Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clonidine in a dose of 2.5 to 3 mg/kg was used as a component of anesthesia in 150 patients aged 60 to 85. Essential hypertension of the second-third stages was diagnosed in 57% patients (group 1), systolic sclerotic arterial hypertension (SSAH) in 43% (group 2). Anesthesia was characterized by stable hemodynamics; however, analysis within the groups showed an increase of systolic and diastolic arterial pressure in 40% patients in group 2. There were no clinical signs of inadequacy of anesthesia. Remembering about the reduction of the reserve potential of the cardiovascular system in this cohort of patients, neurovegetative inhibition was supplemented by peripheral a-adrenoblocker droperidol, starting from the test dose of 1.25 and increasing it to 5 mg over the course of anesthesia; this led to stabilization of the peripheral and improvement of the central hemodynamics. Differences in the changes of central hemodynamics may be explained by specific features of circulation in patients with essential hypertension and SSAH, as well as by a higher tone of the sympathetic component of the CNS in SSAH patients.
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PMID:[Anesthesia using clofelin in different types of arterial hypertension in middle-aged and elderly patients]. 868 41

Patients with essential hypertension often show alterations of the autonomic nervous system. We evaluated the sympathetic and parasympathetic drive to the heart in 12 mildly hypertensive patients and 9 healthy subjects by power spectral analysis of heart rate variability. All subjects underwent measurements of RR interval, low (LF) and high frequency (HF) components of heart rate variability, LF/HF ratio and blood pressure in the resting and sitting positions, both before and after oral clonidine (300 microg), a central sympatholytic agent. In the supine position before clonidine, hypertensive patients had higher blood pressure and lower HF values than healthy subjects. Clonidine induced increases in RR interval and HF in both groups, while LF and LF/HF ratio decreased in healthy subjects, but not in hypertensive patients. On assuming the sitting position, both groups showed reductions in RR and HF and increments in LF and LF/HF. In healthy subjects, the response to the postural challenge was unaffected by clonidine. In contrast, hypertensive patients showed no changes in LF and LF/HF ratio, and a significantly lower decrease in HF. These differences were probably due to the existence of two subsets of patients, one exhibiting similar responses to clonidine as healthy subjects, and the other showing no appreciable response to the drug. These results suggest that hypertensive patients have an altered sympatho-vagal balance to the heart, which can be unmasked by clonidine. This phenomenon should be taken into account to achieve a better control of the overall cardiovascular risk of hypertensive patients.
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PMID:Effects of clonidine on power spectral analysis of heart rate variability in mild essential hypertension. 991 31

Effective therapy (Rx) in primary hypertension (PH) for 50 years, has featured sympathetic nervous system (SNS) mechanisms. Ganglionic blockers and reserpine were pre-eminent in the 1940s (mydriasis, ileus, impotence, peptic ulcer). Guanethidine, and in the 1960s clonidine and methyldopa, were step II agents to thiazide Rx in the 1950s. Reserpine depletes brain (depression) and peripheral (PPH) noradrenaline (NA) storage sites, guanethidine depleted NA storage via blockade of reuptake. Venomotor sympathoplegia resulted in postural hypertension. An analogue, metaiodobenzyguandine is used in diagnosis and Rx of pheochromocytoma. Clonidine lowers both central and PPH neuronal NA release via both stimulation of alpha agonist adrenoreceptors (sedation) and specific imadazoline binding sites (IBS). Methyldopa lowers pressure via PPH induced NA release (retrograde ejaculation) and via alphamethyl NA on central alpha-2 receptors (depression). The alpha-2 and alpha-2 receptor antagonists (alphaRA) cause reflex tachycardia and first-dose hypotension. Recently a two-fold incidence of congestive heart failure after alphaRA in treated primary hypertensives question their role in PH. The beta RA, with or absent alphaRA, remain premier since the 1970s due to mortality benefit in systolic dysfunction and post myocardial infarction, certifying the role of the SNS in the pathogenesis and sequelae and Rx of PH. The future includes beta RA, specific IBS agents, angiotensin (AII) RA with avid presynaptic AII affinity and vasopeptidase inhibitiors that raise peptides and suppress SNS.
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PMID:Sympatholytic therapy in primary hypertension: a user friendly role for the future. 1198 8

The diagnosis of pheochromocytoma is relatively easy when excessive plasma catecholamines can be found. However, whenever plasma catecholamine levels are only moderately increased further evaluation should be performed. Clonidine, a centrally acting alpha adrenergic agouist, can be useful in the differentiation of pheochromocytoma from essential hypertension. Plasma catecholamine failure of suppression three hours after the oral administration of 0.3 mg of clonidine, is considered to be a sign of the presence of pheochromocytoma. In spite of unsatisfactory specificity and predictive value clonidine suppression test provides a helpful diagnostic means together with other biochemical procedures and imaging techniques for a more definitive diagnosis.
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PMID:[Estimation of clonidine test in differential diagnosis of pheochromocytoma from essential hypertension]. 1797 98


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