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 aim of this work was to investigate the influence of blood pressure levels on human platelet alpha 2-adrenergic receptivity. The study was carried out on 12 mild essential hypertensive patients and 7 normotensive parkinsonians with orthostatic hypotension. Alpha 2-adrenoceptors number and affinity were determined by 3H-yohimbine binding, plasma catecholamines were measured by HPLC and adrenaline-induced platelet aggregation by turbidimetry. Results obtained were compared with those of two groups of 12 normotensive control subjects. In hypertensive patients, both platelet alpha 2-adrenoceptors (139 +/- 6 vs 176 +/- 18 fmol/mg protein) and velocity of adrenaline-induced platelet aggregation were decreased whereas plasma adrenaline and noradrenaline remained unchanged. In patients with orthostatic hypotension, there was an increased number of platelet alpha 2-adrenoceptors (313 +/- 52 vs 168 +/- 8 fmol/mg protein) associated with a significant decrease in plasma noradrenaline (62 +/- 11 vs 190 +/- 25 pg/ml). In none of the two groups of patients there was any change in receptor affinity for 3H-yohimbine. These results indicate that human platelet alpha 2-adrenoceptors levels are related to blood pressure values. Moreover, up-regulation in orthostatic hypotension and lack of down-regulation in essential hypertension suggest that only sustained abnormal plasma noradrenaline levels could allow the development of alpha 2-adrenoceptors regulatory mechanisms. These variations can represent tentative compensatory mechanisms for normalization of blood pressure levels.
Arch Mal Coeur Vaiss 1989 Jul
PMID:[Alpha 2-adrenergic receptors and arterial pressure]. 255 34

The presence of Na+ transport abnormalities (decreased affinity of the Na+/K+ pump or the Na+, K+ cotransport for internal Na+, increased Na+:Li+ countertransport, increased Na+ leak), Na+ content, Na+/K+ pump activity and sensitivity to ouabain were investigated in erythrocytes from 13 patients with essential hypertension. According to the presence or absence of Na+ transport abnormalities, the patients were divided into two groups: TrNa(+) (n = 9) and TrNa(-) (n = 4) respectively. Compared with TrNa(-) patients, TrNa(+) patients were characterized by: (i) a higher arterial pressure (131.4 +/- 11.8 vs 110.0 +/- 13.2 mmHg, p less than 0.05), (ii) an increased erythrocyte Na+ content (8.9 +/- 1.0 vs 6.3 +/- 0.8 mmol/l.cells, p less than 0.01) associated with (iii) a decreased rate constant of Na+/K+ pump activity (235 +/- 26 vs 309 +/- 45 h-1, p less than 0.05) and (iv) a higher sensitivity to ouabain (0.76 +/- 0.23 vs 1.12 +/- 0.26 microM, p less than 0.05). Oral administration of canrenone 50 mg per day during 7 weeks decreased mean arterial pressure by 10-30 mmHg in 6 out of the 9 TrNa(+) patients. Conversely, it decreased mean arterial pressure in only one out of the 4 TrNa(-) patients. The hypotensive effect of canrenone in TrNa(+) patients was not associated with normalization of their Na+/K+ pump activity. Canrenone did not modify the sensitivity to ouabain of either the TrNa(+) or the TrNa(-) patients. Before treatment, acute injection of ouabain provoked an inhibition of the erythrocyte Na+/K+ pump, without any change in Na+ content.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1989 Sep
PMID:[Therapeutic response to canrenone of patients with essential hypertension as a function of sodium transport anomalies and ouabain sensitivity of erythrocytes]. 255 40

In this multicentre controlled single blind trial the effectiveness and safety of cicletanine (100 mg/day) were compared with those of enalapril (20 mg/day) and of the combination of both drugs in the same doses in 72 patients (41 men, 31 women, mean age 64.1 +/- 8.3 years) with permanent moderate essential hypertension without severe cardiovascular complications. In the course of the trial, one patient in each of the three therapeutic groups was excluded either for insufficient effectiveness in monotherapy or for photosensitization under the combined treatment. After two months of treatment, the fall in blood pressure and the number of patients with normalized BP were similar in the groups treated with cicletanine or enalapril alone. In contrast, the cicletanine-enalapril combination produced a significantly greater fall of diastolic arterial pressure than cicletanine alone. In addition, there was a greater reduction of functional symptoms associated with arterial hypertension. Apart from the lone case of photosensitization observed with the combined treatment, only minor side-effects were encountered, including an episode of diarrhoea and a case of extrasystoles with the combination, and a case or nausea with lipothymia under cicletanine alone. There were no significant variations of biochemical values.
Arch Mal Coeur Vaiss 1989 Nov
PMID:[Evaluation of the effectiveness of a cicletanine-enalapril combination in hypertensive patients]. 255 22

In a multicentre open trial involving 229 investigators, cicletanine, a new antihypertensive agent, was administered orally in doses of 50 to 100 mg/day either alone (1,238 patients) or combined with another drug (430 patients). In this second group of patients with essential hypertension whose BP had not been normalized by a beta-blocker (n = 157), a calcium inhibitor (n = 67), an angiotensin-converting enzyme inhibitor (n = 134) or an alpha-blocker (n = 7), cicletanine normalized BP (less than 160/95 mmHg) in 48.8% of the patients and significantly lowered BP values which fell from 177.7 +/- 15.9/103.3 +/- 6.3 mmHg to 157.2 +/- 17.6/88.8 +/- 8.7 mmHg. The addition of cicletanine to treatments with beta-blockers, calcium inhibitors and angiotensin-converting enzyme inhibitors normalized BP in 48%, 52% and 47% of patients respectively. A significant reduction of symptoms was noted, notably as regards headache, dizziness, palpitations, lower limb oedema, asthenia, auditory disorders and dyspnoea. The side-effects reported (headache, dizziness, gastralgia, nausea, pruritus) were minor and non-specific; they accounted for the withdrawal of only 8 patients. The only significant, though moderate, biochemical variations observed were decreases in natremia and cholesterolaemia unconfirmed by qualitative analysis. Altogether, cicletanine proved to be effective and well tolerated when administered in combination with other antihypertensive drugs belonging to three main therapeutic classes.
Arch Mal Coeur Vaiss 1989 Nov
PMID:[Antihypertensive effectiveness and tolerance of cicletanine. Results obtained with bitherapy]. 257 67

The antihypertensive effectiveness and the clinical and biochemical safety of cicletanine were evaluated in 84 patients (28 women, 56 men) presenting with permanent essential hypertension without severe cardiovascular complications. The hypertension was insufficiently controlled by a beta-blocker, a centrally acting antihypertensive drug or nifedipine. After 3 months of treatment during which cicletanine was added to each of these three classes of drugs, there was a significant fall of systolic arterial pressure (-18 mmHg with beta-blockers, -17 mmHg with central agents and -26 mmHg with nifedipine) and diastolic arterial pressure (-22, -21 and -28 mmHg respectively), resulting in normalization of blood pressure (less than 160/95 mmHg) in 63%, 43% and 50% respectively of patients in each therapeutic group. The fall of blood pressure was accompanied by a significant decrease of functional symptoms (headache, palpitations, dizziness); in the nifedipine group, the addition of cicletanine resulted in complete regression of anginal attacks. The therapeutic combinations were well tolerated; only two patients were excluded from the study for undesirable effects unascribable to cicletanine. Otherwise, the side-effects observed were minor. The biochemical values measured did not significantly vary, and the variations noted were of small amplitude.
Arch Mal Coeur Vaiss 1989 Nov
PMID:[Cicletanine administered with other antihypertensive agents]. 257 68

The effectiveness and safety of cicletanine hydrochloride, the first representative of the furopyridine family, were evaluated in a 90-day double-blind study involving 120 patients with moderate essential hypertension poorly controlled after at least one month of treatment with a beta-blocker. After a 30-day pre-inclusion period during which a placebo capsule was given together with a stable dose of the beta-blocker, the patients were randomised to one of three therapeutic groups: group 1 (placebo, n = 40), group 2 (cicletanine 50 mg/day, n = 41), group 3 (cicletanine 100 mg/day, n = 39). All three groups were matched in every respect. Eight patients in group I were excluded (5 for ineffectiveness, 2 for unexpected effect, 1 for intercurrent disease) as was 1 patient in group 3 for unexpected effect. On entering the active phase of treatment, supine blood pressures were 171.3 +/- 13.6/103.9 +/- 6.1 mmHg in group 1, 173.5 +/- 12.7/103.6 +/- 5.2 mmHg in group 2 and 171.8 +/- 15.4/104.5 +/- 5.9 mmHg in group 3. A significant (p less than 0.0001) treatment effect on SBP was found in groups 2 and 3 and on DBP in all three groups. The improvement observed in both SBP and DBP was similar in groups 2 and 3 and highly significant when compared with group 1 (p 0.001). At the end of the trial, 5% of group 1 patients, 51.2% of group 2 patients and 74.4% of group 3 patients had normal blood pressure values. The drug was well tolerated clinically and biochemically.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1989 Nov
PMID:[Evaluation of the effectiveness and tolerance of cicletanine in patients with essential hypertension treated with beta-blockers]. 257 69

The aim of this preliminary report is to compare the evaluation of the antihypertensive drug effect, during a controlled trial, using casual measurements and 24 hr B.P. monitoring. 20 patients (16 males, 4 females 55 +/- 10 years old) with primary hypertension (WHO stage I or II) were included with a diastolic blood pressure greater than or equal to 100 mmHg (mean blood pressure from three clinical readings). Casual B.P. and B.P. monitoring (Spacelabs - 4 measurements per hour during a 24 hr period) were established before and after the end of the placebo run in period (one placebo tablet given once daily at 8 h-8 h 30 a.m. for 15 days). Overall sample data: The clinical B.P. decrease (167 +/- 16-109 +/- 7 before and 147 +/- 17-97 +/- 11 after treatment) is higher that the ambulatory B.P. decrease (148 +/- 15-101 +/- 8 before and 138 +/- 21-94 +/- 14 after treatment). Individual patient data: A clinical B.P. decrease (of at least 10 mmHg) was found in 17 patients for systolic B.P. and in 15 patients for diastolic B.P. A significant ambulatory B. P. drop decrease (p less than 0.05) was found in 11 patients for 24 hr systolic and diastolic B.P. The clinical and ambulatory responses to the treatment are in line in 14 patients, but differ in 3 instances. There is a little correlation (for the diastolic B.P.) and no correlation (for the systolic B.P.) between the clinical and the ambulatory B.P. decreases after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Antihypertensive therapeutic effect. Comparison of their evaluation using clinical and ambulatory measurements of arterial pressure. Preliminary study]. 282 46

Circulating digitalis-like compounds have been found elevated in some experimental sodium--and volume--dependent hypertensions, as well as in human essential hypertension. As few studies have been undertaken to assess their enhancement in the genetic hypertension of Okamoto (SHR) we have investigated their presence in plasma using 4 criteria: their apparent immunoreactivity with antidigoxin antibodies, their competition with tritiated ouabain binding to the sodium pump of human red blood cells,-their ability to inhibit the Na+, K+ ATPase activity of rat kidney membranes, and the Na+ fluxes from rat red blood cells. When compared to ordinary Wistar (W) and Wistar Kyoto rats (WKY), SHR exhibited a markedly enhanced apparent immunoreactivity with antidigoxin-antibodies (138 +/- 8; 59 +/- 3; 61 +/- 4 pg/ml, n = 15, 6 et 15, p less than 0.001, and p less than 0.001 respectively). The inhibition of ouabain binding by plasma extracts of the three strains did not differ (10.3 +/- 1.6, 9.9 +/- 1.7 and 12.9 +/- 1.4 ng/ml, n = 9, 18 and 14 respectively). When compared to WKY, SHR plasma extracts inhibited the renal Na+, K+ ATPase activity (75.6 +/- 2.6 vs 89.3 +/- 2.4 mumoles Pi . mg-1 . h-1, n = 11 and 10, p less than 0.01, respectively). When incubated in SHR plasma for one hour, net sodium effluxes from Wistar erythrocytes were inhibited compared to that measured in the presence of W or WKY plasma: (5.91 +/- 0.20 vs 7.68 +/- 0.25 and 7.52 +/- 0.15 mmol/l cells, n = 5, 3 and 5, p less than 0.001, and p less than 0.001 respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Genetic hypertension in the SHR rat and circulating digitalis compounds]. 282 51

Phenylephrine infusions enhance diuresis and natriuresis both in normal subjects and patients with essential hypertension, whereas they have an opposite effect on urinary aldosterone excretion, decreasing it in normal subjects and enhancing it in hypertensive patients. With the new knowledge concerning the atrial natriuretic factor (ANF), it seemed a strong possibility that in normal subjects phenylephrine infusions should exert its effect through the increased release of ANF, as suggested by in vitro studies. Phenylephrine infusions at high pressor dose (to increase diastolic pressure by 25 mmHg) in six healthy volunteers increased plasma ANF and cGMP and decreased plasma renin activity and aldosterone concentrations. Urinary volume, sodium, and cGMP excretion were also increased. Phenylephrine infusions at low pressor dose (to increase diastolic pressure by 12-15 mmHg), in healthy subjects and in five patients with mild essential hypertension, significantly increased plasma ANF concentrations and decreased plasma renin activity to the same degree in both groups. But, whereas in normal subjects plasma aldosterone decreased significantly, it increased in patients with mild essential hypertension despite the simultaneous rise in plasma ANF concentration.
Arch Mal Coeur Vaiss 1988 Jun
PMID:[Effects of phenylephrine on atrial natriuretic factor and the renin-aldosterone axis in normal patients and essential hypertensive patients]. 284 76

The age of patients is an essential factor in the development, duration and severity of hypertension. In essential hypertension there is a change in sympathetic cardiovascular control; during the initial phase, there is an increased response of the beta-adrenergic receptors, i.e. increased cardiac output and plasma renin activity. This response then becomes attenuated and vasoconstriction due to alpha-adrenergic stimulation is observed, accompanied by an increase in intracellular sodium and free calcium. The physiopathological concept of essential hypertension has pharmacotherapeutic implications. In young patients, who often have high renin levels, a better response is observed to monotherapy with betablockers and to treatment with converting enzyme inhibitors. Older patients, who usually have low renins, do not respond as well to betablockers but good results are obtained with calcium antagonists as an alternative to diuretic therapy. Betablockers and calcium antagonists are now the corner store of antihypertensive therapy aimed at protecting the heart.
Arch Mal Coeur Vaiss 1985 Nov
PMID:[Cardiovascular regulation as a function of age. Determinants of antihypertensive treatment based on beta-blockers and calcium inhibitors]. 286


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