The purpose of the present study was to contrast a commonly used ACE inhibitor (enalaprilat) with a novel ACE inhibitor (trandolaprilat) in their ability to inhibit 1) pulmonary capillary endothelialbound ACE activity in vivo, 2) arterial pressure responses to i.v. angiotensin I and bradykinin, and
Expression of pulmonary vascular angiotensin-converting enzyme in primary and secondary plexiform pulmonary hypertension
โ Scribed by Carlos Orte; Julia M. Polak; Sheila G. Haworth; Magdi H. Yacoub; Nicholas W. Morrell
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 251 KB
- Volume
- 192
- Category
- Article
- ISSN
- 0022-3417
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๐ SIMILAR VOLUMES
The pathogenesis of pulmonary hypertension (PH) remains poorly understood. Vasoconstriction, although likely to be a major factor in the disease, varies between patients and studies of a variety of vasoactive substances have sometimes yielded conflicting results. Amongst these substances, alteration
We estimated the activity of pulmonary capillary endothelium-bound (PCEB) angiotensin converting enzyme (ACE) in the rabbit in vivo, before and at 20 min and 2 h postadministration of the ACE inhibitors trandolaprilat (8 ยตg/kg) and enalaprilat (10 ยตg/kg), alone and in combination with the calcium ch