J Wang

St George Hospital, Sydney, New South Wales, Australia

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Publications (4)7.48 Total impact

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    ABSTRACT: L-arginine treatment prevents adrenocorticotrophin (ACTH) induced hypertension in the rat. This study examined whether L-arginine treatment could reverse established ACTH hypertension and its effects on markers of decreased NO activity. Sixty-four male Sprague-Dawley rats were randomly divided into 6 groups given 12 days of treatment: (1) sham (0.9% NaCl, 0.5 ml/kg, subcutaneously, sc, n = 16); (2) ACTH (0.5 mg/kg/day, sc, n = 16); (3) sham + L-arginine (0.6% in food, from treatment day 8 onwards, n = 10); (4) ACTH + L-arginine (n = 10); (5) sham + D-arginine (0.6% in food, from T 8 onwards) (n = 6); and (6) ACTH + D-arginine (n = 6). Systolic blood pressure, water intake, urine volume, and body weight were measured every second day. At the end of the experiments, plasma and urinary nitrate/nitrite (NOx), plasma amino acid concentrations (in groups 1-4), and urinary cyclic guanosine monophosphate (cGMP) concentrations were measured. Sham, sham + L-arginine, and sham + D-arginine treatments did not affect blood pressure. ACTH increased systolic blood pressure (from 121 +/- 1 to 147 +/- 2 mmHg, p < 0.001, pooled control vs treatment day 12, mean +/- sem), and this was partially reversed by L-arginine (group 4: from 141 +/- 2 on day 8 to 133 +/- 1 mmHg on day 12, n = 10, p < 0.001). In contrast, D-arginine did not affect blood pressure in ACTH-treated rats (group 6). ACTH increased water intake and urine volume and decreased body weight, and L-arginine administration did not alter these parameters. ACTH decreased plasma citrulline (group 1 vs 2: 115 +/- 7 vs 67 +/- 6 micro M/L, n = 16, p < 0.001) and NOx concentrations (group 1 vs 2: 8.3 +/- 0.8 vs 4.5 +/- 0.6 microM/L, n= 10, p < 0.001) and these decreases were reversed by L-arginine treatment (group 4: citrulline 98 +/- 9 micro M/L, NOx 9.1 +/- 1.6 micro M/L, group 2 vs 4, both p < 0.05). ACTH produced marked increases in urinary cGMP excretion (group 1 vs 2: 0.5 +/- 0.1 vs 1.9 +/- 0.4 nmol/24 h, p < 0.01). Supplementation with L-arginine partly reversed established ACTH-induced hypertension and restored plasma NOx and citrulline concentrations to levels seen in sham-treated rats. These data are consistent with previous studies suggesting that functional NO deficiency has a role in ACTH-induced hypertension in rats.
    Blood Pressure 01/2000; 9(5):298-304. · 1.39 Impact Factor
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    ABSTRACT: 1. The present study investigated whether a low nitrate/nitrite diet could minimize variability in the measurement of endogenous plasma and urine nitric oxide (NO) metabolites, nitrate and nitrite (NOx) in normal subjects. 2. Nitrate and nitrite concentrations were measured in plasma and urine as indicators of NO production in six subjects during a free diet and then during a low nitrate/nitrite diet for 6 days. 3. The plasma concentration and 24 h urine NOx/creatinine ratio were significantly lower on the low nitrate/nitrite diet than on the free diet (P < 0.01). Nitric oxide production appeared to vary greatly within and between subjects, but these variations were substantially decreased by the fourth day of a low nitrate/nitrite diet. 4. Human plasma and urine NOx measurements should be determined after a low nitrate/nitrite diet for at least 4 days.
    Clinical and Experimental Pharmacology and Physiology 06/1997; 24(6):418-20. · 2.41 Impact Factor
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    ABSTRACT: 1. The effects of L-arginine treatment on dexamethasone-induced hypertension were examined in the Sprague-Dawley rat. Seventy rats were randomly divided into the following eight groups: sham, dexamethasone (5 and 10 micrograms/day, L-arginine (100 and 500 mg/kg per day), L-arginine (100 or 500 mg/kg per day) + dexamethasone (10 micrograms/day), L-arginine (520-797 mg/kg per day in food) + dexamethasone (5 micrograms/day). Systolic blood pressure (SBP), bodyweight and plasma nitrate/nitrite concentration were measured. 2. Dexamethasone (5 and 10 micrograms/day) increased SBP in both sham and L-arginine-treated rats. Dexamethasone at 10 micrograms/day decreased bodyweight, but did not alter plasma nitrate/nitrite concentrations. 3. L-Arginine (500 mg/kg per day, i.p.) increased plasma nitrate/nitrite concentrations in 10 micrograms/day dexamethasone-treated rats. L-Arginine did not alter blood pressure in either sham or dexamethasone-treated rats. 4. Dexamethasone-induced hypertension differs from adrenocorticotropic hormone (ACTH)-induced hypertension in the rat in that it is not modified by L-arginine. Thus, ACTH-induced hypertension cannot be explained simply in terms of glucocorticoid activity.
    Clinical and Experimental Pharmacology and Physiology 01/1997; 24(9-10):730-2. · 2.41 Impact Factor
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    ABSTRACT: Pre-eclampsia is characterised physiologically by plasma volume contraction, intravascular coagulation and intense vasoconstriction. It was originally thought that the renin-angiotensin-aldosterone (RAA) system would be overactive but studies have shown a more complex picture. Plasma renin activity (PRA) and concentration (PRC) and plasma angiotensin II (AII) and aldosterone concentrations (PAC) are reduced compared to normal pregnancy. Total renin concentration is normal and plasma concentrations of high molecular weight angiotensinogen are increased in pre-eclampsia though total angiotensinogen is normal. PRA and PRC respond appropriately to physiologic stimuli in pre-eclampsia except for impaired renin release following frusemide, possibly due to prostacyclin deficiency. Although plasma AII concentrations are reduced there is heightened pressor sensitivity to infused AII--the mechanism(s) for this are unknown. PAC is reduced but the ratio PAC-PRC is twofold greater in pre-eclampsia than normal pregnancy. This does not appear to be due to changes in potassium, atrial natriuretic peptide, dopamine or ACTH, and may be another manifestation of increased (adrenal) sensitivity to AII in pre-eclampsia. There is an inverse relationship between the plasma active renin to prorenin ratio and the clinical severity of the pre-eclampsia. Understanding the mechanisms producing these changes in the RAA system in pre-eclampsia will give strong clues to the overall pathogenesis of this disorder.
    Clinical and Experimental Hypertension 01/1997; 19(5-6):713-26. · 1.28 Impact Factor