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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The central and peripheral haemodynamic effects of the administration of 10 mg nifedipine sublingually in 6 patients with essential hypertension were compared with those observed after the administration of one 20 mg slow release tablet of nifedipine in 7 other hypertensive patients of the same age. The circulatory effects in the forearm were studied by pulsed Doppler velocimetry which allowed simultaneous measurement of the diameter of the brachial artery and of the velocity of blood flow. Both forms of administration significantly reduced the blood pressure by a significant reduction in total peripheral resistance. This reduction in total peripheral resistance was more significant (p less than 0.001 vs p less than 0.01) and more rapid with sublingual administration and was associated with a greater increase in heart rate and cardiac output. Both forms of administration induced an increase in brachial arterial blood flow due to a simultaneous increase in vessel calibre and velocity of blood flow. The results of this study show that both forms of administration act directly on the vessel wall of the arterioles and great arteries leading to a fall in blood pressure associated with an increase in peripheral blood flow. Sublingual nifedipine would seem to be the drug of choice for the treatment of hypertensive crises, whilst the slow release preparation with its lesser baroreflex stimulation would appear better suited for the long-germ treatment of essential hypertension.
Arch Mal Coeur Vaiss 1985 Nov
PMID:[Central and peripheral hemodynamic effects of nifedipine administered orally and sublingually in essential arterial hypertension]. 393 4

Nine patients with untreated essential hypertension (random blood pressure 173/109 +/- 14/7 mmHg) were studied before and after 16 weeks' treatment with oral nifedipine 10 mg three times a day. Direct continuous measurement of the systolic and diastolic blood pressures showed that both values were significantly reduced during the 24 hour period. Nifedipine did not change the variability of the blood pressure. There was no significant change in the heart rate after treatment with nifedipine. Long-term nifedipine induced an increase in blood flow in the forearm and decreased the vascular resistances which confirmed the vasodilator effects of the drug. The absolute responses of the blood pressure during postural changes, the hand grip test and cold pressor test were reduced but the treatment did not change the percentage increase in blood pressure during these tests. Long-term nifedipine therapy did not affect the plasma renin activity. The sensitivity and characteristics of the baroreflex response to intravenous phenylephrine were measured. After long-term nifedipine therapy we observed a normalisation of the sino-aortic baroreflex and an increase in its sensitivity. Normalisation of the blood pressure by nifedipine induced a significant reduction in the index of left ventricular mass.
Arch Mal Coeur Vaiss 1985 Nov
PMID:[Effect of nifedipine on arterial pressure and control of the cardiac reflex]. 393 5

A controlled multicentre trial was organised to compare the effects of 20 mg Nifedipine tablets (N) and 2,5 mg Indapamide tablets (I) during a 4 months' treatment period after a placebo period, in 59 patients with moderate essential hypertension (n = 59). The results of blood pressure measurements of 18 patients treated by nifedipine (1 tablet twice daily) and 22 patients treated by indapamide (1 tablet every morning) were compared. The systolic blood pressure, after 10 minutes recumbency, fell from 165 +/- 10 mmHg to 148 +/- 13 mmHg (p less than 0.01), and the diastolic pressure from 104 +/- 6 mmHg to 86 +/- 7 mmHg (p less than 0.01) in the patients treated with nifedipine. In the indapamide group, the SBP fell from 164 +/- 13 mmHg to 152 +/- 15 mmHg (p less than 0.01) and the DBP from 100 +/- 4 mmHg to 87 +/- 6 mmHg (p less than 0.01). There were no significant changes of heart rate with either drug; plasma creatinine, potassium and uric acid concentrations were also unchanged. There was a higher incidence of headaches and tiredness in the nifedipine group, whilst patients treated with indapamide complained more often of muscular cramps. Flushing was observed in nearly a quarter of the patients in both groups. These results confirm that both nifedipine and indapamide induce significant and persistant falls in systolic and diastolic blood pressure. Although the fall was greater with nifedipine than with indapamide, the difference was not statistically significant. The tolerance was satisfactory in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1985 Nov
PMID:[Comparative effects of nifedipine and indapamide in the treatment of arterial hypertension]. 393 9

Recent studies have suggested a role for adrenaline in the pathogenesis of essential hypertension. In the present study, the effects of several anti-hypertensive agents were compared in normal (plasma adrenaline concentration: 0.267 + 0.040 ng/ml) and adrenomedullectomised (plasma adrenaline concentration: 0.063 + 0.011 ng/ml; p less than 0.01) dogs. The hypotensive and tachycardic effects of phentolamine (1.5 mg/kg i.v.) or dihydralazine (1 mg/kg i.v.) were the same in the two groups of dogs. Verapamil (0.2 mg/kg i.v.)-induced hypotension was less pronounced in dogs without adrenal medulla. In these adrenomedullectomised dogs, clonidine (10 micrograms/kg i.v. or 1 microgram/kg i.c.) elicited tachycardia and its hypotensive properties were delayed. In dogs with neurogenic hypertension, the antihypertensive properties of propranolol (1 mg/kg i.v.) remained unchanged. These results show the importance of adrenal medulla in the antihypertensive action of clonidine, or verapamil. These agents (but not dihydralazine, propranolol or phentolamine) could reduce adrenaline secretion from the adrenal medulla.
Arch Mal Coeur Vaiss 1985 Oct
PMID:[Role of the adrenal medulla in the effect of antihypertensive drugs]. 393 35

Cytosolic free Ca2+ concentrations were measured in platelets from hypertensive and normotensive humans and rats with the use of the fluorescent indicator Quin-2/AM. Without external Ca2+ added, no difference was observed between platelets of hypertensive patients and those normotensive subjects or between platelets of spontaneously hypertensive rats and those of the normotensive Wistar Kyoto and regular Wistar rats. In the presence of 0.5-1 mM external Ca2+, the cytosolic free Ca2+ concentrations were higher both in patients with essential hypertension and rats with genetic hypertension than in their respective normotensive controls. These results suggest that primary hypertension is accompanied by a disequilibrium between cellular Ca2+ influx, storage and extrusion. Such a characteristic if present in other excitable cells and in particular in vascular smooth muscle cells may play a major role in the rise of peripheral resistances.
Arch Mal Coeur Vaiss 1985 Oct
PMID:[Elevation of intraplatelet free Ca2+ in primary hypertension in man and the rat]. 393 48

We have studied the renin aldosterone system and plasma catecholamines in 26 untreated patients with phaeochromocytoma, 21 untreated patients with primary hypertension, and in 10 normal volunteers. Blood pressure (mmHg), plasma renin activity (radioimmunoassay of angiotensin I, ng/ml/h), plasma concentrations of aldosterone (direct radioimmuno-assay, pg/ml), adrenaline and noradrenaline (radioenzymatic assay with catechol-O-methyl transferase, pg/ml) were measured after 1 h of supine rest, 5 mn upright and after walking 1 h. Seven patients with phaeochromocytoma were subsequently given 400 mg acebutolol bid for 3 days, and five were given 1 mg/kg captopril. Supine renin activity was higher in phaeochromocytoma than in primary hypertension and in volunteers (average 2.54, 1.03 and 0.85, F = 7.1, p less than .01) and rose higher after walking (mean increase 3.84, 1.19 and 0.68 respectively, F = 6.3, p less than .01). Aldosterone was higher after walking in phaeochromocytoma than in primary hypertension (534 vs 275 pg/ml, p = .03). Differences in renin and aldosterone could not be explained by age, natriuresis or plasma volume. Catecholamines were as expected much higher in phaeochromocytoma than in the other two groups (p less than .01). At variance with primary hypertensive and normal volunteers, renin was tightly correlated with noradrenaline in patients with phaeochromocytoma (r' = .54, r' = .60, and r' = .74 in supine position, after standing and after walking 1 h, p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1985 Oct
PMID:[Plasma renin and catecholamine activity in pheochromocytoma]. 393 49

The presence of a circulating Na+ pump inhibitor has been assessed in 112 subjects by studying the effects of deproteinized plasma on ouabain binding to erythrocytes and/or inhibition of Na+-K+-ATPase activity. High levels of an inhibitor possessing some digitalis-like properties, were associated with essential hypertension, hypertensive heredity, treatment of hypertension with beta-blocking agents and high sodium intake. Low levels were found in hypertensives on diuretics, patients with chronic renal failure and normotensive controls. These observations are consistent with a possible role of this circulating inhibitor in the control of sodium balance and in hypertension.
Arch Mal Coeur Vaiss 1984 Oct
PMID:[Circulating inhibitor of the Na+-K+ pump in essential hypertension. Physiological and pharmacological variations]. 609 38

Much experimental and clinical evidence points to the fact that increased intracellular Na+ concentration could play an important pathogenic role in hypertension, especially where cells of excitable tissues are concerned. Active extrusion of Na+ (from the cells to the extracellular space) depends mainly on the activity of the system of membrane transport known as the Na+ pump. The extrusion of Na+ occurs in exchange for K+ and the activity of the pump depends on the enzyme Na+-K+-ATPase. The Na+ pump is inhibited by cardiotonic glycosides such as digitalis and ouabain . The results obtained in our laboratory suggest that the activity of the Na+ pump is controlled by an endogenic system acting in a similar manner to ouabain and digitalis. Experimental and clinical studies show: -- that the administration of Na+ increases the inhibitor effect both in urine and plasma; -- that the inhibitor is increased in about 50 p. 100 of patients with essential hypertension; -- that this increase seems to depend on familial or genetic factors. The biochemical identification of this endogenic inhibitor is now under way; it has a small molecular weight (less than 3000), is thermostable and anionic. This factor could have both a regulating role on Na+ turnover and a pathological role in hypertension. Its activity comes into competition cations also capable of inhibiting the Na+ pump, including K+.
Arch Mal Coeur Vaiss 1984 Apr
PMID:[Essential arterial hypertension, cellular intolerance to sodium]. 632 20

The renin-aldosterone system contributes to the regulation of arterial pressure and to the maintenance of sodium and potassium balance. Alterations in plasma potassium concentration have opposite and independent effects on renin secretion by the kidney and on aldosterone secretion by the adrenal gland. Renin secretion tends to be inhibited by hyperkalemia and stimulated by potassium depletion. In contrast, increases of plasma potassium directly stimulate aldosterone secretion. This effect of potassium on aldosterone serves as a protective mechanism against the development of hyperkalemia. Conversely, hypokalemia inhibits aldosterone production. Small changes in plasma potassium have a greater effect on aldosterone than on renin secretion. In patients with essential hypertension, diuretic induced alterations in serum potassium concentrations may affect both renin and aldosterone secretion. We have observed that therapy with a thiazide diuretic results in a reduction of serum potassium and a greater increase in renin activity than therapy with the potassium-retaining diuretic, spironolactone, despite comparable natriuretic responses with both drugs. Conversely spironolactone therapy is associated with a greater increase in aldosterone production. The greater effect of thiazides on renin activity and the greater effect of spironolactone on aldosterone production may be related to the thiazide induced reduction of serum potassium and the spironolactone induced increases of serum potassium.
Arch Mal Coeur Vaiss 1984 Apr
PMID:[Effects of potassium on renin and aldosterone]. 642 66

23 unselected patients with mild to moderate essential hypertension, whose average supine blood pressure after two months' observation on no treatment was 154/99 mm Hg, were entered into an eight week double blind randomised crossover study of one month's treatment with slow release potassium tablets (60 mmol/day) versus placebo without alteration of dietary sodium or potassium intake. By the fourth week mean supine blood pressure had fallen by 4% on potassium supplementation compared with placebo. Urinary potassium excretion increased from 62 +/- 4.7 mmol/24 h on placebo to 118 +/- 7.4 mmol/24 h on potassium. The fall in blood pressure was not related to urinary sodium excretion before entry to the trial or while on placebo. Moderate potassium supplementation caused a small but significant fall in blood pressure in patients with mild to moderate essential hypertension and could be additive to the effects of moderate sodium restriction. This increase in potassium intake could be achieved with a potassium-based salt substitute and a moderate increase in vegetable and fruit consumption. Moderate dietary sodium restriction with dietary potassium supplementation may obviate or reduce the need for drug treatment in some patients with mild to moderate hypertension.
Arch Mal Coeur Vaiss 1984 Apr
PMID:[Moderate supplementation of potassium in essential hypertension]. 642 68


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