ACE Inhibitors by John R. Vane (auth.), Pedro D’Orléans-Juste, Gérard E.

By John R. Vane (auth.), Pedro D’Orléans-Juste, Gérard E. Plante (eds.)

Angiotensin changing enzyme inhibitors (ACEI) symbolize the 1st type of antihypertensive brokers that used to be designed and built at the foundation of a well-defined physiopathological axis of arterial high blood pressure, a vascular dis­ order that's now turning into one of many significant reasons of morbidity/mortality, not just in built societies but in addition within the hugely populated constructing coun­ attempts [1]. CAPTOPRIL, the prototype of the "PRIL" relations, which now contains greater than forty molecule-species, used to be rather harmful and the scientific boost­ ment nearly failed while critical side-effects have been pronounced in an alarmist fash­ ion in respected clinical journals, reminiscent of the hot England magazine of medication and Lancet. Squibb & Sons got here very with regards to retreating CAPTOPRIL from medical research [2]. even though, after second look of the knowledge received from diversified different types of sufferers and applicable dose-adjustments, the scientific use of CAPTOPRIL became out to be progressive. The prototype, in addition to different contributors of the "PRIL" family members grew to become the start line for varied easy and scientific learn courses, concentrating on the interactions of ACEI with the kinin, endothelin, and nitric oxide structures, and the contribution of the receptors for AT I, AT 2, bradykinin Bland B , ETA and ET B to the pharmacological activities 2 of the respective peptides. This learn job ended in the advance of latest pharmacological brokers, reminiscent of the angiotensin receptor antagonists and, extra lately, the impartial endopeptidase inhibitors. within the close to destiny, bradykinin receptor antagonists will also be on hand to modulate ACEI phar­ macological actions.

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Circulation 83: 1849-1865 12 White P, Cumow K, Pascoe L (1994) Disorders of steroid II beta-hydroxylase isozymes. Endocrine Rev 15: 421-438 13 Takeda Y, Miyamori I, Yoneda T, Iki K, Hatakeyama H, Blair lA, Hsieh FY, Takeda R (1995) Production of aldosterone in isolated rat blood vessels. Hypertension 25: 170-173 14 Bonnardeaux A, Davies E, Jeunemaitre X, Fc~ry I, Charru A, Clauser E, Tiret L, Cambien F, Corvol P, Soubrier F (1994) Angiotensin II type I receptor gene polymorphisms in human essential hypertension.

J Hum Hypertens II: 595-597 West M, Summers K, Wong K, Burstow D (1997) Renin-angiotensin system gene polymorphisms and left ventricular hypertrophy. The case against an association. Adv Exp Med Bioi 432: 117-122 Hamon M, Amant C, Bauters C, Richard F, Helbecque N, McFadden E, Lablanche J, Bertrand M, Amouyel P (1997) Association of angiotensin converting enzyme and angiotensin II type 1 receptor genotypes with left ventricular function and mass in patients wwith angiographically normal coronary arteries.

We suggested that the ATl gene is involved in the development of aortic stiffness in hypertensive patients, whereas these results were not observed in normotensive subjects (Tab. 1). The C allele frequency (25%) of ATl was associated with a strong aortic stiffness after adjustment for age and blood pressure. Moreover, an interaction was found between ATl genotype and the ratio of total to high-density lipoprotein cholesterol in terms of the development of aortic stiffness. Thus, a positive correlation was observed between the ratio of total to high-density lipoprotein cholesterol and pulse wave velocity (PWV) in [AC] and [CC] but not [AA] patients.

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