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  • 1
    Electronic Resource
    Electronic Resource
    Renal kallikrein in diabetic patients with hypertension accompanied by nephropathy (1986)
    Springer
    Diabetologia 29 (1986), S. 162-167 
    Details
    ISSN: 1432-0428
    Keywords: Renal kallikrein ; urinary kallikrein excretion ; diabetes mellitus ; hypertension ; nephropathy ; plasma aldosterone concentration ; plasma renin activity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We measured the 24-h excretion of urinary kallikrein in 27 patients with Type 2 (non-insulin-dependent) diabetes and in 10 normal control subjects. Mean (± SD) kallikrein excretion in diabetic patients with nephropathy (6.2±2.4 naphthyl units (NU)/day,n=13) was significantly lower than in control subjects (12.8±3.4NU/day,p〈0.01) and in diabetic patients without nephropathy (9.4±3.4NU/day,n=14,p〈0.05). Kallikrein excretion in hypertensive diabetic patients with nephropathy (5.1±1.6 NU/day,n=8) was significantly lower (p〈0.05) than in normotensive patients with nephropathy (8.3±2.1 NU/day,n=5). There were no significant differences in kallikrein excretion rate (24-h excretion of urinary kallikrein/24-h creatinine clearance) among control subjects (9.9±4.3 NU/ml), diabetic patients with (9.0±3.2 NU/ml) and without (9.3±3.5 NU/ml) nephropathy. However, kallikrein excretion rate in hypertensive diabetic patients with nephropathy (7.7±3.3 NU/ml) was significantly lower (p〈0.05) than in normotensive diabetic patients with nephropathy (11.8 ±2.0 NU/ml,n=10). Respective basal and post-stimulated (with intravenous furosemide 40 mg plus 60 min ambulation) plasma aldosterone concentrations measured in control subjects and in hypertensive diabetic patients with nephropathy were similar and increased to the same extent in the 2 groups (5.5±3.2 versus 5.3±3.2 and 9.3±2.6 versus 10.5±3.4 ng/ml), although the respective plasma renin activity tended to be lower in diabetic patients than in control subjects (0.7±0.6 versus 1.3±0.9 and 1.8±1.8 versus 3.0±2.6 ng−1 · ml−1 · h−1). The results indicate that urinary kallikrein excretion is decreased in hypertensive diabetic patients with nephropathy, and that the decrease might not be attributable to an altered renin-aldosterone system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02427087
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Acute effect of an alpha1-adrenoceptor antagonist on urinary sodium excretion, plasma atrial natriuretic peptide, arginine vasopressin, and the renin-aldosterone system in healthy subjects (1992)
    Springer
    European journal of clinical pharmacology 43 (1992), S. 17-21 
    Details
    ISSN: 1432-1041
    Keywords: Alpha1-adrenoceptor antagonist ; Bunazosin ; Sodium retention ; atria ; natriuretic peptide ; arginine vasopressin ; renin-aldosterone system ; enalapril ; blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary To elucidate the mechanism underlying the sodium retention caused byα 1-adrenoceptor blockade in man, a placebo-controlled, randomised, double-blind study has been made of the acute effects of bunazosin anα 1-antagonist, on urinary sodium excretion, atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and the renin-aldosterone system in 7 healthy men. A single oral dose of bunazosin 2.0 mg caused a significant reduction (P 〈 0.05) in urinary sodium excretion after 0–2 h, 2–4 h, and 4–6 h. The mean values for plasma ANP, AVP, aldosterone, and cortisol concentrations at those times were similar after placebo and bunazosin, and plasma renin activity was significantly increased 2 and 4 h after bunazosin. Pretreatment with oral enalapril 10 mg, an angiotensin converting enzyme inhibitor, did not prevent the bunazosin-induced reduction in urinary sodium excretion. There was a significant positive correlation between the drug-induced changes in blood pressure and urinary sodium excretion. The results suggest that ANP, AVP, and renin-aldosterone may play little role in the sodium retention caused by acuteα 1-adrenoceptor blockade in man.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02280748
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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