ASH XI Special Symposium

AII: A NEW TARGET FOR INTERVENTION IN HYPERTENSION

May 15, 1996


The use of angiotensin-converting enzyme inhibitors has revolutionized the treatment of hypertension and the treatment of patients with renal insufficiency, especially diabetics. Converting enzyme inhibitors, however, may not inhibit angiotensin II formation in all tissues, as there are enzymes other than ACE present in the heart and elsewhere which can convert angiotensin I to angiotensin II, and as there are pathways whereby angiotensin II can be made from angiotensinogen bypassing angiotensin II and again not dependent on ACE. A separate issue is the fact that ACE inhibitor treatment results in increased generation of bradykinin. Whether increased bradykinin generation is a helpful or deleterious action of ACE inhibitors remains to be determined. The recent availability of losartan, as a prototype drug of an angiotensin II (type 1) receptor blocker may be another important step forward in antihypertensive therapy. AII receptor blockers should block the effects of angiotensin II as well as, or even better than, ACE inhibitors, but be devoid of effects on bradykinin. For example, use of AII receptor blockers is not associated with cough, a common problem with ACE inhibitors. Losartan and several of the other available AII blockers are selective antagonists for the type 1 AII receptor. By blocking the cell growth actions of the type I receptor, they should have beneficial effects in reducing AII-mediated damage to the heart, vasculature, and kidneys. Also, AII type 1 receptor blockers such as losartan may indirectly stimulate angiotensin II type 2 receptors, which are present in the failing heart, and which may have beneficial, antiproliferative or antihypertrophic effects.

At the 11th meeting of the American Society for Hypertension, at a special symposium sponsored by an unrestricted education grant from Merck U.S. Human Health Division, a panel of experts who are conducting both basic and clinical research with the AII receptor blockers presented the state of knowledge in this very exciting new area. HDCN, in cooperation with the American Society of Hypertension, and with the generous consent of the speakers, is making available the audiotapes of most of the sessions from this symposium, along with their transcripts. (J.T. Daugirdas, M.D., Editor, HDCN)

Incidentally, if you haven't already, you will need to register with HDCN to access these talks.


The Faculty



Drs. Reid, Unger, Devereux (not shown), de Zeeuw, and Weber

John Reid, M.D., Professor of Medicine and Therapeutics, University of Glasgow, Scotland.
Thomas Unger, M.D., Professor of Phamarcology and Experimental Hypertension, University of Kiel.
Richard B. Devereux, M.D., Professor of Medicine, Cornell University Medical College.
Dick de Zeeuw, M.D., Professor of Clinical Pharmacology, University of Groningen, The Netherlands.
Michael A. Weber, M.D. (Chairman)., Professor of Medicine at the State University of New York Health Sciences Center, Brooklyn, NY.



28.8 modem
14.4 modem

Real Audio recording of Dr. Weber's introduction



Dr. Michael Weber.
Let me start by welcoming all of you here this morning on behalf of the American Society of Hypertension. These are our 11th annual meetings. Each year the meetings have gotten larger, more ambitious, more diverse. I think those of you who stay for the full program, which I hope is everyone in this room, will find that it is going to be a very exciting and a very fulfilling meeting. Today this is the first session of the meetings. It is a symposium that is being put on by the Society, supported by an unrestricted educational grant from Merck. I would like to thank our colleagues at Merck for their support of this program and for their support of other important activities of the Society. Today we are going to talk, obviously, about angiotensin II, as a target for intervention in cardiovascular disease. Naturally we are going to have some focus on hypertension. But I think as the program evolves, you will see that the heart, the kidney, the arteries and all the other critical structures that are important for us are going to be discussed in depth and detail. I'm delighted that we have been able to assemble such a distinguished faculty, and I'm looking forward to a very exciting morning.


The talks

* AII: A target for treatment. (Dr. Reid)
* AII Receptors: Signalling pathways, cell growth, and differentiation. (Dr. Unger)
* AII: Left ventricular structure and clinical events. (Dr. Devereux)
* Renal effects of AII: Physiology and Pathophysiology. (Dr. de Zeeuw)
* Clinical implications of AII blockade. (Dr. Weber)



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