Clonidine hypertension caused

III. Clinical presentation. Manifestations of intoxication result from generalized sympathetic depression and include pupillary constriction, lethargy, coma, apnea, bradycardia, hypotension, and hypothermia. Paradoxic hypertension, caused by stimulation of peripheral alpha-1 receptors, may occur with clonidine, oxymetazoline, and tetrahydrozoline (and possibly guanabenz) and is usually transient. The onset of symptoms is usually within 30-60 minutes, although peak effects may occur more than 6-12 hours after ingestion. Full recovery is usual within 24 hours. In an unusual massive overdose, a 28-year-old man who accidentally ingested 100 mg of clonidine powder had a three-phase intoxication over 4 days initial hypertension, followed by hypotension, and then a withdrawal reaction with hypertension. 

Potentiation of the antihypertensive effect of clonidine by ACE inhibitors can be clinically useful. However, limited evidence suggests that the effects of captopril may be delayed when patients are switched from clonidine. Note that sudden withdrawal of clonidine may cause rebound hypertension. 

Guanfacine. Guanfaciae, used ia patients having mild to moderate hypertension, can lower blood pressure 50/25 mm Hg (systoHc/diastoHc) ia hypertensive patients. Side effects such as sedation, dry mouth, and asthenia are less as compared to those of guanaben2 and clonidine. Guanfaciae reduces blood cholesterol and triglyceride and does not cause glucose iatolerance. 

The answer is a. (Hardman, p 789. Katzung, pp 162—163.) Withdrawal of clonidine, particularly doses greater than 1 mg/d, is well known to cause such a syndrome (including severe hypertension, tachycardia, anxiety tremor, headache, abdominal pain, and sweating), even after one or two missed doses. 

The primary indication for clonidine use is in mild and moderate hypertension that has not responded adequately to treatment with a diuretic or a p-blocker. Since clonidine causes sodium and water retention and plasma volume expansion, it generally is administered in combination with a diuretic. A vasodilator can be added to the clonidine-diuretic regimen in the treatment of resistant forms of hypertension. Such drug combinations can be quite effective, since the reflex increases in heart rate and cardiac output that result from vasodilator administration are reduced or negated by clonidine-induced decreases in heart rate and cardiac output. 

For severely hypertensive patients, clonidine has been used in combination with a diuretic, a vasodilator, and a -blocker. Some care must be taken, however, because the coadministration of clonidine and a p-blocker may cause excessive sedation. Clonidine is especially useful in patients with renal failure, since its duration of... 

Tricyclic antidepressants potentiate the pressor effects of directly acting sympathomimetic amines, such as adrenaline (epinephrine) or noradrenaline (norepinephrine), to cause hypertension. Small amounts of these, such as may be present in local anaesthetic solutions, can be dangerous. Tricyclic antidepressants will inhibit the antihypertensive effects of the older anti hypertensive drugs, such as adrenergic neurone-blocking agents, e.g. guanethidine, a-methyl-DOPA, and clonidine. 

Reduction in arterial blood pressure by clonidine is accompanied by decreased renal vascular resistance and maintenance of renal blood flow. As with methyldopa, clonidine reduces blood pressure in the supine position and only rarely causes postural hypotension. Pressor effects of clonidine are not observed after ingestion of therapeutic doses of clonidine, but severe hypertension can complicate a massive overdose. 

One method used for the control of hypertension is reduction of the impulses flowing from the CNS to the sympathetic nervous system which controls the tone of the cardiovascular system. The veratrum alkaloids do this at doses that are near the emetic dose, and reserpine acts both centrally and peripherally. The imidazoline clonidine (175) and some analogues in which the chlorine is replaced by fluorine or methyl groups decrease sympathetic outflow and cause vasomotor relaxation. However, they cause sedation, lack of saliva and renewed hypertension on withdrawal of the drug. 

Clonidine, an antihypertensive drug, also has been used in the treatment of mania. Sudden withdrawal can produce a rebound hypertensive crisis. Consistent with the brain-disabling principles, it can produce a variety of psychiatric symptoms, including sedation, vivid dreams or nightmares, insomnia, restlessness, anxiety, and depression. More rarely, it can cause hallucinations. Unfortunately, this drug is too commonly used as a so-called mood stabilizer in children. When mistakenly prescribed with stimulants, it causes an elevated risk of cardiac arrhythmia and cardiac arrest in children. 

The authors recognized that mirtazapine alone could have caused the hypertensive event. In postmarketing surveillance of mirtazapine, hypertension occurred in at least 1% of patients. However, it is likely that the patient lost antihypertensive control because mirtazapine antagonized the antihypertensive effect of clonidine. Mirtazapine, a tetracyclic antidepressant, stimulates the noradrenergic system through antagonism at central alpha2 inhibitory receptors, which is precisely opposite to the effect of clonidine. 

Tetanus toxin often causes disturbances in autonomic control, resulting in sympathetic overactivity and high plasma catecholamine concentrations. The first-line treatment for autonomic dysfunction is by sedation with a benzodiazepine and opioid. Infusion of the short-acting i-blocker esmolol, or the o -adrenergic agonist clonidine, helps to control episodes of hypertension. Intravenous magnesium sulphate is also used to reduce autonomic disturbance. 

Clonidine (Catapres) is an imidazoline which is an agonist to ctj-adrenoceptors (postsynaptic) in the brain, stimulation of which suppresses S5unpathetic outflow and reduces blood pressure. At high doses it also activates peripheral a -adrenoceptors (pre-synaptic autoreceptors) on the adrenergic nerve ending these mediate negative feedback suppression of noradrenaline release. In overdose clonidine can stimulate peripheral Oj-adrenoceptors (postsynaptic) and thus cause hypertension by vasoconstriction. Clonidine was discovered to be hypotensive, not by the pharmacologists who tested it in the laboratory but by a physician who used it on himself as nose drops for a common cold. The tl is 6 h. 

Clonidine reduces blood pressure with little postural or exercise related drop. Its most serious handicap is that abrupt or even gradual withdrawal causes rebound hypertension. This is characterised by plasma catecholamine concentrations as high as those seen in hypertensive attacks of phaeochro-mocytoma. The onset may be rapid (a few hours) or delayed for as long as 2 days it subsides over 2-3 days. The treatment is either to reinstitute clonidine, i.m. if necessary, or to treat as for a phaeochro-mocytoma. Clonidine should never be used with a p-adrenoceptor blocker which exacerbates withdrawal hypertension (see phaeochromocytoma). Common... 

The hypertensive crisis that can follow the withdrawal of clonidine can be accentuated by beta-blockers. It has also been reported that when beta-blockers are used in conjunction with drugs that cause arterial vasoconstriction they can have an additional effect on peripheral perfusion, which can be hazardous. Thus, combining beta-blockers with ergot alkaloids, as has been recommended for migraine, can cause severe peripheral ischemia and even tissue necrosis (408). 

Unlike clonidine, moxonidine does not appear to cause sedation or to impair psychomotor performance or cognitive function. However, possible potentiation of the effect of benzodiazepines can ocenr. There is no evidence of a withdrawal syndrome or rebonnd hypertension associated with sudden withdrawal. 

Tolazoline can antagonize the effects of intravenous clonidine and prevent the brief hypertensive reaction that it often causes (SEDA-2,192) (SEDA-3,180). 

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