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)

The effects of timolol (10 mg thrice daily) and hydrochlorothiazide (50 mg/day) have been compared in a double-blind factorial trial in 20 patients with essential hypertension. There were four randomised test phases of 8 weeks each during which patients received timolol alone, hydrochlorothiazide alone, timolol plus hydrochlorothiazide, and no treatment (placebo). Blood-pressure was measured weekly, alternately at the outpatient clinic and at the patient's home. Supine mean arterial pressure fell from 119 mm Hg in the placebo phase to 110 mm Hg in the hydrochlorothiazide phase, 106 mm Hg in the timolol phase, and 101 mm Hg in the combined timolol plus hydrochlorothiazide phase. Factorial analysis revealed that these effects of the two drugs were additive without any potentiation or antagonism. Mean plasma-renin activity (P.R.A.) was 5-02 ng/ml/3 h in the placebo phase falling to 1-79 in the timolol phase and rising to 9-54 in the diuretic phase, but remaining unchanged in the combined treatment phase (5-40 ng/ml/3 h). The data suggest that the hypotensive action of timolol is not dependent on the concomitant fall in P.R.A. The methods described provide a valuable tool for quantitating the effects of a given drug, and hence a valid basis for objective comparison.
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PMID:Effects of timolol and hydrochlorothiazide on blood-pressure and plasma renin activity. Double-blind factorial trial. 6 May 66

In an attempt to resolve conflicting reports about the identity of a low-renin subgroup in essential hypertension, the distribution of plasma-renin activity (P.R.A.) has been examined in 82 hypertensive subjects before and after stimulation with bendrofluazide. The unstimulated basal P.R.A. showed no evidence of a separate subgroup of patients with low P.R.A. values although the distribution was slightly skewed with a tail to the right when compared with 83 normotensive subjects. In 38 of the patients post-stimulation P.R.A. observed in age and sex matched normotensive controls exposed to the same stimulus. However the percentage rise in P.R.A. in all 83 patients was less than half that of the controls. Thus the identification of a low-renin subgroup of hypertensive patients is critically determined by the standard of comparison employed: if the percentage rise is considered subnormal responsiveness is a feature of essential hypertension. If absolute post-stimulation values are used, there is a substantial group of patients with "low renin hypertension". The demarcation of such a group is, however, essentially arbitrary.
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PMID:Low renin hypertension. A distinct entity. 6 62

Inactive renin which can be converted to an enzymologically active form by acidification to pH 3-3 by dialysis was found in normal subjects and in patients with untreated essential hypertension. The molecular weight of this inactive renin (43 000) is 2000 +/- 900 (S.E.M.) daltons higher (p less than 0.05) than that of naturally occurring active renin and the two forms of renin could be clearly separated by ion-exchange chromatography with diethylaminoethyl-"Sepharose'. Patients with low-renin essential hypertension had proportionately larger amounts of inactive renin than usual, so that the total renin in these patients approached the normal range. Inactive renin seems likely to be a form in which the enzyme is secreted since in a patient with renal-artery stenosis its concentration was greater in the renal-vein blood coming from the affected kidney.
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PMID:An inactive higher-molecular-weight renin in normal subjects and hypertensive patients. 6 45

20 patients with severe essential hypertension (average blood-pressure 211/123 mm Hg) had an inadequate fall in blood-pressure with beta blockade alone. They were given in random order either 5 and then 10 mg of bendrofluazide a day or prazosin 2 mg three times daily rising to 5 mg if required. The trial was a within-patient comparison of the two drug regimens. 10 patients who did not achieve a satisfactory fall in pressure with either agent were then given all three drugs together. When bendrofluazide 5 or 10 mg was added to beta blockade there was an average fall in mean blood-pressure, standing, of 13%. When prazosin was added to beta blockade the average fall in mean blood-pressure, standing, was 16%. 18 patients who completed the trial had an average final blood-pressure, standing, of 139/93 mm Hg. In the prazosin period 8 patients continued to complain of dizziness after the first 24 h. With bendrofluazide serum-potassium levels fell below 3-6 mmol/l in half the patients within the first two weeks of treatment. It is concluded that patients with essential hypertension already treated with beta blockade who need an additional agent will get a further fall in blood-pressure with 5 mg of bendrofluazide. Prazosin appears to be a potent and appropriate third agent.
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PMID:Evaluation of beta blockade bendrofluazide, and prazosin in severe hypertension. 6 3

Plasma-noradrenaline (P.N.A.) has been determined in normotensive controls and in patients with essential hypertension while resting and after postural stimulation. A linear relationship was found between age and P.N.A. in normotensives during recumbency and in the upright posture. This relationship did not occur in the hypertensives and was due to raised P.N.A. levels in many younger patients. On standing, ten out of thirty-four patients under the age of 50 years with essential hypertension had significantly greater P.N.A. than the age-matched controls. No differences were found, however, between controls and patients in the older age-group. It is proposed that stimulation of the sympathetic nervous system by postural challenge provides a means for identifying a subgroup of younger patients with essential hypertension in whom sympathetic overactivity may play an important rule.
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PMID:Plasma-noradrenaline in essential hypertension. 6 82

Plasma-prolactin concentration was up to four times higher in male patients with essential hypertension than in normotensive controls. Oral administration of bromocriptine, a dopaminergic agonist, suppressed plasma-prolactin and lowered arterial pressure. It is proposed that in the hypertensive patients the raised prolactin levels reflect a defect in central dopamine control which is normalised by bromocriptine. The antihypertensive effect of bromocriptine suggests that the dopaminergic system is involved in blood-pressure regulation and that reduced central dopaminergic activity may be a factor in the maintenance of essential hypertension.
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PMID:Hyperprolactinaemia and antihypertensive effect of bromocriptine in essential hypertension. Identification of abnormal central dopamine control. 6 27

HLA-typing was performed in 149 patients with essential hypertension, 86 males and 63 females. In 66 patients with significantly elevated serum levels of immunoglobulins, HLA-B27 was increased to 18%, from 8% in the controls (P less than 0.007). This was not significant when correcting the P-value for the number of antigens analyzed, but confirms reports of an association of this antigen with serum levels of immunoglobulins. HLA-Bw15 was found to be increased two-fold in patients with a family history of hypertension (P corrected less than 0.05) and in patients with autoantibodies (not significant). This is discussed in relation to the increase of Bw15 in juvenile diabetes and in Systemic Lupus Erythematosus, diseases in which vascular damage also occurs.
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PMID:HLA antigens in essential hypertension. Relation to familiar disposition and serum immunoglobulins. 7 Aug 61

Plasma concentrations of arginine-vasopressin (antidiuretic hormone) have been measured in 40 patients with benign essential hypertension and 12 patients with malignant-phase hypertension. Values tended to be low in the benign phase and high in the malignant phase. 5 normal subjects were infused with synthetic arginine-vasopressin, producing plasma concentrations up to five times the highest value recorded in malignant-phase hypertension, without any effect on blood-pressure. There is no evidence that vasopressin has a direct role in the pathogenesis of benign essential hypertension or its transition to the malignant phase. On the contrary, abnormal vasopressin concentrations may be caused by hypertension.
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PMID:Changes of vasopressin in hypertension: Cause or effect? 7 91

Human plasma contains renin, which is enzymatically active at neutral pH (active renin), and a non-dialysable factor, which has renin-like activity after treatment at low pH (inactive renin). In vitro activated plasma-renin and purified human renal renin showed identical enzyme-kinetic properties. Quantitative estimations of inactive renin in renal venous plasma from 5 patients with renal-artery stenosis demonstrated its release by the kidney. Acute stimulation of renin release by isoprenaline, tilting, or diazoxide in 13 normotensive individuals and in 9 patients with essential hypertension increased active plasma-renin and reduced inactive plasma-renin. Inactive plasma-renin was increased and active plasma-renin decreased during suppression of renin release by propranolol in 12 patients with essential hypertension. In 55 patients with various disorders, inactive and active plasma-renin were directly correlated. However, the concentration of inactive renin, for a given value of active renin, varied widely from patient to patient. These results indicate that so-called inactive renin is indeed physiologically related to active renin. They also suggest that inactive renin can be activated not only in vitro, but also in vivo. Different renin assays measure different relative amounts of active and inactive renin. This may call for reinterpretation of results obtained by various methods, especially in situations where changes in plasma concentrations of the two forms of renin are in opposite directions.
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PMID:Inactive renin in human plasma. 7 64

Parallel fluctuations of potential difference (P.D.) across oral and rectal mucosa are probably related to the activity of autonomic nerves rather than adrenal steroids. Unlike rectal mucosa, oral mucosa does not respond to exogenous or endogenous aldosterone. Therefore subtraction of oral P.D. from rectal P.D. gives a closer indication of mineralocorticoid activity than does rectal P.D. alone. In normal subjects plasma-aldosterone correlated well with subtraction P.D. (r = 0.74; P is less than 0.001). A subtraction P.D. higher than 26 mV in subjects on a normal sodium intake indicated primary or secondary hyperaldosteronism; if the level was lower than 11 mV four hours after intramuscular injection of 0.25 mg tetracosactrin this suggested mineralocorticoid deficiency. Measurement of oral and rectal P.D. permits rapid and inexpensive diagnosis of aldosterone excess and deficiency. The method may also be used in study of the mineralocorticoid effect of other adrenal steroids: as assessed with this bioassay, the plasma 18-OH-deoxycorticosterone, which is raised in some patients with essential hypertension, lacked any in vivo mineralocorticoid activity.
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PMID:Subtraction potential difference: In-vivo assay for mineralocorticoid activity. 7 36


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