minor histological changes were seen and there was no deposition of IgG, C3 or fibrinogen. No changes were seen in WKY. Thus, it was concluded that nephrosclerosis and cardiac hypertrophy in SHR-SP are prevented by captopril. The role of the renin-angiotensin and kallikrein-kinin systems in organ pathogenesis in SHR-SP is discussed.

Animals↗
PubMed1985

Effects of enalapril maleate (MK-421) on renovascular hypertension.

The effects of enalapril maleate (MK-421), a new angiotensin converting enzyme inhibitor, were studied on 5 patients with renovascular hypertension (RVH) due to unilateral renal artery stenosis. The therapeutic dosage was increased when the blood pressure (BP) was not controlled for more than 3 days. Blood sampling was performed before, and 5 hr and 24 hr after the first administration, and on the 3rd day with each dosage. The BP was normalized on 5 mg/day in 1 case, 10 mg in 1 case, 20 mg in 2 cases, and 40 mg plus mefruside in 1 case. Plasma renin activity (PRA) was significantly increased after 5 hr and recovered after 24 hr with 2.5 mg of the enalapril maleate, when the BP was not affected. This indicates that the increase in PRA is likely due to the reduced negative feedback of angiotensin II. When the blood pressure was lowered, PRA was increased and plasma aldosterone concentration (PAC) was decreased significantly. This rise of PRA may depend not only on the reduced negative feedback but also on the fall of BP. It is also considered that the PAC was decreased through the decrease in plasma angiotensin II. A fall of the glomerular filtration rate in one case and also a fall of the perfusion of the kidney of the stenotic side in another case were observed by radioisotope renograms. MK-421 administration was a useful treatment for RVH, and clearly normalized the BP of all the patients studied. However, there was a risk of a fall of renal function on the stenotic side due to the decrease in perfusion pressure.

Adolescent↗
PubMed1985

Production and release of inactive renin by human vascular smooth muscle cells.

Human arterial smooth muscle cells were obtained from surgically excised tissues and cultured by the explant method. The cultured cells had both active and inactive forms of an angiotensin I forming enzyme. About a five-fold increase in the activity was obtained by trypsin treatment. This renin-like enzyme was also found in abundance in the culture media, mostly in an inactive form. Most of the enzyme activity, either before or after the activation, was suppressed by an antibody specific to human renin. The inactive enzyme was activated to some extent also by acidification and by cold exposure. The molecular weight of the inactive enzyme was estimated to be approximately 49,000 by gel filtration. These results suggest that human vascular smooth muscle cells can produce renin and release an inactive form of renin, and can be a potential source of plasma inactive renin under certain conditions such as the anephric state.

Angiotensin I↗
PubMed1985

Effects of enalapril maleate on plasma level of inactive renin in renovascular hypertension.

Changes in plasma levels of active and inactive renin after the treatment with enalapril maleate (MK-421), a new angiotensin converting enzyme inhibitor, were studied in five patients with renovascular hypertension (RVH) due to unilateral renal artery stenosis. The dosage was increased when the blood pressure (BP) was not normalized for more than 3 days. Blood sampling was performed before, and 5 hours and 24 hours after the first administration, and on the 3rd day with each dosage. Active and inactive renin concentrations (ARC and IRC) showed a reciprocal change in 4 cases, 5 hours after the first dose. In the chronic treatment, ARC and IRC before the morning dose did not change apparently until the BP was normalized, when both ARC and IRC were evidently increased. It was suspected that a conversion from inactive to active renin may occur in the patients with RVH, when the active renin secretion is stimulated suddenly by the first dose of MK-421. The chronically diminished perfusion pressure in the kidney may stimulate the secretion of inactive renin, but the decrease in endogenous angiotensin II may not.

Adolescent↗
PubMed1984

High level of plasma inactive renin in Bartter's syndrome.

In 10 cases of Bartter's syndrome, plasma active and inactive renin (AR and IR) were measured by two different methods. First, plasma renin activity (PRA), and total renin activity (TRA) after activating IR with trypsin, were measured by radioimmunoassay (RIA) of angiotensin I (AI) generated from endogenous substrate. And secondly, plasma active renin concentration (ARC) and total renin concentration (TRC) were measured by RIA of AI generated in the presence of an excess of exogenous substrate. The difference between TRA and PRA, and between TRC and ARC were designated as inactive renin activity (IRA) and inactive renin concentration (IRC), respectively. Small amounts of IRA were found only in 2 cases and no IRA in 8 cases. However, the existence of large amounts of IR in Bartter's syndrome was revealed by the IRC determination. This suggests that the shortage of endogenous renin substrate, consumed by the markedly increased AR, may have interfered with the detection of IRA in Bartter's syndrome, though the IR is markedly increased as well. The molecular weights of AR and IR were determined by Sephadex G-100 gel filtration in 3 cases. Both AR and IR seemed to be smaller than those of normal subjects.

Adolescent↗
PubMed1984

Angiotensin II analogue infusion test in renovascular hypertension under low sodium intake and under spironolactone administration: is angiotensin II analogue infusion test useful in determining the mode of treatment?

An angiotensin II antagonist (1-Sar, 8-Ileu-angiotensin II) was infused into 5 hypertensive patients with unilateral renal artery stenosis under 5-day low sodium diet (2 g NaCl/day) and under 7-day spironolactone administration (300 mg/day). In the sodium depleted state, 1 case showed depressor response, 2 cases pressor response and the other 2 no response. During the spironolactone administration, 3 cases showed depressor, 1 case pressor, and another case no response. Angiotensin II analogue (A II A) infusion test under spironolactone administration was more effective than under sodium depletion. However, there were cases which showed pressor response, i.e. false negative, under low sodium diet and under spironolactone administration. The hypertension of these patients was cured by converting enzyme inhibitor, percutaneous transluminal renal angioplasty (PTRA) or bypass surgery. A II A infusion test has been used for screening, diagnosis and determination of the surgical repair of renovascular hypertension. However, the proportion of depressor response was low in our cases, yet pressor responders and non-responders were also cured by PTRA. PTRA is a painless and low risk procedure of the treatment of renovascular hypertension, so PTRA will become the preferential mode of therapy for the treatment of renovascular hypertension of the cases with no depressor response by AIIA infusion.

Adolescent↗
PubMed1984

Successful treatment of the crisis of scleroderma with enalapril maleate (MK-421).

A 74-year-old man has been known to have scleroderma for 5 years. Two months before the hospitalization, his blood pressure was rapidly elevated, and progressive renal impairment and ulcerations of the fingers manifested. Then he was diagnosed to have a crisis of scleroderma. The treatment with a new long-acting angiotensin I converting enzyme inhibitor, enalapril maleate (MK-421), normalized the blood pressure and protected the progress of renal impairment without side effects.

Aged↗
PubMed1984

A case of 17 alpha-hydroxylase deficiency syndrome associated with right adrenal tumor.

A 35-year-old woman, who had been hypertensive for about 17 years and had lacked menarche, showed hypokalemia, low plasma cortisol and aldosterone levels, suppressed renin activity, and marked elevation of plasma corticosterone. The patient was diagnosed as having 17 alpha-hydroxylase deficiency from functional studies. In addition, a right adrenal tumor was found by adrenal venography. Adrenal venous sampling showed that this tumor might be secreting corticosterone and possibly also deoxycorticosterone (DOC). The genotype was 46,XY, so she was diagnosed as having male pseudohermaphroditism. Right adrenalectomy and contralateral adrenal biopsy were done. The retained testicles were removed. Dexamethasone administration normalized the blood pressure and serum potassium. This is the first report of 17 alpha-hydroxylase deficiency with a right adrenal tumor.

Adrenal Gland Neoplasms↗
PubMed1984

Synchronous changes in active and inactive renin secretion after furosemide in patients with primary aldosteronism.

Changes in plasma active and inactive renin concentrations (ARC and IRC) were measured in 10 patients with primary aldosteronism (PA) due to adrenal adenomas. Before the resection of adrenal adenomas, venous blood samples were taken at supine resting state, after 1-hour standing and 30 min. after furosemide injection and these samplings were repeated after surgical treatment. Plasma inactive renin was measured after activation with trypsin. Before the treatment ARC and IRC did not change by standing or furosemide. After the treatment, however, ARC was increased clearly by standing or furosemide, and IRC was also increased by furosemide injection. Both ARC and IRC at supine resting state were increased after the surgery. When the renin-angiotensin system is suppressed chronically by the over-produced aldosterone in patients with PA, not only active but also inactive renin secretions are suppressed, and fail to respond to orthostasis or furosemide. The secretion of IR could be stimulated after the removal of aldosteronoma.

Adenoma↗
PubMed1984

Studies on the active and inactive renin in renovascular hypertension.

Active and inactive plasma renin concentrations (ARC and IRC) from both renal veins and the femoral artery, and the molecular weight (MW) of active and inactive renin (AR and IR) from both renal veins were measured in 6 patients with renovascular hypertension due to unilateral renal artery stenosis. Venous ARC on the affected side was higher than that on the unaffected side and arterial ARC. In 4 patients ARC increased and IRC decreased after circulating through the stenotic kidney, while in the other 2 cases venous IRC on the stenotic side was higher than arterial IRC. The MW of AR on the stenotic and non-stenotic sides were 40000-48000 and 45000-48000, respectively, and those of IR varied from 45000-53000 and 48000-55000, respectively. These values seem to be smaller than those of normal subjects. The renin molecule may be small immediately after the release from the kidney and become larger in the circulation. In 3 cases, whose ARC increased and IRC decreased after passing through the stenotic kidney, AR and IR from the stenotic kidney were smaller than those from the non-stenotic kidney. Some mechanism of AR and IR molecule reduction may work in the stenotic kidney to activate IR.

Chromatography, Gel↗
PubMed1983

Studies on the molecular weight of active and inactive renins in essential hypertension.

The molecular weight (MW) of active renin (AR) and inactive renin (IR) was investigated in individual plasma samples from 15 essential hypertensive and 5 normal subjects. The patients with essential hypertension were classified into 3 subgroups: low plasma renin activity (PRA), normal PRA and high PRA. The MW of AR and IR was estimated by Sephadex G-100 gel filtration. IR in the eluates was activated with trypsin. Plasma renin activity and renin activity in eluates were measured by radioimmunoassay of angiotensin I. At least 3 sizes of AR (MW: 48,000, 53,000 and 57,000) and 2 sizes of IR (MW: 53,000 and 57,000) were discovered, and the MW of AR was less than or equal to the MW of IR. The larger AR was predominant in the low PRA group and the smaller one in the high PRA group. This was also true for IR. This relation was also observed in the 2 types (high renin and low renin) of pooled plasma. In high renin pooled plasma the MW of AR and IR was about 48,000 and 54,000, respectively, while both were about 56,000 in low renin pooled plasma. It appears that the larger type of AR and IR remains in the circulation in the suppressed renin state, and that the smaller type of renins enters into the circulation when the secretion of renins is enhanced.

Enzyme Precursors↗
PubMed1982

Active and inactive renins in human urine.

Urinary excretions of active and inactive renin were studied in normal subjects and in patients with hypertensive or renal disease. Excessive excretion of active and inactive renins was observed in some patients with no significant correlation to their plasma levels or the degree of proteinuria. Inactive renin excretion correlated to active renin excretion, but the clearance was lower than that of the active form. No correlation was found between the urinary kallikrein excretion and the active/inactive renin ratio in the urine or the plasma. Urinary renin activity was increased by acidification and by trypsin treatment, but not by cold exposure. Both active and inactive renins in the urine showed multiple peaks corresponding to molecular weights between 45,000 and 64,000 by gel filtration.

Cold Temperature↗