Studies on catecholamines, renin and aldosterone following catapresan® (2-(2,6-dichlor-phenylamine)-2-imidazoline hydrochloride) in hypertensive patients

Hökfelt, Bernt; Hedeland, H; Dymling, John‐Fredrik

doi:10.1016/0014-2999(70)90212-8

Cited by 170 publications

(36 citation statements)

References 13 publications

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“…Hokfelt, Hedeland & Dymling (1970) described a rebound phenomenon after interruption of 6-30 days of clonidine treatment (0.3-0.9 mg/day) in some of his patients. The symptoms consisted of phaeochromocytoma-like complaints, and the excretion of urinary catecholamines and blood pressure showed a marked increase.…”

Section: Discussionmentioning

confidence: 99%

“…Patients on clonidine therapy should be warned to take the tablets regularly and keep a sufficient stock of tablets at hand. Tapering off of the therapy does not guarantee prevention of the withdrawal symptoms (see case 3) (Hokfelt et al, 1970). P-adrenergic receptor antagonists can prevent many symptoms but theoretically can provoke a further increase of the blood pressure (Bailey & Neal, 1976), which can be managed by a-adrenoceptor blockade (Hansson et al, 1973).…”

Section: Discussionmentioning

confidence: 99%

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Clonidine withdrawal. Mechanism and frequency of rebound hypertension.

Geyskes¹,

Boer²,

Mees³

1979

Brit J Clinical Pharma

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1. The frequency and pathophysiology of the clonidine withdrawal syndrome was studied in fourteen hypertensive patients on chronic clonidine therapy. 2. After sudden cessation of clonidine (900 microgram daily) almost all of the patients showed an excessive increase of the heart rate and blood pressure. Seven of the fourteen patients had subjective symptoms, in three severe enough to require interruption of observation by therapeutic intervention 12 to 60 h after the last dose of clonidine. After clonidine withdrawal, NAE increased to abnormally high values in correlation with the blood pressure (P less than 0.01) and heart rate (P less than 0.001), whereas PRA even decreased initially, probably secondary to the rise of the blood pressure, and only rose, although not significantly, 48 h after withdrawal. PRA was not correlated with NAE, heart rate, or blood pressure. 3. It is concluded that the clonidine withdrawal phenomenon is a frequently occurring and potentially dangerous syndrome. Overactivity of the sympathetic nervous system is mainly responsible, without the mediation of the renin angiotensin system. This also explains our experience that adrenergic beta‐receptor blocking drugs do not prevent the rise in BP, although they alleviate some of the symptoms.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Clonidine withdrawal. Mechanism and frequency of rebound hypertension.

Geyskes¹,

Boer²,

Mees³

1979

Brit J Clinical Pharma

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“…This, in turn, leads to reduced sympathetic nervous activity and decreased blood pressure (Kobinger, 1973). Another antihypertensive mechanism of clonidine involves its suppressive effect on renin secretion (Hokfelt, Hedelund & Dymling, 1970;Baer, Brunner, Bard & Laragh, 1971). As the sympathetic nervous system and the renin-angiotensin system contribute to the maintenance of arterial blood pressure, we have investigated the acute and chronic effects of guanfacine on plasma noradrenaline concentration and plasma renin activity in patients with essential hypertension in order to assess whether the drug's antihypertensive effect is related to changes in these two parameters.…”

Section: Introductionmentioning

confidence: 99%

Guanfacine in essential hypertension: effect on blood pressure, plasma noradrenaline concentration and plasma renin activity.

Schoeppe¹,

Brecht²

1980

Brit J Clinical Pharma

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1 The acute and chronic effects of guanfacine on blood pressure, plasma noradrenaline concentration and plasma renin activity were investigated in 23 patients (15 males, 8 females) with essential hypertension (WHO grade I-II). 2 Guanfacine induced a decrease in plasma noradrenaline concentration and plasma renin activity concomitant with a fall in blood pressure and heart rate in both the acute and the chronic study. 3 The adrenergic response to upright posture, reflected by an increase in plasma noradrenaline concentration and plasma renin activity, was not abolished after chronic guanfacine therapy. 4 The decrease in blood pressure 15 min after intravenous administration of guanfacine was inversely correlated with the basal sympathetic activity before treatment and with the decrease in plasma noradrenaline. 5 After chronic treatment with guanfacine no significant correlation existed between blood pressure reduction and the concomitant changes in peripheral sympathetic and/or plasma renin activity. 6 Despite the lack of a close correlation it is suggested that the antihypertensive effect of guanfacine in patients with essential hypertension is at least partially mediated by an inhibition of the sympathetic nervous and plasma renin activity.

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“…In this respect, the reader should note that alpha-adrenergic blockade decreases pulmonary extravascular leakage in the setting of experimental haemorrhage [137] f) diuresis [138] in the setting of ascites [139−141], cardiac failure [142] and critical care [143] g) lowered pro-inflammatory IL6 [144], increased anti-inflammatory IL10 [145] The use of SV in the setting of early severe diffuse ARDS remains seldom used [39,40]. This lack of enthusiasm may be related to the absence of epidemiological data: a) clearly, the mode of ventilation was selected appropriately, e.g., [21], with a reduction in CCU stay.…”

Section: Sedationmentioning

confidence: 99%

Early severe acute respiratory distress syndrome: What’s going on? Part II: controlled vs. spontaneous ventilation?

Petitjeans

Pichot

Ghignone

et al. 2016

Anaesthesiol Intensive Ther

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The second part of this overview on early severe ARDS delineates the pros and cons of the following: a) controlled mechanical ventilation (CMV: lowered oxygen consumption and perfect patient-to-ventilator synchrony), to be used during acute cardio-ventilatory distress in order to "buy time" and correct circulatory insufficiency and metabolic defects (acidosis, etc.); b) spontaneous ventilation (SV: improved venous return, lowered intrathoracic pressure, absence of muscle atrophy). Given a stabilized early severe ARDS, as soon as the overall clinical situation improves, spontaneous ventilation will be used with the following stringent conditionalities: upfront circulatory optimization, upright positioning, lowered VO 2 , lowered acidotic and hypercapnic drives, sedation without ventilatory depression and without lowered muscular tone, as well as high PEEP (titrated on transpulmonary pressure, or as a second best: "trial"-PEEP) with spontaneous ventilation + pressure support (or newer modes of ventilation). As these propositions require evidence-based demonstration, the reader is reminded that the accepted practice remains, in 2016, controlled mechanical ventilation, muscle relaxation and prone position. Anestezjologia Intensywna Terapia 2016, tom 48, nr 5, 354-366Key words: acute respiratory distress syndrome, ARDS, severe ARDS; acute hypoxic non-hypercapnic respiratory failure; driving pressure; tidal volume, Vt, low tidal volume, ultra-low tidal volume; positive end-expiratory pressure, PEEP; transpulmonary pressure; controlled mechanical ventilation; spontaneous ventilation; spontaneous breathing; pressure support, airway pressure release ventilation; sedation, cooperative sedation; alpha-2 adrenergic agonist, clonidine, dexmedetomidineThe previous chapter overviewed, for residents rotating through the critical care unit (CCU), basic pathophysiology required to analyze early severe acute respiratory distress syndrome (ARDS). An emphasis was placed on spontaneous ventilation both in the setting of the healthy volunteer and of severe ARDS. This chapter will address the pros and cons of controlled mechanical ventilation, with the help of muscle relaxation, as opposed to the putative advantages of spontaneous ventilation. So far, spontaneous ventilation has not achieved evidence-based demonstration: thus, as in part I, conjectures are within [….], following [1]. i. MUSCLE RELAXATiON VERSUS SPONTANEOUS VENTiLATiON?When muscle relaxation is considered, the overall picture appears to be simplified with 48 h of muscle relaxation [2]. A sober interpretation may be considered. a. Muscle relaxationIn severe ARDS (P/F < 120), muscle relaxation [2] lowered the mortality (45 to 31%; difference of −32%; P = 0.04), multiple organ failure (MOF), and barotrauma and led to more ventilator-free days and identical CCU-acquired paresis. Muscle relaxation was hypothesized to minimize excessive transpulmonary pressure, patient-to-ventilator asynchrony [2], ventilator-induced lung injury (VILI), atelectrauma, overdistension,...

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Studies on catecholamines, renin and aldosterone following catapresan® (2-(2,6-dichlor-phenylamine)-2-imidazoline hydrochloride) in hypertensive patients

Cited by 170 publications

References 13 publications

Clonidine withdrawal. Mechanism and frequency of rebound hypertension.

Clonidine withdrawal. Mechanism and frequency of rebound hypertension.

Guanfacine in essential hypertension: effect on blood pressure, plasma noradrenaline concentration and plasma renin activity.

Early severe acute respiratory distress syndrome: What’s going on? Part II: controlled vs. spontaneous ventilation?

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