Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fenoldopam, a dopamine-1 (D1) agonist, was administered by a 6-h intravenous infusion to patients with refractory hypertension [diastolic blood pressure (DBP) greater than 115 mmHg while on triple therapy] in order to achieve a fall in DBP of 30 mmHg. The evolution of blood pressure, heart rate, glomerular filtration rate (GFR), renal plasma flow (RPF), urine volume, renal excretion of sodium, potassium, chloride, calcium, uric acid, phosphate, plasma renin activity (PRA), aldosterone and prolactin were evaluated. A significant fall in blood pressure (P less than 0.01) accompanied by an increase in heart rate (P less than 0.01) was attained after 30 min. GFR and RPF increased significantly (P less than 0.01) but the filtration fraction fell. Urine volume and urinary output of sodium, potassium, chloride, calcium, uric acid and phosphate increased markedly (P less than 0.01). Meanwhile, plasma potassium fell (P less than 0.01) and the hormonal parameters showed no significant change. We concluded that in refractory hypertension fenoldopam has potent renal and systemic vasodilatory properties through which blood pressure falls. The hypotensive effect of fenoldopam is also facilitated by its marked diuretic and natriuretic properties. The absence of variations of plasma prolactin confirm the D1 selectivity of fenoldopam and the lack of increase in PRA indicates that fenoldopam blocks the renin-angiotensin-aldosterone system.
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PMID:Renal effects of fenoldopam in refractory hypertension. 290 90

Enalapril, an orally-active, long-acting, nonsulphydryl angiotensin-converting enzyme (ACE) inhibitor, is extensively hydrolysed in vivo to enalaprilat, its bioactive form. Bioactivation probably occurs in the liver. Metabolism beyond activation to enalaprilat is not observed in man. Administration with food does not affect the bioavailability of enalapril; excretion of enalapril and enalaprilat is primarily renal. Peak serum enalaprilat concentrations are reached 4 hours post-dose, and the profile is polyphasic with a prolonged terminal half-life (greater than 30 hours) due to the binding of enalaprilat to ACE. Steady-state is achieved by the fourth daily dose, with no evidence of accumulation. The effective accumulation half-life following multiple dosing is 11 hours. Higher serum concentrations and delayed urinary excretion occur in patients with severe renal insufficiency. Enalapril reduces blood pressure in hypertensive patients by decreasing systemic vascular resistance. The blood pressure reduction is not accompanied by an increase in heart rate. Furthermore, cardiac output is slightly increased and cardiovascular reflexes are not impaired. Once- and twice-daily dosage regimens reduce blood pressure to a similar extent. Enalapril increases renal blood flow and decreases renal vascular resistance. Enalapril also augments the glomerular filtration rate in patients with a glomerular filtration rate less than 80 ml/min. Enalapril reduces left ventricular mass, and does not affect cardiac function or myocardial perfusion during exercise. There is no rebound hypertension after enalapril therapy is stopped. Enalapril does not produce hypokalaemia, hyperglycaemia, hyperuricaemia or hypercholesterolaemia. When combined with hydrochlorothiazide, enalapril attenuates the undesirable diuretic-induced metabolic changes. Therapeutic doses of enalapril do not affect serum prolactin and plasma cortisol in healthy volunteers or T3, rT3, T4 and TSH in hypertensive patients. Enalapril has natriuretic and uricosuric properties. The antihypertensive effect of enalapril is potentiated by hydrochlorothiazide, timolol and methyldopa, but unaffected by indomethacin and sulindac. No interactions occur between enalapril and frusemide, hydrochlorothiazide, digoxin and warfarin. The bioavailability of enalapril is slightly reduced when propranolol is coadministered, but this does not appear to be of any clinical significance. Enalapril increases cardiac output and stroke volume and decreases pulmonary capillary wedge pressure in patients with congestive heart failure refractory to conventional treatment with digitalis and diuretics.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enalapril: a review of human pharmacology. 299 84

The effect of short-term (6 weeks) and long-term (7 years) guanfacine treatment on some metabolic and endocrine parameters was studied in patients with moderate hypertension. Short-term treatment decreased blood pressure and heart rate, and also produced a significant fall in urinary excretion of noradrenalin and prolactin. Long-term treatment, in addition, produced a progressive decrease in prolactin, total cholesterol and triglyceride levels, but did not change growth hormone levels and oral glucose tolerance test. The decreased mortality and morbidity which was observed under guanfacine treatment may depend not only on important antihypertensive activity of guanfacine, but also on its beneficial effect on known cardiovascular risk factors.
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PMID:Prolactin, renin, growth hormone, lipoproteins and glucose under guanfacine treatment. 311 90

In order to elucidate the mechanism of pregnancy-induced hypertension (PIH) from the point of view of vascular resistance, we measured the intracellular Na+ concentrations and the membrane Na+ effluxes using red blood cells from normal pregnant females and patients with PIH. We also discussed the influences of hormones such as estrogen, progesterone, dehydroepiandrosterone sulfate (DHAS), hydrocortisol, human placental lactogen (hPL), human chorionic gonadotropin (hCG), and prolactin and parathyroid hormone (PTH) on the membrane Na+ effluxes. The intracellular Na+ concentrations were lower and the Na+-K+-ATPase activities were slightly higher both in the luteal phase and in the first trimester of normal pregnancy than those in the follicular phase, after which the former gradually increased and the latter gradually decreased until term to the mean values of those in the whole menstrual period. In mild PIH, the intracellular Na+ concentrations were not significantly increased, and the Na+-K+-ATPase activities were significantly increased compared to those in the third trimester of normal pregnancy, which suggests the compensatory increase of the Na+-K+-ATPase activities as opposed to the increase of the intracellular Na+ concentrations. In severe PIH, the intracellular Na+ concentrations were significantly increased compared with those in the third trimester of normal pregnancy and slightly increased compared with those in mild PIH, whereas the Na+-K+-ATPase activities were slightly decreased compared with those in mild PIH, which indicates a breakdown of the compensatory increase of the Na+-K+-ATPase activities. The intracellular Na+ concentrations in PIH are significantly correlated to diastolic pressure, systolic pressure and mean blood pressure. When the male red blood cells were incubated with the hormone, dose-dependently the Na+-K+-ATPase activities were significantly elevated by hydrocortisol and slightly elevated by progesterone and hPL, and they were significantly depressed by estrogen and prolactin and slightly depressed by PTH. These results suggest that the peripheral vascular resistance might be increased in the third trimester of normal pregnancy compared with that in the first trimester because the intracellular Na+ concentrations were elevated, and the Na+-K+-ATPase activities in the cell membrane were decreased along the course of pregnancy as a result of the effects of various hormones in the maternal blood.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A study on the membrane Na+ efflux of pregnancy-induced hypertension (PIH)]. 320 19

Cyclosporin is a potent, widely used specific immunosuppressive agent which affects T-helper cells, and has little myelotoxicity. Its pharmacokinetics are complex and many of its actions remain poorly understood. Numerous side effects have been reported, affecting most organs. Most troublesome have been renal injury, systemic hypertension and vascular changes. Oral use is more effective than intramuscular and safer than the intravenous route. Interactions with other drugs include those which affect hepatic metabolism and those which reduce clearance. Aminoglycosides, macrolide antibiotics, imidazole derivatives, calcium channel blockers, sulphonamides and steroids are included in such interactions. Other metabolic effects of cyclosporin are more subtle and include hyperchloraemic alkalosis, changes in serum potassium and magnesium and effects on testosterone and prolactin levels. Acute poisoning with cyclosporin has been reported, again without myelosuppression. Cyclosporin is an important agent with multisystem toxicity, which requires precise monitoring of drug concentrations, liver and renal function, haemoglobin levels and plasma electrolytes. Cyclosporin pharmacodynamics and interactions with other drugs need to be carefully considered if lower rates of toxicity are to be achieved.
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PMID:Adverse reactions and interactions of cyclosporin. 328 88

A personal series of 256 cases of acromegaly/gigantism seen over a 20-year period from 1963 is described. The insidious nature of the condition resulted in delay in diagnosis which was often made by a doctor when seeing the patient for an unrelated problem. Other features which commonly led to the diagnosis being made were headache, change in appearance, carpal tunnel syndrome, amenorrhoea and diabetes. The Hardy system for grading the radiological appearance of the pituitary tumour was used. Widely invasive tumours were not common but tended to occur in patients with younger age of onset and high GH levels. The occurrence of various symptoms and clinical features was noted and the changes resulting from reducing the GH level to normal. The incidence of hypertension, but not of coronary artery disease, is increased and the blood pressure may be reduced following successful treatment. The effects on the upper and lower respiratory tract are reported as well as sleep apnoea and problems associated with anaesthesia. Skin manifestations included sweating, pigmented skin tags, acanthosis nigricans and cutis verticis gyrata. In the skeletal system the incidence of kyphoscoliosis and osteoarthritis especially of the hip is reported: the question of hip replacement is discussed. Diabetes mellitus disappeared in most cases if the acromegaly was cured. In men but not in women the incidence of colloid nodular goitre was increased as was hyperthyroidism in middle-aged women. In two patients a parathyroid adenoma was present: hypercalcaemia was present in five additional patients, but the cause was not determined. The common occurrence of amenorrhoea in the younger women was noted, it was not always associated with hyperprolactinaemia, and often responded to successful treatment of the acromegaly. The association of acromegaly with hirsutism and galactorrhoea is confirmed. The incidence of impotence and loss of libid in the men is discussed: in a proportion of those in whom the acromegaly was cured, potency returned, but in a number depression occurred and what was believed to be psychogenic impotence persisted. Hyperprolactinaemia was found in 49 out of 151 patients with active acromegaly in whom the prolactin level was measured. Previous reports have indicated a doubling of death rates in acromegalics. In this series there were 47 deaths observed compared to 37.2 expected. The increased death rate was in women of all ages and in men under the age of 55, The increased deaths in the women were from cardiovascular and cerebrovascular causes and from breast cancer.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acromegaly. 330 90

A sample of 73 men and women aged 22-63 years and working in six different occupations (air traffic controllers, waiters, physicians, symphony orchestra musicians, baggage handlers, and airplane mechanics) participated in a longitudinal study four times during a year. The spontaneous variations in job strain (determined as the self-reported ratio between psychological demands and decision latitude) were substantial. The average difference between the occasion with the highest level of strain and the occasion with the lowest level was 25% of the total mean. Systolic blood pressure during workhours, as well as self-reported sleep disturbance, increased when demands increased in relation to decision latitude. Among men with a depressive tendency (according to a diary) morning plasma prolactin levels increased markedly with increasing job strain. Among subjects with a positive family history of hypertension the increase in systolic blood pressure at work was particularly pronounced, and among the men in this group a lower than expected level of morning cortisol was found measured during the period with the highest level of strain.
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PMID:Changes in job strain in relation to changes in physiological state. A longitudinal study. 339 55

Prolactin may play an important role in the pathogenesis of pregnancy-induced hypertension (PIH) and preeclampsia. In 105 normotensive nulliparous women at 28 to 32 weeks of gestation, the relationship between serum prolactin concentration (PRL) and blood pressure behaviour was examined under standardized conditions. Neither postural change from left lateral to supine recumbency nor the infusion of low doses of angiotensin-II-amide had an effect on PRL levels. Similar mean PRL levels were found in pregnant women with a low angiotensin pressor dose (ADP less than 10 ng x kg-1 x min-1) or "angiotensin sensitivity", a positive supine pressor response (delta pd greater than or equal to 20 mmHg) or an increased serum uric acid concentration (greater than 3.6 mg/dl), which are criteria for an increased risk of developing hypertensive complications. However, in the group of subjects with angiotensin sensitivity, a significant correlation was found (a) between PRL levels and the APD and (b) between PRL levels and diastolic blood pressure increase after 5 min of supine recumbency. These results may reflect diminished dopaminergic activity in the central nervous system, which could influence both blood pressure and prolactin secretion.
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PMID:Relationship between serum prolactin concentration, vascular angiotensin sensitivity and arterial blood pressure during third trimester pregnancy. 340 Oct 43

Pituitary cell reaggregates from 14-day-old and adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were cultured in serum-free, chemically defined medium supplemented with the thyroid hormone triiodothyronine and the glucocorticoid dexamethasone. After 1 wk in culture, aggregates were transferred into a perifusion system, and the effect of angiotensin II (ANG II) on prolactin (PRL) and growth hormone (GH) release was studied. In aggregates from adult SHR, ANG II displayed a significant and dose-dependent GH releasing activity, whereas a negligible effect or no effect was seen in aggregates from adult WKY. In contrast, no difference in the stimulation of PRL release by ANG II was found. To exclude the possibility that the enhanced GH responsiveness was secondary to longstanding hypertension, aggregates from animals in the prehypertensive stage were studied. Both the GH and PRL responses to ANG II were significantly higher in aggregates from 14-day-old SHR than in aggregates from 14-day-old WKY. These data indicate that abnormal GH and PRL responses to ANG II exist in pituitary cell aggregates from SHR long before hypertension develops. Because these differences were found in pituitary cells maintained in culture for 1 wk, they do not seem to be secondary to changes in brain regulation of pituitary function but rather are caused by factors intrinsic to the pituitary.
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PMID:Enhanced ANG II activity in anterior pituitary cell aggregates from hypertensive rats. 341 35

Ketanserin, a serotonin-2-receptor antagonist, was administered to 12 subjects with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 6 weeks of ketanserin (40 mg every 12 hours), blood pressures measured 12 hours after dosing were not significantly different from those obtained after placebo. However, 2 hours after ketanserin administration, supine systolic and diastolic blood pressures declined 11 +/- 10 mm Hg (P less than 0.01) and 6 +/- 5 mm Hg (P less than 0.005) from predose values, whereas placebo caused no change in either systolic or diastolic blood pressure. Except for a slight decline in serum prolactin levels 12 hours after dosing with ketanserin, no changes were observed in pituitary hormone levels, serum testosterone, plasma catecholamines, plasma renin activity, aldosterone, or lipoproteins. Stroke volume, measured 2 hours after dosing, increased with ketanserin therapy, but cardiac output, systemic resistance, and heart rate were unchanged. Ketanserin has a moderate antihypertensive effect and neutral metabolic-hormonal profile when used as monotherapy for the treatment of hypertension. However, further studies are needed to define the frequency of dosing that will provide 24 hours of antihypertensive activity.
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PMID:Metabolic and hemodynamic effects of antihypertensive treatment with ketanserin. 341 1


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