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  • Articles: DFG German National Licenses  (3)
  • plasma renin activity  (2)
  • Bunazosin  (1)
  • 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
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Effects of dilevalol, an R, R-isomer of labetalol, on blood pressure and renal function in patients with mild-to-moderate essential hypertension (1988)
    Springer
    European journal of clinical pharmacology 35 (1988), S. 9-15 
    Details
    ISSN: 1432-1041
    Keywords: dilevalol ; hypertension ; labetolol R-R-isomer ; renal function ; plasma renin activity ; plasma aldosterone ; side-effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of oral dilevalol (an R, R-isomer of labetalol), a new β-adrenoceptor blocker with β2-receptor stimulating and α-recepter blocking properties on blood pressure, renal function, plasma renin activity (PRA) and plasma aldosterone have been studied in 15 patients with mild-to-moderate essential hypertension treated with it for 6 weeks. Two patients with apparent treatment failure and one patient who developed muscle pain and cramps, and had an elevated creatine phosphokinase level, were excluded from the study. Dilevalol monotherapy 100 mg once daily for 6 weeks significantly lowered both the systolic and diastolic blood pressure compared to placebo. Total renal vascular resistance was significantly reduced, and RBF and GFR remained unchanged. Dilevalol significantly decreased PRA. The results suggest that prolonged daily treatment with dilevalol preserves renal function and produces a concomitant hypotensive action in patients with mild-to-moderate essential hypertension. The ancillary pharmacological properties of dilevalol rather than PRA suppression may be relevant to its renal effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00555500
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    Paper (German National Licenses)
    Fulltext
  • 3
    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
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    Paper (German National Licenses)
    Fulltext
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