Hypotensive Action of Methyldopa

Smirk, Horace

doi:10.1136/bmj.1.5324.146

Cited by 48 publications

(13 citation statements)

References 10 publications

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“…Environmental stresses, such as clamping of the kidney, salt solutions, and chronic catecholamine excess, all produce a higher eventual blood pressure level than in control animals (Smirk, 1963). These findings suggest that blood pressure-elevating stimuli, when superimposed upon appropriate genetic endowment, cause further increases in pressure and acceleration of the hypertensive disease process-a concept that is believed to apply in humans as well.…”

Section: Blood Pressure and Psychological Variablesmentioning

confidence: 65%

Genetic and familial factors in essential hypertension and related traits

Siervogel

1983

American J Phys Anthropol

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The health significance of essential hypertension (high blood pressure of undefined origin) is well established. It is a major factor contributing to coronary heart disease, stroke, and kidney failure. It directly affects about one in five Americans. Factors which are known to be associated with blood pressure include: body composition as it relates to overall mass and fat mass; physiological variables involving the sympathetic and parasympathetic nervous systems; biochemical variables such as renin, aldosterone, kallikrein, lipids, and lipoproteins, etc.; environmental variables such as sodium intake, heavy metals, and noise; and psychological variables involving personality type and mental stress.There is a definite, well-established genetic involvement in hypertension, but specific genetic mechanisms remain a mystery. Familial aggregation occurs for many of the associated traits listed above. For some, specific polymorphic major genes have been identified, but for others genetic factors are unidentified. Essential hypertension is undoubtedly a heterogeneous group of diseases with the common end result of elevated blood pressure. Because of its health significance, there is considerable interest in identifying genetic mechanisms resulting in essential hypertension. One area that currently shows some potential for the identification of a specific genetic mechanism is related to the transmembrane transport of sodium and potassium cations.A genetic component has long been suspected in essential hypertension, but a clear and definitive genetic mechanism has yet to be identified. Since there are many variables that can affect blood pressure, this review of the genetics of essential hypertension necessarily involves a discussion of related traits. Before focusing on the genetic and familial aspects of hypertension a description of the normal course of human blood pressure is presented and some of the traits related to it are discussed. NATURAL HISTORY OF BLOOD PRESSUREUntil recently, reports describing blood pressure patterns during the neonatal period were relatively few, largely because of the difficulty of accurately measuring blood pressure in infants by noninvasive techniques. The ultrasonic technique utilizing the Doppler effect greatly facilitated noninvasive systolic blood pressure determination in infants (McLaughlin et al., 1971). Accurate automatic methods are currently available using the oscillometric principal coupled with a microcomputer and a standard limb blood presure cuff (Friesen and Lichtor, 1981). Even in adults newer methods are being developed (Wolthuis et al., 1981).© 1983 Alan R. Liss, Inc. [Vol.26,1983 Systolic blood pressure tends to increase sharply during the first two weeks of life from a mean of 70 mmHg at 2 days to 84 mmHg at 2 weeks. It continues to increase at a slightly slower rate over the next 4 weeks to a mean of about 93 mmHg at 6 weeks (Earley et aI., 1980); from 6 weeks to 1 year af age there is little change in systolic pressure (deSwiet et aI., 1975(deSwiet et ...

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Section: Blood Pressure and Psychological Variablesmentioning

confidence: 65%

Genetic and familial factors in essential hypertension and related traits

Siervogel

1983

American J Phys Anthropol

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“…This drug produces tiredness and drowsiness in most patients: some may become tearful and depressed (71)(72)(73)(74)(75)(76). Smirk (72) reported depression and weeping in 5 of 53 patients; Dubach (77) reported that 2 patients treated with this drug manifested depression with psychomotor retardation.…”

Section: Methyldopamentioning

confidence: 99%

“…The incidence of really troublesome depression has been reported to be about 4% (79,80). Insomnia, nightmares and hallucinations may also occur with depression occasionally (72,75). The combination of methyldopa with other drugs can cause neuropsychiatrie problems: hallucinations with pargyline (81); nightmares or depression with Rauwolfia (82); agitation with amitriptyline (83), and puerperal depression and hallucination with phenothiazines (84).…”

Section: Methyldopamentioning

confidence: 99%

Drug-Induced Mood Disorders

Ananth¹,

Ghadirian²

1980

Int Pharmacopsychiatry

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Various drugs including antihypertensives, anxiolytics, antibiotics, antidepressants, corticosteroids, choline, indomethacin, levodopa, metronidazole, neuroleptics, oral contraceptives, sulphonamides and physostigmine have been reported to produce depression as a side effect. Clinically, these drug-induced depressions may go unnoticed and thus create therapeutic problems. Although causal relationship is difficult to establish, depression occurring during the course of drug treatment needs an evaluation of all the medications that the patient has been receiving. We believe that postpsychotic depressions include three types of depression: pendular depression — primarily disease related; chronic depression - primarily environment related, and amine-depletion depression - drug related. Thus, drug-induced depressions constitute a subgroup of postpsychotic depression. Clinically, it is essential to carefully monitor patients receiving drugs known to produce depression. Thus, prompt recognition of the drug-induced depressions may assist in initiating proper therapeutic measures.

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“…The incidence of depression in one series was 13% (Prichard et al 1968) but the incidence of really troublesome depression has been given as about 4% (Johnson et al 1966;Hamilton, 1968). Insomnia, nightmares and hallucinations may occur occasionally (Smirk, 1963); insomnia has been reported as a withdrawal effect (Horwitz et ,al. 1987).…”

Section: Antihypertensive Drugs and Depressionmentioning

confidence: 99%

“…Methyldopa causes depletion of brain noradrenaline, serotonin and dopamine, a t least in the * Received 17 January 1973 experimental animal (Sourkes, 1965). Drowsiness is a common side effect initially unless the starting dose is small; tiredness may be a prominent feature and the patient may become tearful and depressed (Gillespie et al 1962;Smirk, 1963;Lauwers et al 1963;Johnson et al 1966; Horwitz elt al. 1967).…”

Section: Antihypertensive Drugs and Depressionmentioning

confidence: 99%

Hypertension and Depression and Their Treatment

Simpson¹

1973

Aust N Z J Psychiatry

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Hypotensive Action of Methyldopa

Cited by 48 publications

References 10 publications

Genetic and familial factors in essential hypertension and related traits

Genetic and familial factors in essential hypertension and related traits

Drug-Induced Mood Disorders

Hypertension and Depression and Their Treatment

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