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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of the study of depressor (PGE+A) and pressor (PGF2 alpha) prostaglandins in the blood plasma and of PGE2 and PGF2 alpha excretion in the urine of 52 patients with an acute stage of Itsenko-Cushing disease are presented. It has been established that the different components of the PG system have dissimilar changes: the absence of differences in the content of depressor and significant increase in pressor PG, which may be the cause of hypertension in Itsenko-Cushing disease. Stress due to insulin hypoglycemia and furosemide load brought about disturbances in the reaction of the PG system, which were more pronounced in the system pressor component. Disturbances of the PG system which were more pronounced in the presence of stable hypertension were established in all patients.
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PMID:[Prostaglandins in Itsenko-Cushing syndrome]. 277 63

Hypertension, common in diabetic patients, worsens not only the risk of cardiovascular complications, but also that of microangiopathic complications (nephropathy, retinopathy) of diabetes mellitus. It is thus important to ensure the perfect control of even mild hypertension in diabetic patients. However, treatment sometimes becomes difficult given that certain categories of antihypertensive drugs interfere with blood glucose control and/or lipid metabolism, interfere with the symptomatology of hypoglycemia, or promote orthostatic hypotension, a complication of autonomic neuropathy. A study was undertaken to determine the effects of rilmenidine, administered for 16 weeks, in 29 diabetic patients treated with insulin and experiencing mild-to-moderate hypertension (supine diastolic blood pressure, 96.7 +/- 0.5 mmHg). Administered as single-drug therapy, rilmenidine rapidly normalized blood pressure (systolic blood pressure, less than 160 mmHg; diastolic blood pressure, no more than 90 mmHg--supine) in 17 patients; this persisted throughout the trial period. Addition of a diuretic after 12 weeks in the remaining 12 patients led to normalization of blood pressure in nine additional patients. Blood glucose control (evaluated at home by weekly blood glucose measurements and by glycosylated hemoglobin levels) was unaffected by treatment. Plasma levels of cholesterol (total, high-density lipoprotein and low-density lipoprotein), triglycerides and proteinuria (or microalbuminuria) showed no change during the course of the trial. In conclusion, rilmenidine offers an effective and safe treatment for mild-to-moderate hypertension in diabetic patients treated with insulin and does not interfere with their blood glucose control.
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PMID:Treatment of hypertension in diabetic patients. 278 24

Beta-adrenoceptor blockade (beta-blocker) has recently been introduced for use in treating hypertension of pregnancy. The aim of this investigation is to determine the effects of beta-blocker (alprenolol and labetalol) on parturition and on the fetal cardiovascular and metabolic system in normotensive pregnant rats. The continuous administration of alprenolol to pregnant Wistar rats revealed the following: a small placenta intrauterine growth retardation delayed parturition intrauterine death (21.8%) morbidity (30.3%) and, hypoglycemia of neonates. In the cases which received the administration of both labetalol and alprenolol, the growth of fetuses was retarded. However, there was twice as much growth retardation of the fetuses treated with alprenolol. No other abnormalities were observed. The administration of alprenolol in pregnant rat uteri (in vitro) resulted in stimulation of myometrial contractility (oxytocic reaction) and lowered the c-AMP levels in the bath medium. However, when labetalol was administered, uterine activity was reduced in a dose-dependent manner (tocolytic reaction) with a concurrent rise in c-AMP levels in the bath medium. The effect of alprenolol on rat uterine blood flow using the thermocouple method resulted in a decrease of 18-30 percent but with labetalol there was only a slight decrease (0-5%).
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PMID:[Effects of beta-adrenoceptor blockade on parturition and fetal cardiovascular and metabolic system]. 286 Jan 90

Hypertension in diabetic patients is more common than in controls, contributes substantially to their increased cardiovascular morbidity and mortality, and should be treated as accurately as diabetes mellitus itself. After appropriate exclusion of secondary forms, the first therapeutic step consists of reduction of overweight, salt intake, and smoking; the omission of interfering drugs; and adequate instruction. Step 2 has usually been the prescription of a diuretic drug, in spite of its known side effects on carbohydrate and lipid metabolism. A new possible alternative may be a calcium antagonist. Results in 10 hypertensive diabetic persons suggest that at a dose that normalizes blood pressure, neither carbohydrate nor lipid metabolism is altered, uric acid decreases, the exaggerated cardiovascular reactivity toward norepinephrine becomes normal, and the pressor dose for angiotensin II tends to rise. Body weight, blood volume, exchangeable sodium, as well as plasma and urinary sodium, potassium, and creatinine levels were unchanged. The third therapeutic step is the addition of a cardioselective beta blocker in a moderate dose. This avoids the disadvantages of beta 2-adrenergic blockade such as decreased insulin output, prolonged hypoglycemia, diminished glucagon secretion, and increased vasospasticity during hypoglycemic states, as well as aggravation of peripheral vascular disease. Alternatives are other sympatholytics with their known tendency to cause or increase orthostatic and sexual problems or, again, a calcium antagonist. In step 4, a hydralazine-type drug or prazosine is added. The fifth step, which adds minoxidil or captopril to the previous drugs, should only be taken after a specialist reevaluates the overall situation.
Hypertension
PMID:Antihypertensive therapy in diabetic patients. 286 38

Many antihypertensive drugs have adverse effects on glycemic control when they are used in diabetic patients. This was noted for thiazide diuretics in 1960, and the mechanism of the effects remains uncertain. Indirect evidence suggests that changes in the serum potassium are at least contributory, although the principal mechanism of thiazide-induced hyperglycemia is probably a reduction in the insulin response to glucose. Beta blockers also adversely affect blood sugar control but only by a small margin. The main cause for concern with beta blockers, however, is their effect during hypoglycemia in which nonselective agents delay blood sugar recovery. In diabetic patients, the institution of antihypertensive therapy should be followed by a reassessment to note any changes in sugar, potassium, and lipids, or side effects.
Hypertension
PMID:Glucose tolerance during antihypertensive therapy in patients with diabetes mellitus. 286 40

Adverse effects of beta-adrenergic receptor blocking drugs can be divided into two categories: 1) those that result from known pharmacological consequences of beta-adrenergic receptor blockade; and 2) other reactions that do not appear to result from beta-adrenergic receptor blockade. Adverse effects of the first type include bronchospasm, heart failure, prolonged hypoglycemia, bradycardia, heart block, intermittent claudication, and Raynaud's phenomenon. Neurological reactions include depression, fatigue, and nightmares. It is not yet proven whether the beta 1-selective adrenergic blockers or those with partial agonist activity reduce the overall frequency of adverse reactions seen with propranolol. Patient age does not appear, in itself, to be associated with more beta-blocker side effects. Side effects of the second category are rare. They include an unusual oculomucocutaneous reaction and the possibility of oncogenesis. There are also many drugs that interact with beta-blockers, which may increase toxicity. Finally, there are specific patient characteristics where one beta-blocker may be more effective and safer than another.
Hypertension 1988 Mar
PMID:Beta-adrenergic receptor blockers. Adverse effects and drug interactions. 289 72

The effects of beta-blockers administered to mothers with arterial hypertension were investigated in 38 neonates of varying gestational age and weight. During the first 48 hours of extra-uterine life, heart rate was continuously monitored and blood pressure and glycaemia were measured every 3 hours. Left ventricular function was studied by echocardiography on the first day post-partum, once again between the 5th and 10th days. Hypoglycaemia was observed in 42% of the neonates; 47% had one or several episodes of bradycardia and 2 had arterial hypotension. Most important, a significant improvement of left ventricular function was observed between the first and the 5th-10th days. This time-related change was not found in a control group. The cardiac dysfunction was more pronounced in neonates who had an episode of bradycardia, and although it is usually asymptomatic, it probably accounts for the fortunately rare cardiovascular collapses observed in some newborn babies.
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PMID:[Metabolic and cardiovascular effects of beta-blockers taken by the mother in newborn infants]. 289 60

beta-Blocking therapy is used extensively is conditions as diverse as hypertension, angina pectoris, arrhythmias, thyrotoxicosis, hypertrophic cardiomyopathy, migraine, glaucoma, and myocardial infarction. Studies show they beneficially influence sinus node and atrioventricular conduction, but excessively high doses may cause sinus arrest or sinoatrial block. Nonselective beta-blockade in asthmatic patients may aggravate bronchoconstriction, whereas increased airways resistance is less likely with beta 1-selective, partial agonist, or alpha-beta-blocking drugs. Hypoglycemia can be prolonged; beta 1-selective or partial agonist drugs may cause less interference with glucose metabolism. beta-Blockade affects free fatty acids, lipids and lipoproteins, thyroid hormones, and parathormone. beta-Blockade may normalize abnormal platelet aggregation. Finally, the choice of the most effective drug depends on the clinician's knowledge of the various pharmacodynamic and pharmacokinetic drug profiles, allied with familiarity of the patient's medical condition.
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PMID:Circulatory and metabolic aspects of beta-adrenoceptor blockade. 290 49

Pharmacological treatment of hypertension can, cause clinically significant alterations in endocrine function and glucose homeostasis. The aim of this study was to investigate the antihypertensive efficacy and the influence on carbohydrate metabolism of carvedilol and metoprolol in non-insulin-dependent diabetics with mild to moderate hypertension. The patients received either carvedilol 25mg twice daily or metoprolol 50mg twice daily for a period of 4 weeks; if diastolic blood pressure was over 90mm Hg at this time, the dosage was doubled for the subsequent 4 weeks. 49 of 89 enrolled patients completed the trial according to the protocol and were statistically evaluated. After 4 weeks of carvedilol treatment, 23 of 25 patients (92%) showed a good response to therapy (reduction of diastolic blood pressure below 90mm Hg). Doubling of dosage in the carvedilol group did not further increase the response rate after another month of treatment. The response rate after 4 and 8 weeks of metroprolol treatment was 79 and 83%, respectively. In both treatment groups, blood glucose concentrations were maintained within narrow limits. Glycated haemoglobin A1, which provides a profile of the mean blood glucose levels present during the preceding weeks, also remained unchanged. Oral antidiabetic medication taken by the patient remained constant and no hypoglycaemia was reported. When used in therapeutic doses in non-insulin-dependent diabetics, carvedilol is thus unlikely to cause a deterioration of carbohydrate metabolism.
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PMID:Influence of carvedilol on blood glucose and glycohaemoglobin A1 in non-insulin-dependent diabetics. 290

In a single blind randomized study the effects of a 4-week administration of propranolol (160 mg/day) and penbutolol (40 mg/day) on metabolic control and insulin-induced hypoglycemia were tested in 8 non-insulin-dependent diabetics with diastolic blood pressure between 95 and 110 mmHg. The recovery from hypoglycemia was not delayed by either drug; hypoglycemic nadir and Conard's K did not change significantly. Symptoms of hypoglycemia were inhibited to a lesser extent and pulse rate decrease was lower after penbutolol vs baseline (65 +/- 2.4 vs 77 +/- 2.4 beats/min, p less than 0.01) than after propranolol vs baseline (61 +/- 1.06 vs 77 +/- 2.4 beats/min p less than 0.001). Both drugs produced similar and significant effects on blood pressure both systolic and diastolic. There were no significant effects on fasting plasma glucose concentration, HbA1c, IRI, urinary C-peptide, triglycerides, total and HDL cholesterol and FFA. IRG decreased after penbutolol vs baseline 60 min after insulin injection (170 +/- 30.8 vs 125 +/- 15.4 pmol/l, p less than 0.05). These results indicate that the use of beta-blockers, in particular penbutolol, for mild to moderate hypertension may be considered the treatment of choice also in non-insulin-dependent diabetics at the therapeutic doses employed.
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PMID:Beta-blockers in hypertensive non-insulin-dependent diabetics: comparison between penbutolol and propranolol on metabolic control and response to insulin-induced hypoglycemia. 306 86


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