Cyclosporine-induced sympathetic activation and hypertension after heart transplantation

Article Abstract:

Cyclosporine is a drug used to suppress the immune system after organ transplantation that has led to great improvement in survival rates, but one of its side effects is a new form of high blood pressure (hypertension). This is especially apparent in heart transplant patients, 90 percent of whom develop hypertension and often require treatment with antihypertensive agents. The mechanisms that underlie cyclosporine-induced hypertension have not been characterized. To evaluate whether the drug causes sustained activation of sympathetic nerve cells (neurons) leading to elevated blood pressure, studies of the heart's electrical activity in 14 heart transplant recipients were performed. Using microelectrodes inserted into sympathetic nerves in the leg, investigators measured the activity of the neurons. Simultaneously, calf blood flow was also measured. Studies were also performed on five heart transplant patients who did not receive cyclosporine; fourteen patients with myasthenia gravis who took cyclosporine and a placebo (inactive) drug as part of another study; five with uncomplicated essential hypertension; and nine healthy subjects with normal blood pressure. Results showed that heart transplant recipients who took cyclosporine had a higher rate of sympathetic discharge (80 bursts per minute) than normal controls (28 bursts per minute), recipients who did not take cyclosporine, and patients with essential hypertension. Sympathetic nerves fired during a larger proportion of cardiac cycles in the cyclosporine group than the non-cyclosporine group. The myasthenia gravis patients had a higher rate of sympathetic firing when they received cyclosporine than when they received the placebo drug. Cyclosporine was also associated with considerable increases in vascular resistance (the opposition of the vascular system to blood flow). In heart transplant recipients, these effects may be especially pronounced because feedback loops that normally tell the heart to decelerate have been surgically interrupted. (Consumer Summary produced by Reliance Medical Information, Inc.)

Transplantation of organs, tissues, etc., Organ transplantation, Tissue transplantation, Transplantation

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Cyclosporine, sympathetic activity, and hypertension

Article Abstract:

Although cyclosporine, a drug that suppresses the immune system, has led to major improvements in survival after organ transplantation, it is also associated with significant side effects, including high blood pressure (hypertension). An article in the September 13, 1990 issue of The New England Journal of Medicine presents results that show cyclosporine is associated with increased firing of sympathetic nerves (which regulate blood vessel constriction and certain cardiac functions), as well as increased vascular resistance (resistance to the flow of blood). Possible answers to two questions relevant to these results are discussed. The first concerns the role of the sympathetic nervous system in hypertension. It appears that increased sympathetic neuron activity is present in the earlier phases of hypertension (in young people with hypertension), but its role in chronic hypertension is less clear. In fact, several facts argue against the importance of sympathetic activation in chronic blood pressure elevation, including the association of sympathetic activation and normal blood pressure (as in heart failure), as well as the occurrence of hypertension without excess sympathetic activity. Secondly, other than direct effects on blood vessels, the sympathetic system could influence aspects of kidney function, growth of muscle tissue in the heart and blood vessels, and changes in the permeability of vascular muscle to sodium (making it more responsive to contractile stimuli). These issues are discussed in detail. It seems likely that the hypertensive effects of cyclosporine are not solely the result of sympathetic activation, but, rather the outcome of combined effects on that system, the kidney, and the blood vessels. (Consumer Summary produced by Reliance Medical Information, Inc.)

editorial

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Sympathetic overactivity in patients with chronic renal failure

Article Abstract:

Overactive sympathetic-nerve discharge may be a factor in the high incidence of high blood pressure seen among patients with chronic renal (kidney) failure. It appears that in patients undergoing hemodialysis for kidney failure there is long-term stimulation of the kidneys' afferent nerves, triggering excessive sympathetic-nerve discharge. The rate of discharge in the peroneal nerve was compared among 18 hemodialysis patients, 5 hemodialysis patients who had undergone the removal of both kidneys and 11 normal subjects. The discharge rate among patients receiving hemodialysis who still had their kidneys was significantly higher than among those who had them removed and was two and one-half times higher than that of normal subjects. Furthermore, 14 of the 18 patients with kidneys had high blood pressure but only one of the five patients without kidneys had high blood pressure. Kidney removal seems to lower sympathetic discharge and the risk for high blood pressure among patients with chronic kidney failure.

Chronic kidney failure

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