Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen of 22 elderly male patients (aged 60-74 years) who had previously taken only hydrochlorothiazide 50 mg completed a study evaluating the safety, efficacy, and tolerability of 12-20 weeks of transdermal clonidine (Catapres TTS) as monotherapy for mild hypertension. Thirteen of the sixteen patients (81%) responded to transdermal clonidine which was begun after 28 days of placebo. Five patients discontinued transdermal clonidine therapy because of intolerable skin irritation, and one because of daytime fatigue. Clonidine caused none of the metabolic effects we observed with hydrochlorothiazide: no change in serum potassium, uric acid, cholesterol, or triglyceride. Eleven of the 22 patients (50%) who began the study experienced a skin reaction under the transdermal clonidine patch. The incidence of dry mouth and fatigue in patients using transdermal clonidine was dose-related and similar to reports of dry mouth and fatigue in patients taking oral clonidine tablets. Rebound hypertension occurred in one patient upon withdrawal of transdermal clonidine. There was no effect of transdermal clonidine or hydrochlorothiazide on cognitive function or emotional state tested with three questionnaires. Overall, transdermal clonidine, in various doses, was as effective as hydrochlorothiazide in elderly male hypertensive patients. The effectiveness of both was inversely proportional to the level of untreated blood pressure. The high incidence of skin reactions limited prolonged use of transdermal clonidine in our patients.
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PMID:Transdermal clonidine compared with hydrochlorothiazide as monotherapy in elderly hypertensive males. 271 69

Rebound hypertension with a neurological complication occurred during an attempt to substitute transdermal for oral clonidine in a patient with severe hypertension. Published studies have not established an unequivocal correlation between previous oral clonidine dose and the dose of transdermal clonidine required for equally effective antihypertensive therapy. Close observation of blood pressure may be advisable for at least one week following substitution of transdermal for oral clonidine, especially in patients with severe hypertension.
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PMID:Rebound hypertension during initiation of transdermal clonidine. 341 42

The present study was designed to investigate the role of the central nervous system in the rebound hypertension precipitated by abrupt cessation of chronic clonidine (Cl) treatment. Male Wistar rats were treated with Cl (100 micrograms/kg, s.c.) twice daily for 7 days. Systolic blood pressure and heart rate were measured at different time intervals during Cl treatment. Rebound hypertension occurred 16-18 h after the last injection of Cl, but not in control animals given saline (0.1 ml) twice a day for 7 days. Rats were anesthetized with ether during this rebound phase of Cl withdrawal, an electrode inserted into the posterior hypothalamus, and a cannula introduced into the lateral cerebral ventricle. The posterior hypothalamus was electrically stimulated, and voltage-response curves obtained for control and Cl-treated rats revealed that the pressor responsiveness to hypothalamic stimulation was significantly potentiated in the Cl-treated rats. In addition, the depressor response to a single injection of Cl (10 micrograms) into the lateral cerebral ventricle was significantly attenuated in the Cl-treated rats. Additional experiments were performed in pithed rats to determine the involvement of peripheral adrenergic mechanisms in the rebound hypertension. When rats were pithed during the hypertensive phase of withdrawal, the blood pressure of treated rats decreased to a level which was similar to that of control animals. While the pressor responses to total spinal stimulation were similar in both the groups, the effect of exogenous norepinephrine was significantly attenuated in Cl-treated rats., These results suggest that a hyperresponsiveness of central noradrenergic pressor pathways contributes to the rebound hypertension noted following the abrupt cessation of clonidine treatment.
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PMID:Involvement of central noradrenergic mechanisms in the rebound hypertension following clonidine withdrawal. 617 42

1. Twenty-two patients with moderately severe essential hypertension were treated for a period of 12 months with guanfacine (BS 100-141), a new centrally-acting antihypertensive agent. A twice daily schedule was followed and the dose range of guanfacine was 1-8 mg daily. 2. In twenty patients satisfactory blood pressure responses (diastolic pressure below 95 mmHg) were achieved in both the supine and the standing position. Pulse rate decreased slightly, though not significantly. 3. Tolerance to the pressure-lowering effect of the drug developed during the third or fourth month of therapy. This could be overcome by either increasing dosage or adding a diuretic. 4. All patients reported side-effects, mainly dryness of the mouth and fatigue. These side-effects became less or disappeared at the end of 3 months. Rebound hypertension on discontinuation of therapy occurred in two patients. 5. Plasma concentrations of noradrenaline and adrenaline as well as plasma renin activity were decreased after 1 week of treatment with the drug. 6. Guanfacine in conjunction with a diuretic is a useful drug in the long-term treatment of hypertension. Reduced central sympathetic outflow may be the major mechanism underlying the antihypertensive effect of the drug.
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PMID:Evaluation of long-term treatment of essential hypertension with guanfacine. 699 80

Minoxidil, a potent peripheral vasodilator, was used concomitantly with other antihypertensive drugs for severe hypertension in three children for 47 to 158 weeks at the dosage of 40 to 50 mg/day. Two patients had three and two courses of minoxidil, respectively. Attempts were made to withdraw minoxidil in all children because of severe hypertrichosis. Minoxidil was withdrawn over periods varying from four to 12 weeks. Rebound hypertension manifesting as hypertensive encephalopathy occurred in all when minoxidil was withdrawn rapidly. The occurrence of rebound hypertension correlated with the total cumulative dose of minoxidil in mg/kg/week given prior to the withdrawal (P less than 0.05) and the rapidity (four to eight weeks) with which minoxidil was withdrawn (P less than 0.05), but not with the total duration of therapy, duration at maximal dosage, or the amount of minoxidil in mg/kg on the day prior to withdrawal. Rebound hypertension also did not occur when minoxidil was withdrawn gradually (12 weeks) or if the patient was receiving a small dose (2.5 to 5 mg/day). Pretreatment with an alpha-blocking agent (prazosin) or the discontinuation of the concomitantly administered beta-blocker (propranolol) prior to the withdrawal seemed to prevent rebound hypertension. We suggest that the dosage of minoxidil should be decreased very gradually.
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PMID:Rebound hypertension following minoxidil withdrawal. 735 90

Centrally acting antihypertensive drugs, or sympatholytics, have a long history of efficacy, including some of the earliest major clinical trials, but they are now little used in the UK and elsewhere. This has been due to the introduction of new drugs with better tolerability than the centrally acting agents. In the case of clonidine there was also concern about rebound hypertension. However, at least some hypertensives may benefit from a centrally acting drug and a new class of agents, the imidazoline agonists, has recently been developed. One of these, moxonidine, is available in the UK. Clinical studies so far suggest that its efficacy is comparable to currently used drugs and that adverse effects are less severe than with earlier sympatholytics. Rebound hypertension has not been described, so this may lead to a revival in interest in these drugs as antihypertensive agents.
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PMID:Centrally acting antihypertensives: not obsolete after all. 968 37

The medical care of chronic renal failure patients is often complicated by the comorbid conditions of hypertension and coronary artery disease in the perioperative period. The limitations on solute and water excretion imposed by renal dysfunction increase the susceptibility of this population to both salt deficit and surfeit, as well as hyponatremia and hypernatremia perioperatively. Accurate assessment and successful treatment of these complications in renal failure patients require understanding of the concept of electrolyte-free water, proper utilization of diuretics, and calculated prescription of fluid therapy. The presence of hyperkalemia in the adapted renal failure patient generally indicates a severe reduction in glomerular filtration, such that nonrenal hypokalemic treatments are imperative. IV calcium-based therapy and infusion of insulin with glucose represent the mainstays of immediate therapy, and sodium bicarbonate therapy should be given only when severe acidemia is present. Perioperative aggravation of preexistent hypertension is common. Rebound hypertension attributable to injudicious adjustment of the medical regimen should be diligently searched for first, before any new therapies are recommended. Relief of pain or anxiety may be all that is necessary. Briefly acting calcium channel blocker therapy should not be employed in these cases, and smooth IV control by a variety of agents is preferable, the choice of the agent contingent on the clinical scenario.
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PMID:Selective review of key perioperative renal-electrolyte disturbances in chronic renal failure patients. 1033 49