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)

A clinical and laboratory examination was conducted with a hypotensive drug Katapresan used alone and in combinations with Reserpine and saluretics in 30 patients with stage II and III of essential hypertension. Katapresan was shown to be an active hypotensive agent, often effective in patients resistant to other drugs. For long-term therapeutic courses the most effective combination is Katapresan with Hypothiazide and Reserpine. Katapresan may result in a deceleration of atrioventricular conduction, a slowing down of the electric systole, a reduction of the contractile function of the myocardium. The drug does not affect the metabolism of potassium and sodium ions.
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PMID:[Clinical evaluation of the hypotensive drug catapresan]. 88 32

Background data revealed that some American and Japanese patients with essential hypertension, including many who were not being treated with any anti-hypertensive drug, had a deficiency of coenzyme Q10. Eight clinically used anti-hypertensive drugs have now been tested for inhibition of two mitochondrial coenzyme Q10-enzymes of heart tissue, succinoxidase and NADH-oxidase. Diazoxide and propranolol significantly inhibited the CoQ10-succinoxidase and CoQ10-NADH-oxidase, respectively. Metoprolol did not inhibit succinoxidase, and was one-fourth as active as propranolol for inhibition of NADH-oxidase. Hydrochlorothiazide, hydralazine, ans clonidine also inhibited CoQ10-NADH-oxidase. Reserpine did not inhibit either CoQ10-enzyme, and methyldopa was a very eak inhibitor of succinoxidase. The internationally recognized clinical side-effects of propranolol may be due, in part, to inhibition of CoQ10-enzymes which are indispensable in the bioenergetics of cardiac function. A pre-existing deficiency of coenzyme Q10 in the myocardium of hypertensive patients could be augmented by subsequent treatment with propranolol, possibly to the "life-threatening" state described by others.
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PMID:Bioenergetics in clinical medicine. III. Inhibition of coenzyme Q10-enzymes by clinically used anti-hypertensive drugs. 119 30

40 patients with essential hypertension were subjected to an analysis of efficacy and safety of the three-component-combination Briserin (Reserpine, Clopamide, Dihydroergocristine). After double-blind and randomized allocation, one group received the two constituents Reserpine/Clopamide, another the full combination Briserin and a third first Reserpine/Clopamide and Briserin afterwards. Both types of treatment proved equi-effective in terms of blood pressure reduction with the blood pressure values falling below 150/90 mm Hg within one week. The most important finding resided in the improved orthostatic tolerance due to Briserin. Maximal systolic pressure drop during standing and the tachycardia associated were significantly reduced by Briserin, i.e. by the influence of Dihydroergocristine. In addition, there was a corresponding difference in terms of subjective complaints due to orthostasis. The same held true for general symptoms related to hypertension such as headache, dizziness, undue tiredness and sleeplessness. Patients preferred treatment with Briserin as compared to the other regimen. The discussion deals with the clinical-pharmacological impact of the orthostatic regulation quality within the framework of antihypertensive treatment.
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PMID:[Hypertension therapy with Briserin: what role do dihydroergocristine components play?]. 679 82

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