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Guanethidine and Related Agents: III. Antagonism by Drugs Which Inhibit the Norepinephrine Pump in Man

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Guanethidine and Related Agents: III. Antagonism by Drugs Which Inhibit the Norepinephrine Pump in Man Guanethidine and related agents: III. Antagonism by drugs which inhibit the norepinephrine pump in man Jerry R. Mitchell, … , Luis Arias, John A. Oates J Clin Invest. 1970;49(8):1596-1604. https://doi.org/10.1172/JCI106377. Antagonism of the antihypertensive action of guanethidine by the tricyclic antidepressants, desipramine and protriptyline, has been demonstrated in controlled studies. These antidepressants also prevent the effect of the related ring-substituted guanidinium adrenergic neuron blockers, bethanidine and debrisoquin. That the rise in blood pressure when desipramine is added to guanethidine therapy is not due simply to a pressor action of the two drugs in combination was demonstrated by the lack of an increase in blood pressure when guanethidine was added to desipramine therapy. Investigations were conducted to determine whether antagonism of guanethidine's clinical effect could result from blockade by the tricyclic antidepressants of the norepinephrine pump in the adrenergic neuron membrane, thereby preventing the uptake of guanethidine into the neuron by this pump. Like guanethidine, the indirectly acting pressor amine, tyramine, enters the neuron via the norepinephrine pump. Desipramine, protriptyline, and amitriptyline in clinical doses all were found to block the pressor action of tyramine while potentiating the pressor effect of norepinephrine. The amino acid, methyldopa, does not enter the neuron via the norepinephrine pump, and its antihypertensive action is not altered by concomitant administration of tricyclic antidepressants. It is concluded from the evidence in this investigation together with the results of previous studies in experimental animals that clinical doses of desipramine-like drugs inhibit the norepinephrine pump in the peripheral adrenergic […] Find the latest version: https://jci.me/106377/pdf Guanethidine and Related Agents III. ANTAGONISM BY DRUGS WHICH INHIBIT THE NOREPINEPHRINE PUMP IN MAN JERRY R. MrrCHELL, JOHN H. CAVANAUGH, Luis AIuAs, and JOHN A. OATES From the Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37203 A B S TR A C T Antagonism of the antihypertensive ac- pump in the peripheral adrenergic neuron in man and tion of guanethidine by the tricyclic antidepressants, thereby prevent uptake of guanethidine to its site of desipramine and protriptyline, has been demonstrated action. in controlled studies. These antidepressants also pre- vent the effect of the related ring-substituted guani- dinium adrenergic neuron blockers, bethanidine and INTRODUCTION debrisoquin. That the rise in blood pressure when Observations by Leishman, Mathews, and Smith (2) desipramine is added to guanethidine therapy is not due suggested that imipramine may block the effect of simply to a pressor action of the two drugs in combi- guanethidine in hypertensive patients. Studies in ex- nation was demonstrated by the lack of an increase in perimental animals also have shown that imipramine- blood pressure when guanethidine was added to desipra- like antidepressants will prevent some of the actions of mine therapy. guanethidine (3, 4). Because of the notion that there Investigations were conducted to determine whether is a relation between the psyche and hypertension, the antagonism of guanethidine's clinical effect could result use of such psychotherapeutic agents in the hyper- from blockade by the tricyclic antidepressants of the tensive population is widespread. Accordingly, studies norepinephrine pump in the adrenergic neuron mem- were undertaken to obtain data on the clinical signifi- brane, thereby preventing the uptake of guanethidine cance of interactions between these drugs and guanethi- into the neuron by this pump. Like guanethidine, the dine, and to determine whether similar interactions indirectly acting pressor amine, tyramine, enters the occurred with the related guanidinium antihypertensives, neuron via the norepinephrine pump. Desipramine, pro- bethanidine and debrisoquin. The possibility that the triptyline, and amitriptyline in clinical doses all were antagonism resulted from an inhibition of transport of found to block the pressor action of tyramine while these antihypertensives to their site of action was potentiating the pressor effect of norepinephrine. The investigated. amino acid, methyldopa, does not enter the neuron via the norepinephrine pump, and its antihypertensive ac- METHODS tion is not altered by concomitant administration of tri- The studies were conducted in the Clinical Research Center cyclic antidepressants. It is concluded from the evidence of Vanderbilt University Hospital and in the Nashville in this investigation together with the results of pre- Veterans Administration Hospital. vious studies in experimental animals that clinical doses Demonstration of drug antagonism. 13 hypertensive adults (10 men and 3 women) were placed on a regular of desipramine-like drugs inhibit the norepinephrine hospital diet containing 100 mEq of sodium per day. These patients when hospitalized had persistent hypertension of This work was presented in part to the Southern Society moderate to severe degree; on admission their blood pres- for Clinical Investigation, 1 February 1969, and in a pre- sures while standing ranged from 190 to 250 mm Hg in liminary communication (1). systole and 115 to 160 mm Hg in diastole. Four patients Received for publication 22 July 1969 and in revised form intermittently had mild azotemia (blood urea nitrogen, 22 February 1970. 30-50 mg/100 ml) but none had liver disease. All medica- 1596 The Journal of Clinical Investigation Volume 49 1970 TABLE I Interactions between Antihypertensive and Antidepressant Drugs in Patients Average of mean blood pressures in the standing position 4SE Pre- Post- antagonist Antagonist antagonist Patient Antihypertensive drug and dosage Antagonist drug and dosage period period period L. L. C. Guan, 150 mg daily, 31 days DMI, 75 mg daily, 3 days 93 ±3* 116 43 94 ±5* then 125 mg daily, 6 days D. C. W. Guan, 100 mg daily, 19 days DMI, 50 mg daily, 2 days 112 ±-5t 138 ±2 114 ±1t T. D. P. Guan, 150 mg daily, 18 days DMI, 75 mg daily, 1.3 days 108 ±3* 130 +5 98 ±44t L. J. Guan, 60 mg daily, 20 days DMI, 75 mg daily, 5 days 103 ±4* 128 ±3 108 ±5§ J. H. D. Guan, 70 mg daily, 18 days DMI, 75 mg daily, 3.3 days 103 ±4§ 119 ±3 107 +1§ G. T. E. Guan, 220 mg daily, 30 days DMI, 150 mg daily, 9 days 101 ±41t 116 ±1 111 ±5 E. L. Guan, 50 mg daily, 9 days Pro, 20 mg daily, 3.5 days 115 45* 155 ±66 D. C. W. Beth, 80 mg daily, 16 days DMI, 50 mg daily, 1 day 105 ±2* 142 ±4 106 i2* W. R. D. Beth, 20 mg daily, 30 days DMI, 50 mg daily, 1 day 102 43* 146 ±33 R. H. C. Beth, 15 mg daily, 16 days DMI, 75 mg daily, 2 days 94 ±4* 142 ±:1 126 ±3* W. S. Debr, 60 mg daily, 30 days DMI, 75 mg daily, 1.3 days 88 ±5* 127 ±3 116 43§ H. E. A. Debr, 240 mg daily, 29 days DMI, 75 mg daily, 6 days 80 ±5* 107 ±-1 94 ±1* L. L. B. Meth, 3.0 g daily, 24 days DMI, 75 mg daily, 5 days 99 +4 96 ±5 100 ±4 W. R. D. Meth, 2.5 g daily, 28 days DMI, 75 mg daily, 4.7 days 90 ±4 87 43 E. N. Meth, 3.0 g daily, 15 days DMI, 75 mg daily, 6 days 104 ±-5 96 ±5 Patients receiving a clinically effective dose of guanethidine (Guan), bethanidine (Beth), debrisoquin (Debr), or methyl- dopa (Meth) were given desipramine (DMI) or protriptyline (Pro) as described in Methods. * Differs from antagonist period, P < 0.005. 1 Differs from antagonist period, P < 0.01. § Differs from antagonist period, P < 0.05. tions, with the exception of digitoxin in one patient, were was the proposed antagonist in 14 of the studies, while discontinued for at least 1 wk before the experimental protriptyline was given in the 15th. period. Except for the initial study (patient L. L.) placebo cap- Observations on blood pressure and apical pulse rate were sules identical in appearance and mode of administration to made at the same hour four times daily with the patient desipramine and protriptyline were used during pre and both in the supine and standing (at least 2 min) positions. postexperimental control periods of the studies with guan- The effects of the drug on computed mean blood pressure ethidine, debrisoquin, and methyldopa, in order that patients (diastolic blood pressure plus one-third pulse pressure) would not know when administration of the antidepressant were evaluated. The average mean blood pressure in the drugs was initiated. The placebo did not raise the blood standing position was calculated for each day from the four pressure. daily blood pressure determinations. For statistical analy- After the clinically effective dose of one of the antihyper- sis, the average of each patient's daily mean blood pressures tensive drugs (guanethidine sulfate, bethanidine sulfate, in the standing position for days 1 through 5 (bethanidine, debrisoquin sulfate, or methyldopa) was determined for a debrisoquin, methyldopa patients) or days 2 through 5 patient, that dose was continued throughout the study. The (guanethidine patients) of the antagonist period was com- total daily dose was divided into two or three doses given pared by the two-tailed Student's unpaired t test with the between 9 a.m. and 9 p.m. each day. The antihypertensive corresponding data for both the preantagonist period (the drug was administered alone in that fashion for a control 5 days preceding administration of antagonist) and days period of at least 5 days before adding the proposed 8 through 10 of the postantagonist period (days 11 through antagonist, desipramine hydrochloride or protriptyline hydro- 13 for patients G. T. E. and L.L. C. who received increased chloride. The antagonist was given in divided doses 30 min doses of antagonist).
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