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)

Coenzyme Q10 has been administered to five patients having essential hypertension and deficiencies of activity of succinate dehydrogenase-co-enzyme Q10 reductase in leucocyte preparations ranging from 20-40%. For a 74-year old male, the systolic pressure was reduced (p less than 0.001), the diastolic pressure was reduced (p less than 0.05), the specific activity of the coenzyme Q10-enzyme was increased (p less than 0.001), and the deficiency of coenzyme Q10 activity was negated (p less than 0.01). Four patients receiving CoQ10 for 3-5 months showed reductions (p less than 0.05 to p less than 0.001) of diastolic pressure, and 3 of these 4 showed reductions (p less than 0.05 to p less than 0.01) of diastolic pressure. Initial deficiencies of enzyme activity were reduced (p less than 0.01 to 0.05) in two patients. Three other patients did not show the high level of deficiency on treatment as initially observed. These effects of CoQ10 on the reduction of systolic and diastolic blood pressures, increase in CoQ10-enzyme activity, and reduction of CoQ10-deficiency are presumably due to improved bioenergetics through correction of a deficiency of coenzyme Q10.
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PMID:Bioenergetics in clinical medicine. VIII. Adminstration of coenzyme Q10 to patients with essential hypertension. 78 64

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

A total of 109 patients with symptomatic essential hypertension presenting to a private cardiology practice were observed after the addition of CoQ10 (average dose, 225 mg/day by mouth) to their existing antihypertensive drug regimen. In 80 per cent of patients, the diagnosis of essential hypertension was established for a year or more prior to starting CoQ10 (average 9.2 years). Only one patient was dropped from analysis due to noncompliance. The dosage of CoQ10 was not fixed and was adjusted according to clinical response and blood CoQ10 levels. Our aim was to attain blood levels greater than 2.0 micrograms/ml (average 3.02 micrograms/ml on CoQ10). Patients were followed closely with frequent clinic visits to record blood pressure and clinical status and make necessary adjustments in drug therapy. Echocardiograms were obtained at baseline in 88% of patients and both at baseline and during treatment in 39% of patients. A definite and gradual improvement in functional status was observed with the concomitant need to gradually decrease antihypertensive drug therapy within the first one to six months. Thereafter, clinical status and cardiovascular drug requirements stabilized with a significantly improved systolic and diastolic blood pressure. Overall New York Heart Association (NYHA) functional class improved from a mean of 2.40 to 1.36 (P < 0.001) and 51% of patients came completely off of between one and three antihypertensive drugs at an average of 4.4 months after starting CoQ10. Only 3% of patients required the addition of one antihypertensive drug. In the 9.4% of patients with echocardiograms both before and during treatment, we observed a highly significant improvement in left ventricular wall thickness and diastolic function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of essential hypertension with coenzyme Q10. 775 51