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Biomedical subjects

A Iaina

Publications and source records attributed to A Iaina.

At least 55 records · Page 3Linked to original sources
PubMed1997

Avoiding the supine position during sleep lowers 24 h blood pressure in obstructive sleep apnea (OSA) patients.

Obstructive sleep apnea (OSA), is a common clinical condition affecting at least 2-4% of the adult population. Hypertension is found in about half of all OSA patients, and about one-third of all patients with essential hypertension have OSA. There is growing evidence that successful treatment of OSA can reduce systemic blood pressure (BP). Body position appears to have an important influence on the incidence and severity of these sleep-related breathing disturbances. We have investigated the effect of avoiding the supine position during sleep for a 1 month period on systemic BP in 13 OSA patients (six hypertensives and seven normotensives) who by polysomnography (PSG) were found to have their sleep-related breathing disturbances mainly in the supine position. BP monitoring was performed by 24-h ambulatory BP measurements before and after a 1 month intervention period. We used a simple, inexpensive method for avoiding the supine posture during sleep, namely the tennis ball technique. Of the 13 patients, all had a reduction in 24-h mean BP (MBP). The mean 24-h systolic/diastolic (SBP/DBP) fell by 6.4/2.9 mm Hg, the mean awake SBP/DBP fell by 6.6/3.3 mm Hg and the mean sleeping SBP/DBP fell by 6.5/2.7 mm Hg, respectively. All these reductions were significant (at least P < 0.05) except for the sleeping DBP. The magnitude of the fall in SBP was significantly greater in the hypertensive than in the normotensive group for the 24 h period and for the awake hours. In addition, a significant reduction in BP variability and load were found. Since the majority of OSA patients have supine-related breathing abnormalities, and since about a third of all hypertensive patients have OSA, avoiding the supine position during sleep, if confirmed by future studies, could become a new non-pharmacological form of treatment for many hypertensive patients.

Adult↗
PubMed1997

Sleep-related breathing disturbances: their pathogenesis and potential interest to the nephrologist.

For about 120 years we have been looking for the 'cause' of essential hypertension. It is possible that we have merely been wandering through its graveyard, looking at the pathogenetic mechanisms but never the actual cause? Here we pass the gravestone of increased sympathetic activity; there the gravestone of low renin activity. Here high endothelin; there low EDRF. Here high thromboxane A2; there low prostacyclin. It is possible that all these and so many other pathogenetic factors are all due to one basic defect? Is it possible that, in the dead of night while patients with EH have been sleeping, the villain has been lurking in their mouths, stuck somewhere at the back of their throats, hidden from view yet choking them hundreds of times a night. But this intermittent strangulation has not occurred silently. On the contrary, it has made its presence felt in the most irritating way, with snores, groans, grunts, gasps and frightening periods of total apnea. But we, their physicians, never asked about these symptoms, or, if we did, we never paid heed to them. This is clear from the fact that, most cases of OSA occur in association with EH yet are not diagnosed. Perhaps the next 'arousal response' should be the arousal of physicians' consciousness so that they can at long last wake up to the existence of the close connection between sleep-related breathing disorders and hypertension and breathe some new life into the treatment of two old diseases-essential hypertension and secondary hypertension. Early diagnosis and treatment of the sleep-related breathing disorders may not only make the patient feel much better, (something our antihypertensive medications do not always do), but may reduce the blood pressure and prevent the progression of renal and cardiovascular damage as well.

Blood Pressure↗
PubMed1997

Methylene blue--a promising treatment modality in sepsis induced by bowel perforation.

In this study, we compared the effects of methylene blue (MB) and an L-arginine analogue on host outcome, blood pressure, lung injury, and nitric oxide (NO) production in rats following fecal peritonitis induced by cecal ligation and puncture (CLP). Sepsis syndrome was induced in 90 rats: 30 were treated with MB, 30 with an NO synthase inhibitor, and 30 with normal saline. We found significantly less alveolar damage, higher blood pressure, better respiratory function, and delayed mortality among animals treated with MB compared to the control group. We conclude that the ability of MB to reduce alveolar damage and therefore to delay mortality in this animal septic shock model may give this harmless substance a role among the treatment modalities of septic shock syndrome induced by fecal peritonitis.

Animals↗
PubMed1997

Glomerular basement membrane polyanionic sites and nitric oxide in genetically salt-sensitive and resistant hypertensive rats.

Cationic colloid gold, a polycationic histochemical probe, was used to analyze the distribution of glomerular basement membrane (GBM) polyanions, including heparan sulfate protoglycan in genetic salt-sensitive (SBH/Y) and resistant (SBN/Y) hypertensive rats, with or without high dietary salt intake. GBM morphology, renal function and nitric oxide, as measured by plasma and urine nitrite (NO2) and nitrate (NO3) were also determined. In the salt-sensitive rats the high-salt dietary intake resulted in severe hypertension, proteinuria and decreased glomerular filtration rate. After 1 month of high-salt intake, the average width of the GBM of salt-sensitive rats was higher by 27% than that of salt-resistant rats. The number of GBM anionic sites (lamina rata externa and interna) was much lower in both salt-sensitive and salt-resistant groups after 1 month of salt loading, 8.04+/-0.36 and 7.8+/-0.25 counts/cm, respectively, compared to the respective values of non-salt-loaded animals, 20.58+/-1.08 counts/cm in the SBH/Y (p < 0.001) and 21+/-1.86 counts/cm in the SBN/Y (p < 0.001). A decreased nitric oxide production was found in the salt-sensitive rats before and after salt loading compared with the salt-resistant group. No correlation was found between the nitric oxide changes and the GBM modifications. It is concluded that high-salt intake may be deleterious to the permselectivity of the GBM. It is suggested that salt restriction in hypertension may have a beneficial effect in preventing GBM permselectivity changes and proteinuria.

Animals↗
PubMed1997

Metformin enhances clearance of chylomicrons and chylomicron remnants in nondiabetic mildly overweight glucose-intolerant subjects.

OBJECTIVE: To assess the effect of metformin on the metabolism of intestinally derived lipoproteins in nondiabetic individuals who were mildly overweight and glucose intolerant. RESEARCH DESIGN AND METHODS: A total of nine subjects with a BMI > or = 25 kg/m(2) and fasting serum glucose < or = 6.1 mmol/l and who were glucose intolerant were studied. The subjects underwent a vitamin A fat-loading test before and after a 3-month treatment with 850 mg metformin twice a day. The metabolic behavior of the postprandial lipoproteins was compared with that found in a group of 19 healthy normolipidemic individuals who participated in a previous study. RESULTS: Mean total plasma, chylomicron fraction, and nonchylomicron fraction retinyl palmitate (RP) pretreatment levels were 3.4-fold, 3.59-fold, and 3-fold higher, respectively, in the study group than in the normolipidemic group and were reduced by 50, 56, and 32%, respectively, after 3 months of metformin treatment. The decrease of chylomicron levels after treatment was positively correlated to the fasting triglyceride values before treatment (r = 0.73, P = 0.039) and to the serum insulin level at 120 min of standard glucose loading before treatment (r = 0.91, P = 0.002). CONCLUSIONS: Metformin was shown to be beneficial in the clearance of postprandial lipoproteins in nondiabetic individuals who were mildly overweight and glucose intolerant.

Cholesterol↗
PubMed1996

Metabolism of agmatine into urea but not into nitric oxide in rat brain.

Agmatine is a guanidino compound abundant in bacteria and plants where it serves as a precursor for polyamine synthesis. It can interfere with several neurotransmission-related functions and can exert neuroprotective effects after brain injury. Agmatine was recently identified in mammalian brain and its synthesis by arginine decarboxylation was characterized. Its metabolism by the brain is, however, unknown. Here we report evidence indicating that agmatine can be selectively metabolized in the rat brain (cerebellum) into urea and thus, may lead to formation of putrescine, the precursor of polyamine synthesis. In addition, while agmatine can inhibit brain nitric oxide synthase, it did not serve as a substrate for nitric oxide formation.

Agmatine↗
PubMed1996

Clearance of chylomicron remnants in normolipidaemic patients with coronary artery disease: case control study over three years.

OBJECTIVE: To test the hypothesis that subjects who clear chylomicron remnants slowly from plasma may be at higher risk of coronary artery disease than indicated by their fasting plasma lipid concentrations. DESIGN: Case control study over three years. SETTING: An 800 bed general municipal hospital. SUBJECTS: 85 normolipidaemic patients with coronary artery disease selected prospectively and matched with 85 normolipidaemic subjects with normal coronary arteries on angiography. INTERVENTIONS: All subjects were given a vitamin A fat loading test which specifically labels intestinal lipoproteins with retinyl palmitate. MAIN OUTCOME MEASURE: Postprandial lipoprotein metabolism. RESULTS: The area below the chylomicron remnant retinyl palmitate curve was significantly increased in the coronary artery disease group as compared with the controls (mean 23.4 (SD 15.0) v 15.3 (8.9) mumol/l.h; 95% confidence interval of difference 4.37 to 11.82). CONCLUSION: Normolipidaemic patients with coronary artery disease had significantly higher concentrations of chylomicron remnants in plasma than normolipidaemic subjects with normal coronary vessels. This may explain the mechanism underlying the susceptibility to atherosclerosis of coronary artery disease patients with normal fasting lipid values. As diet and drugs can ameliorate the accumulation of postprandial lipoproteins in plasma, the concentration of chylomicron remnants should be measured in patients at high risk of coronary artery disease.

Adult↗
PubMed1996

Prediction of renal impairment in elderly patients with congestive heart failure treated with captopril.

This study assessed the usefulness of the oral captopril test in the prediction of renal impairment among elderly patients with congestive heart failure (CHF). Forty-seven patients aged > or = 65 years with CHF (EF < 40%) participated in a prospective nonrandomized series. Blood samples for plasma renin activity (PRA) were drawn before and 60 minutes after 50 mg of oral captopril. Twenty-four hours later, captopril was administered (up to 75 mg/day over a 4 day period), and renal laboratory and clinical assessment were performed at baseline and for a 9 day period. In 7 of 47 patients (14.9%), deterioration of renal function was observed. During the captopril test, the PRA increased significantly after 1 hour in almost all patients and the mean blood pressure decreased from 99.2 +/- 14.6 mmHg to 92.2 +/- 13.7 mmHg (p < 0.001). All patients whose baseline PRA level was < 1.9 ng/ml/hr and whose stimulated PRA was < 3.2 ng/ml/hr maintained a stable renal function throughout the study period. Significant statistical correlation (p < 0.05) was found between the initial PRA, the changes in PRA or mean blood pressure during the captopril test, and the change in plasma creatinine and creatinine clearance in the entire group, and was even more evident in a subgroup of patients with an ejection fraction > or = 30%. All these correlations were not statistically significant in the patients with an ejection fraction < 30%. It is thus concluded that measurement of pretreatment PRA levels might be a useful laboratory tool for predicting the renal safety of captopril use in patients with CHF whose EF > or = 30%.

Administration, Oral↗
PubMed1996

Nitric oxide in ischaemic acute renal failure of streptozotocin diabetic rats.

Changes in nitric oxide (NO) levels were determined in ischaemic acute renal failure in streptozotocin-induced diabetes mellitus rats. Two weeks after streptozotocin administration and immediately after right nephrectomy, the left renal artery was occluded for 60 min. Similar procedures were carried out in non-diabetic rats. The nitrite (NO2) + nitrate (NO3) levels were measured in plasma and urine. The effects of chronic oral supplementation with L-arginine and an NO synthase inhibitor (N-omega-nitro-L-arginine) were also studied in both diabetic and non-diabetic rats before and after renal artery clamping. The rats with diabetic acute renal failure had a much lower creatinine clearance (90 +/- 22 microliters.min-1. 100g body weight-1, p < 0.005), and higher fractional excretion of sodium (FENa)% (10.90 +/- 4.2, p < 0.001) and protein excretion (2078 +/- 69 micrograms/ml creatinine clearance, p < 0.001) compared with the respective values in the non-diabetic groups (163 +/- 30; 1.46 +/- 86; 453.3 +/- 31). The plasma and urine NO2 + NO3 levels were significantly higher in the untreated diabetic rats compared with the untreated normal rats before ischaemia (p < 0.001). The ischaemic acute renal failure in non-diabetic rats increased the plasma and urinary NO2 + NO3 excretion after ischaemia. The urinary excretion of these metabolites decreased significantly and their plasma levels remained unchanged in the ischaemic diabetic rats. The L-arginine administration resulted in a small but significantly higher creatinine clearance after clamping in the non-diabetic rats. The NO synthase inhibitor caused deterioration in renal function in all ischaemic and non-ischaemic groups. In summary, the greater vulnerability to ischaemia of the diabetic kidney seems to be associated with both impaired response to and impaired production of NO.

Acute Kidney Injury↗
PubMed1996

The effect of human recombinant erythropoietin on the growth of a human neuroblastoma cell line.

Erythropoietin is a growth factor. Cancer can be described as disturbance of the fine balance of positive and negative growth control mechanisms. The effect of human recombinant erythropoietin (EPO) was studied on the cell growth and differentiation of a human neuroblastoma cell line (h-NMB). Cell growth curves, trypan blue staining and thymidine uptake were used to assess cell proliferation and death. To assess cell differentiation, neutral endopeptidase (cell membrane enzyme marker), creatine kinase (cytosolic enzyme marker), dopamine uptake (dopamine transporter marker) and cell morphology were determined. Specific EPO receptor mRNA, by RT-PCR technique, was demonstrated. The incubation of erythropoietin with the tumor cell line resulted in inhibition of cell proliferation as evidenced in a diminished cell growth. EPO was shown to have induced a differentiation process as seen from the two different enzymatic markers, membranal and cytosolic, and from the cells dopamine uptake studies. However, the morphological changes did not document a full differentiation effect. EPO specific antibodies blocked the effects of EPO on cell proliferation and creatine kinase activity. In this study, EPO did not produce any sign of proliferation in the nervous tumor cell line used.

Base Sequence↗
PubMed1996

Intravenous iron supplementation for the treatment of the anemia of moderate to severe chronic renal failure patients not receiving dialysis.

Iron deficiency may develop in hemodialysis patients, especially when erythropoietin is given. The role of iron deficiency in the anemia of predialysis chronic renal failure (CRF), however, is much less clear. We have intravenously (IV) administered iron as ferric saccharate in a total dose of 200 mg elemental iron monthly for 5 months to 33 CRF patients who remained anemic despite oral iron supplementation and who had no laboratory signs of iron overload. None was receiving erythropoietin therapy. In 22 of the patients there was an increase in the hematocrit values by the end of the study. These patients were considered responders to intravenous iron (IV Fe) therapy. In 11 patients the iron administration was not associated with improvement of the anemia (nonresponders). Before onset of the IV Fe therapy there were no differences between the responders and nonresponders with regard to degree of anemia, serum ferritin, iron saturation, renal function, or blood pressure. One additional patient was excluded from the study because of a mild reaction during an IV test dose before the study. No worsening of kidney function and no other side effects were noted. In four patients (three responders and one nonresponder) the control of blood pressure necessitated antihypertensive drug therapy adjustment. In conclusion, IV Fe supplementation in two thirds of anemic CRF patients not receiving dialysis resulted in a significant improvement of the anemia, thus avoiding the necessity of erythropoietin or blood administration. This could be achieved by increasing the plasma ferritin levels to 200 to 400 microns/L and/or increasing the iron saturation to 25% to 35%. Intravenous ferric saccharate appears to be a safe and effective method of administering iron for the correction of anemia in CRF patients not receiving dialysis.

Administration, Oral↗
PubMed1996

Nitric oxide in streptozotocin-induced diabetes mellitus in rats.

1. The present study was performed to determine the relationship between diabetic glomerular hyperfiltration and nitric oxide as modulated by the chronic administration of L-arginine and/or N-omega-nitro-L-arginine, a known nitric oxide synthase inhibitor in streptozotocin-induced diabetic rats. 2. Normal rats and rats drinking hypertonic glucose (10%) were used as time-controlled groups. Six weeks after administration of streptozotocin the diabetic rats had significantly higher creatinine clearance (667 +/- 53 microliters min-1 100 g-1 body weight) than before and streptozotocin (456 +/- 38 microliters min-1 100 g-1 body weight, P < 0.005) and very high plasma (37.8 +/- 10.9 mumol/l) and urinary (3.492 +/- 0.179 nmol min-1 100 g-1 body weight) nitrite+nitrate (stable metabolites of nitric oxide) values compared with before streptozotocin administration [19.3 +/- 2.8 mumol/l (P < 0.001) and 0.420 +/- 0.051 nmol min-1 100 g-1 body weight (P < 0.001) respectively]. The 6-week diabetic rats had higher systolic blood pressure (124.2 +/- 2.9 mmHg, P < 0.05) than before streptozotocin (108 +/- 8 mmHg), but had a value similar to that of the hypertonic-glucose-drinking rats. 3. The diabetic rats supplemented with L-arginine did not show an increase in creatinine clearance and had a lower urinary excretion of nitrite+nitrate (0.999 +/- 0.27 nmol min-1 100 g-1 body weight, P < 0.005) than the respective untreated streptozotocin-induced diabetic rats. Creatinine clearance increased in the normal and glucose-drinking rats that received L-arginine. The administration of L-arginine resulted in significant reduction in blood pressure in all groups studied. The chronic nitric oxide synthase inhibitor resulted in high blood pressure, and in a significant decrease in creatinine clearance and urinary nitrite+nitrate excretion in all groups studied. In both diabetic and glucose-drinking rats, the L-arginine therapy resulted in significantly lower plasma and urinary glucose levels than in their respective untreated control groups. 4. The nitric oxide synthase inhibitor increased the plasma and urinary glucose concentration in both diabetic and glucose-drinking rats. 5. Our results indicate that diabetic rats are characterized by high plasma concentrations and elevated urinary excretion of nitrite+nitrate, suggesting a state of high nitric oxide production. The vascular response to nitric oxide in diabetic rats may be different at the glomerular and peripheral vascular bed.

Alloxan↗
PubMed1996

Intravenous ferric saccharate as an iron supplement in dialysis patients.

In the present prospective study we examined the long-term effect of intravenous supplementation with ferric saccharate (IV Fe) in the treatment of the anemia of chronic dialysis patients. All patients, 64 on chronic hemodialysis (HD) and 9 on chronic ambulatory peritoneal dialysis (CAPD), were treated intravenously with this preparation in a dose of 100 mg elemental iron twice monthly. There were five groups. Group 1: 41 HD patients who were receiving erythropoietin (EPO) for at least 6 months prior to the addition of IV Fe. In this group, when IV Fe was given over 6 months, the hematocrit (Hct) increased from a mean of 28.7 to 33.7%. Over the next 6 months, the EPO dose was gradually reduced by a mean of 61.1%, but the mean Hct remained unchanged. Group 2: 11 HD patients who started IV EPO simultaneously with the IV Fe. In this group, over 6 months, the mean Hct increased from 28.1 to 34.1. Over the next 6 months, the EPO dose was gradually reduced by 75.7%, but the mean Hct remained unchanged. Group 3: 12 HD patients who received IV Fe alone for 12 months. The mean Hct increased from 30.5 to 37.9%. Group 4: 4 CAPD patients who had been receiving subcutaneous EPO for at least 6 months prior to IV Fe therapy. Over the subsequent 6 months of IV Fe, the mean Hct increased from 28.4 to 33.3%. Group 5: 5 CAPD patients not on EPO who received IV Fe for 6 months. The mean Hct increased from 27.7 to 35.6%. No adverse effects were seen in any patients throughout the study. In conclusion, adequate Fe supplementation may allow the target Hct of about 33% to be reached without, or with only very low doses of EPO. IV Fe as ferric saccharate is a new and safe form of parenteral iron therapy of the anemia of chronic dialysis patients.

Adult↗
PubMed1995

Improvement of cardiac performance by intravenous infusion of L-arginine in patients with moderate congestive heart failure.

OBJECTIVES: The aim of this study was to evaluate the hemodynamic effect of L-arginine infusion in patients with congestive heart failure. BACKGROUND: Endothelium-dependent vasodilation is impaired in patients with congestive heart failure. Nitric oxide, which was identified as endothelium-derived relaxing factor, is generated by nitric oxide synthase from L-arginine. Our hypothesis was that administration of L-arginine in patients with congestive heart failure may increase nitric oxide production and have a beneficial hemodynamic effect. METHODS: Twelve patients with congestive heart failure (New York Heart Association class II or III) due to coronary artery disease (left ventricular ejection fraction < 35%) were given 20 g of L-arginine by intravenous infusion over 1 h at a constant rate. Stroke volume, cardiac output and left ventricular ejection fraction were determined with Doppler echocardiography at baseline and at 30 and 60 min and 1 h after the end of infusion. Blood and urinary levels of nitrite/nitrate (NO2/NO3), stable metabolites of nitric oxide, were measured and clearance was calculated. RESULTS: One hour of infusion of L-arginine resulted in a significant increase in stroke volume (from 68 +/- 18 ml to 76 +/- 23 ml [mean +/- SD], p = 0.014) and cardiac output (from 4.07 +/- 1.22 liters/min to 4.7 +/- 1.42 liters/min, p = 0.006) without a change in heart rate. Mean arterial blood pressure decreased (from 102 +/- 11 mm Hg to 89 +/- 9.5 mm Hg, p < 0.002), and systemic vascular resistance decreased significantly. Within 1 h after cessation of L-arginine infusion, blood pressure, stroke volume, cardiac output and systemic vascular resistance were statistically not different from baseline values. Clearance of NO2/NO3 increased significantly during L-arginine administration (from 13.28 +/- 0.42 ml/min to 29.97 +/- 1.09 ml/min, p < 0.001). CONCLUSIONS: Infusion of L-arginine in patients with congestive heart failure results in increased production of nitric oxide, peripheral vasodilation and increased cardiac output, suggesting a beneficial hemodynamic and possibly therapeutic profile.

Aged↗
PubMed1995

Bezafibrate therapy in patients with isolated low high-density lipoprotein cholesterol levels may have a beneficial effect in prevention of atherosclerosis.

Although a low plasma high-density lipoprotein cholesterol (HDL-C) level is a well-accepted risk factor for coronary artery disease (CAD), it is unclear whether pharmacologic agents can effectively increase HDL-C levels and/or reduce the incidence of CAD in patients with isolated low HDL-C levels. An important determinant of HDL levels is the efficiency of postprandial lipoprotein catabolism. The purpose of the present study was to evaluate the efficacy of bezafibrate therapy in increasing HDL-C levels in these patients and to examine its effect on postprandial lipoprotein levels. Fasting and postprandial lipid and lipoprotein levels were studied in 23 patients with isolated low HDL-C levels before and during 3 and 6 months of bezafibrate treatment. Postprandial lipoprotein levels were evaluated using the vitamin A-fat loading test, in which these intestinally derived lipoproteins are specifically labeled with retinyl palmitate (RP). Patients with isolated low HDL had significantly higher levels of chylomicron RP than a control group of 19 normolipidemic subjects. The area below the chylomicron RP curve was 17,773 +/- 6,821 versus 13,936 +/- 6,217 micrograms/L.h, respectively (P < .005). No differences were found in chylomicron remnant levels between the groups. Bezafibrate therapy reduced the chylomicron RP area by 27%, from 17,773 +/- 6,821 to 12,895 +/- 2,576, and the nonchylomicron RP area by 25%, from 6,059 +/- 3,310 to 4,430 +/- 1,963 (P < .0001). It increased fasting HDL-C levels from 35 +/- 3 to 38 +/- 1.4 mg/dL after 3 months (P < .001) and to 40 +/- 2.2 mg/dL after 6 months (P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Postprandial intestinal-derived chylomicron and chylomicron remnants in essential hypertensive patients before and after prolonged captopril therapy.

The metabolism of the postprandial intestinal-derived lipoproteins, chylomicron and chylomicron remnants, is not known in patients with essential hypertension. After a fat meal, using the vitamin A test as a marker, retinyl palmitate was measured in the total plasma, chylomicron, and chylomicron remnant fractions in 14 untreated nondiabetic essential hypertensive patients with normal fasting lipids and lipoproteins. The vitamin A fat loading test was repeated in eight hypertensive patients after 3 months of captopril therapy. Fifteen matched normotensive subjects were used as controls. The untreated essential hypertensive patients had significantly higher chylomicron fraction concentration curves (AUC 17,469 +/- 2553 micrograms/L/h) P < .001 compared with the control group (AUC 13,208 +/- 1245 micrograms/L/h), by two-way analysis of variance with repeated measurements. After 3 months of captopril therapy, the chylomicron fraction (AUC 9701 +/- 1566 micrograms/L/h), and chylomicron remnants fraction (AUC 3487 +/- 580 micrograms/L/h) were much lower (P < .001) than before captopril therapy. Oral glucose tolerance tests were borderline in five of the eight hypertensives before captopril treatment but returned to normal after 3 months of therapy. In summary, postprandial intestinal-derived lipoprotein metabolism is altered in essential hypertensive patients. Captopril therapy caused significant improvement in the postprandial chylomicron metabolism.

Captopril↗
PubMed1995

Oral administration of L-arginine and captopril in rats prevents chronic renal failure by nitric oxide production.

The effect of oral supplementation of L-arginine, the substrate of nitric oxide, (1.25 g/liter water) and captopril (15 mg/liter water) was studied in 5/6 nephrectomized rats for a period of three months. N-omega-nitro L-arginine, a nitric oxide synthase inhibitor, was given orally (70 mg/liter water) with or without L-arginine or captopril. The urinary excretion of nitrite (NO2) + nitrate (NO3), the known metabolites of nitric oxide, was taken as an index of nitric oxide production. Chronic renal failure rats were characterized by a low creatinine clearance, high FENa%, proteinuria, hypertension and a low urinary excretion of NO2 + NO3; 0.152 +/- 0.06 (P < 0.001) nmol/micrograms creatinine compared with 0.481 +/- 0.004 (P < 0.001) in normal rats and 0.479 +/- 0.11 (P < 0.001) in untreated sham-operated rats. Both L-arginine and captopril were effective in the normalization of all these parameters. The combination of L-arginine and captopril had no additive effects. The nitric oxide synthase inhibitor significantly diminished the captopril beneficial effect. It is concluded that chronic renal failure in rats is a low nitric oxide production state. The supplementation of L-arginine is shown to overcome this condition. It is suggested that the beneficial effect of captopril on chronic renal failure is through a specific L-arginine--nitric oxide synthase--nitric oxide pathway.

Administration, Oral↗