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  • 1
    ISSN: 1432-1041
    Keywords: Key words Imidapril ; Angiotensin converting enzyme ; Heart failure; ACE inhibitor ; blood pressure ; circulating ACE
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: To study the haemodynamic profile and tolerability of imidapril, a new long-acting ACE inhibitor, and to investigate the effect of inhibition of circulating ACE on blood pressure in patients with stable chronic heart failure. Methods: Twenty-four patients with stable, chronic heart failure (New York Heart Association (NYHA) functional Class II–III) were randomised to receive either 2.5 mg or 5 mg imidapril. Other vasodilators were withheld for ≥ 5 half-lives. Blood pressure and ACE activity were carefully monitored for 24 h after dosing. Results: Both 2.5 mg and 5 mg imidapril decreased systolic blood pressure, while diastolic blood pressure fell only after 5 mg imidapril. The two doses produced a significant and similar inhibition of circulating (serum) ACE. No serious adverse effects were observed, although symptomatic hypotension occurred in 1 patient (5 mg). The decrease in blood pressure was not related to baseline ACE activity, serum sodium or serum creatinine concentration. Conclusions: Imidapril significantly lowered systolic blood pressure and was well tolerated. The difference in the first dose response to the two doses with respect to diastolic blood pressure suggests that this haemodynamic effect of ACE-inhibition is not related to inhibition of circulating ACE.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: Review-tissue renin-angiotensin systems ; heart failure ; experimental-clinical
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In this paper, we review the hypothesis that activated tissue renin-angiotensin systems play a detrimental role in heart failure. The main arguments for this idea are discussed: a) tissue renin-angiotensin systems behave functionally distinct from the circulating renin-angiotensin system; b) tissue renin-angiotensin systems are activated in heart failure; c) activated tissue renin-angiotensin systems induce cardiovascular dysfunction. Finally, this hypothesis predicts that optimal treatment in heart failure requires the inhibition of tissue renin-angiotensin systems. However, studies pertaining to this prediction are still lacking, particularly in human subjects.
    Type of Medium: Electronic Resource
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