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  • Renin angiotensin system  (1)
  • hypertrophy  (1)
  • ramiprilat  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of ramipril in hypertensive patients with renal insufficiency (1989)
    Springer
    European journal of clinical pharmacology 37 (1989), S. 249-256 
    Details
    ISSN: 1432-1041
    Keywords: ramipril ; renal insufficiency ; hypertension ; pharmacokinetics ; ramiprilat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary In an open trial, the pharmacokinetics of ramipril and its active metabolite ramiprilat were studied in 25 hypertensive patients with various degrees of renal insufficiency given 5 mg ramipril p.o. for 14 days. Ramipril was rapidly absorbed and reached a peak concentration after 1–2 h. Cmax was greater in patients with severe renal insufficiency, which might indicate a reduced renal elimination rate, although, the rapid decline of the concentration-time curve for ramipril was almost independent of renal function. The mean initial apparent half-lives on Days 1 and 12, respectively, were 2.8 and 3.4 h (Group I: creatinine clearance 5–15 ml/min), 1.8 and 2.3 h (Group II: creatinine clearance 15–40 ml/min), and 1.9 and 1.9 h (Group III: creatinine clearance 40–80 ml/min). No accumulation was observed after multiple dosing. In contrast, the kinetics of its active acid metabolite ramiprilat was significantly influenced by renal function. The mean times to the peak plasma concentration were 5.7 h in Group I, 4.4 h in Group II and 3.8 h in Group III. The initial decline in plasma ramiprilat was dependent upon renal function; the mean initial apparent half-lives (Days 1 and 12, respectively) were 16.0 and 14.8 h (Group I), 10.1 and 9.5 h (Group II) and 10.6 and 8.0 h (Group III). Mean trough concentrations and absolute accumulation also increased with worsening renal function, and the renal clearance of ramiprilat was significantly correlated with the creatinine clearance. The subsequent long terminal phase at low plasma ramiprilat concentrations represented slow dissociation of the ACE-inhibitor complex. The study indicates that in patients with severe renal insufficiency (creatinine clearance below 30 ml/min) smaller doses of ramipril are required than in patients with normal or borderline renal function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00679779
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Adaptive and genetic alterations of the renin angiotensin system in cardiac hypertrophy and failure (1996)
    Springer
    Basic research in cardiology 91 (1996), S. 65-71 
    Details
    ISSN: 1435-1803
    Keywords: Renin angiotensin system ; hypertrophy ; afterload ; angiotensin converting enzyme ; polymorphism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The risk to suffer from cardiovascular events may be modulated, in part, by neurohormonal systems. Neurohormones such as angiotensin II or aldosterone may be activated secondary to congestive heart failure or in the course of an acute myocardial infarction. These systems, if activated, will subject the failing heart to increased hemodynamic load and, thus, further compromise cardiac function. In addition, structural changes of the heart and vessels occurring with pressure or volume overload may be amplified by the growth promoting effects of these agents. Taken together, the interaction of underlying cardiovascular disease and activated neurohormones may often determine clinical symptoms and prognosis. More recently, growing evidence suggests that the basal, genetically determined, activity of the renin angiotensin aldosterone system may relate to the development of cardiovascular disease as well. In particular, variants of the angiotensinogen and angiotensin converting enzyme genes have been associated with essential hypertension, myocardial infarction, or left ventricular hypertrophy. In this regard, the data suggest that the renin angiotensin aldosterone system may be one of the primary causes, rather than only a secondary co-factor, in the pathogenesis of these most important cardiovascular disorders. In light of the various options of pharmacological intervention, it seems important that ongoing clinical and molecular-genetic research will further define the role of the renin angiotensin system in clinical conditions or genetic risk profiles.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00795365
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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