A Mechanism of Chlorothiazide-Enhanced Effectiveness of Antihypertensive Ganglioplegic Drugs

Dustan, Harriet P.; Cumming, Gordon R.; Corcoran, A. C.; Page, Irvine H.

doi:10.1161/01.cir.19.3.360

Cited by 133 publications

(23 citation statements)

References 15 publications

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“…Sodium restriction causes reduction in extracellular fluid and plasma volumes (28,(30)(31)(32), and in cardiac output (31,32). These hemodynamic effects could account for the decreases in systemic pressure and renal plasma flow observed in the hypertensive patients.…”

Section: Reactivity Of Renal and Systemic Circulations To Vasoconstrimentioning

confidence: 99%

Reactivity of Renal and Systemic Circulations to Vasoconstrictor Agents in Normotensive and Hypertensive Subjects*

Gombos¹,

Hulet²,

Bopp³

et al. 1962

J. Clin. Invest.

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Section: Reactivity Of Renal and Systemic Circulations To Vasoconstrimentioning

confidence: 99%

Reactivity of Renal and Systemic Circulations to Vasoconstrictor Agents in Normotensive and Hypertensive Subjects*

Gombos¹,

Hulet²,

Bopp³

et al. 1962

J. Clin. Invest.

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“…37 At first sight, the blood pressure lowering action of thiazides seems obvious; diuretics will cause a reduction in plasma volume, diminish venous return and depress cardiac output and blood pressure. This mechanism does seem sufficient to explain most or all of the reduction in blood pressure seen in hypertensive subjects following acute administration of thiazides, [38][39][40][41][42] and re-expansion of plasma volume by infusion of dextran, with or without sodium, restores blood pressure to pre-treatment levels. 39,40 In association with the fall in cardiac output following acute administration of thiazide, there is a rise in total peripheral vascular resistance (TPR) that is mediated largely by the sympathetic nervous system (SNS) 43 and activation of the reninangiotensin-aldosterone system.…”

mentioning

confidence: 99%

How do thiazide and thiazide-like diuretics lower blood pressure?

Hughes

2004

J Renin Angiotensin Aldosterone Syst

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“…Caution should be employed in considering this finding in connection with the reported observations on resting output in hypertensive human subjects (24)(25)(26)(27)(28). The experiments are not comparable, and ours were not designed to show differences in resting hemodynamic parameters.…”

Section: Discussionmentioning

confidence: 83%

“…The work of several investigators suggests that resting cardiac output in hypertensive humans is unchanged or reduced by treatment with chlorothiazide (24)(25)(26)(27). To our knowledge there are no measurements of resting cardiac output in dogs before and after administration of chlorothiazide.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Norepinephrine on Cardiac Output, Arterial Blood Pressure, and Heart Rate in Dogs Treated With Chlorothiazide*†

Eckstein¹,

Abboud²,

Pereda³

1962

J. Clin. Invest.

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Forearm blood flow in normal human subjects was found to decrease progressively during intravenous infusions of norepinephrine as the rate of infusion increased (2). After 1 week of treatment with chlorothiazide, the same subjects responded to the same doses of norepinephrine with progressive increases in flow. 20, 1961 (1). Supported by Grant H-2644 from the National Heart Institute, Bethesda, Md., and aided by grants from the Iowa and American Heart Associations.t Established Investigator of the American Heart Association.§ Advanced Research Fellow of the American Heart Association.1 1 Postgraduate Trainee under Grant HTS-5367 from the National Heart Institute. that treated and untreated animals were available for study on the morning of the eighth day.The dogs were lightly anesthetized with 10 mg thiopental sodium per kg and treated with 0.3 mg decamethonium bromide per kg. A cuffed endotracheal tube was inserted immediately, and intermittent positive pressure breathing was instituted with a Harvard respiratory pump. Two cardiac catheters were introduced through the external jugular vein so that their tips lay in the main pulmonary artery and right atrium. Needles were inserted into the left carotid and femoral arteries and into a femoral vein. Pressures were recorded from the femoral artery and right atrium with Statham strain gauges. Drugs were given through the needle in the femoral vein. The catheter in the pulmonary artery was filled with indocyanine green dye and connected through a three-way stopcock to a dye reservoir and injection system. The needle in the carotid artery was connected through small-bore, nylon tubing to the cuvet of a Gilford densitometer. Dye curves were obtained by drawing blood through the densitometer with a constant speed pump after injections into the pulmonary artery. Endexpiratory CO2 concentration was monitored with a Spinco CO2 analyzer. Dye curves, CO2 concentration, and blood pressure were recorded with a Sanborn direct-writing oscillograph.Ventilation was adjusted by manipulating the controls on the respiratory pump so that end-expiratory CO2 concentration, after it became stable, was about 4 per cent. The rate and depth of breathing were not changed after this initial adjustment. Repeated doses of 0.075 mg decamethonium per kg were given at 20-minute intervals to maintain skeletal muscle relaxation. After the animal was prepared, 15 to 20 minutes were allowed for blood pressure and heart rate to become stable. Then l-norepinephrine bitartrate was infused intravenously at rates of 0.1, 0.2, and 0.4 Ag of norepinephrine base per kg per minute. Each dose was repeated once in each animal. The doses were given in random order both in the untreated and treated groups, using the same 6 X-6 Latin square (3). Observations on cardiac output, heart rate, and blood pressures were made immediately before and at the end of 2.5 minutes of norepinephrine infusion. Exactly 10 minutes were allowed between infusions. Electrically integrated mean right atrial pressures were recorded thro...

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A Mechanism of Chlorothiazide-Enhanced Effectiveness of Antihypertensive Ganglioplegic Drugs

Cited by 133 publications

References 15 publications

Reactivity of Renal and Systemic Circulations to Vasoconstrictor Agents in Normotensive and Hypertensive Subjects*

Reactivity of Renal and Systemic Circulations to Vasoconstrictor Agents in Normotensive and Hypertensive Subjects*

How do thiazide and thiazide-like diuretics lower blood pressure?

The Effect of Norepinephrine on Cardiac Output, Arterial Blood Pressure, and Heart Rate in Dogs Treated With Chlorothiazide*†

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