Summary
Nineteen ninety-six certainly was the year of bradykinin regarding its assault on the minds of clinicians interested in cardiovascular disease. This assault was further amplified by the introduction, in Canada, of the first angiotensin receptor antagonist, an agent that appeared to be devoid of activities involving bradykinin. Intriguingly, this assault was also fueled by some pharmaceutical companies who had ACE inhibitors, but no angiotensin receptor antagonists. The suggestion was that bradykinin was good, not bad.
The closer one gets to the field of vascular regulation, the more complicated the situation becomes. There are now many defined vasoactive substances, but even with the use of the probes and scientific methods of today, a comprehensive understanding will not likely emerge. The bottom line will quite likely depend upon well-conducted, randomized clinically controlled studies that would compare agents with a bradykinin effect, namely, ACE inhibitors, with those without a bradykinin effect. Thus far, the trials have shown great similarity between the agents in the field of hypertension and those of cardiac failure.
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Barnes, C.C. (1998). Exploring the Difference Between Angiotensin Converting Enzyme Inhibitors and Angiotensin II-Receptor Antagonists. A Focus on Bradykinin. In: Dhalla, N.S., Zahradka, P., Dixon, I.M.C., Beamish, R.E. (eds) Angiotensin II Receptor Blockade Physiological and Clinical Implications. Progress in Experimental Cardiology, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5743-2_15
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