Mechanisms of hypertension in cardiac transplantation and the role of cyclosporine

Ventura, H.O., Malik, F.S., Mehra, M.R., Stapleton, D.D. and Smart, F.W. (1997) Mechanisms of hypertension in cardiac transplantation and the role of cyclosporine. Current Opinion in Cardiology, 12 4: 375-381.

Author Ventura, H.O.
Malik, F.S.
Mehra, M.R.
Stapleton, D.D.
Smart, F.W.
Title Mechanisms of hypertension in cardiac transplantation and the role of cyclosporine
Journal name Current Opinion in Cardiology   Check publisher's open access policy
ISSN 0268-4705
1531-7080
Publication date 1997-07
Sub-type Critical review of research, literature review, critical commentary
Volume 12
Issue 4
Start page 375
End page 381
Total pages 7
Place of publication Philadelphia, PA, United States
Publisher Lippincott Williams & Wilkins
Language eng
Abstract The use of cyclosporine in solid organ transplantation has been shown to be associated with the development of hypertension and nephrotoxicity. Several mechanisms, including endothelin-mediated systemic vasoconstriction, impaired vasodilatation secondary to reduction in nitric oxide, and altered cytosolic calcium translocation, have been proposed to underlie cyclosporine-induced hypertension. In addition, other studies have shown activation of the sympathetic nervous system and the renin-angiotensin system, as well as abnormalities in prostaglandin metabolism, as culpable mechanisms. Hemodynamic features of cyclosporine-induced hypertension consist of elevated peripheral vascular resistance, ventricular vascular uncoupling contributing to left ventricular hypertrophy, and abnormalities in the diastolic function of the allograft. Combined calcium-channel blockers and angiotensin-converting enzyme inhibitors have been used for the treatment of this clinical problem, and they achieve blood pressure control in 65% of patients. Moreover, these agents may also be beneficial in preventing development of cardiac allograft vasculopathy, a long-term nemesis in cardiac transplantation.
Keyword Induced renal vasoconstriction
Induced sympathetic activation
Left ventricular hypertrophy
Nitric oxide
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collection: School of Medicine Publications
 
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Created: Mon, 14 Mar 2011, 10:16:47 EST