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

A randomised double-blind crossover trial was done to assess the efficacy of chlorothiazide as an antihypertensive drug in patients with severe renal failure. There was a significant reduction in standing (mean drop 13/6 mm Hg) and supine (mean drop 13/5 mm Hg) blood-pressure, without postural hypotension. Chlorothiazide has a place in the management of hypertension in patients with severe renal failure and its antihypertensive effect is probably due to a change in peripheral vascular resistance and not to volume contraction.
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PMID:Double-blind trial of antihypertensive effect of chlorothiazide in severe renal failure. 9 80

1. In plasma samples from normal subjects and patients with untreated essential hypertension, the concentration of inactive renin (as measured after acidification) was on average 4-5 times higher than the concentration of active renin (as measured without acidification).2. Plasma angiotensin II concentration was correlated to active renin but not to inactive renin. 3. A hyperacute stimulation induced by infusion of saralasin resulted in a marked rise of active renin, whereas inactive renin remained unchanged. 4. An acute stimulation induced by frusemide and ambulation led to a considerable rise in active renin and a slight, but significant, rise of inactive renin. 5. Stimulation with oral thiazide over 5 days induced a seven-fold rise of active renin, with a doubling of inactive renin. Thiazide treatment for 3 months led to a four-fold rise of active renin and a three-fold rise of inactive renin. 6. There was no difference between the concentrations of inactive renin in systemic plasma, ipsilateral and contralateral renal venous plasma in 12 patients with renovascular hypertension, neither before nor after infusion of saralasin with the associated fall in blood pressure. 7. We conclude that the time constants pertinent to secretion or release of active and inactive renin in man are of different orders of magnitude.
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PMID:Different secretion patterns of active and inactive renin in man. 28 41

This study was undertaken to evaluate the effect of chronic diuretic therapy with chlorothiazide on the course of salt hypertension in hypertension-resistant (R) and hypertension-sensitive (S) strains of rats. Investigation of the effects of chlorothiazide on blood pressure, 24-hour urinary 24Na and aldosterone excretion, and plasma renin activity (PRA) produced the following observations: (1) Chlorothiazide failed to prevent the development of salt hypertension in S rats. (2) After 12 weeks, S rats on high salt puls chlorothiazide exhibited a rapid fall in blood pressure to levels indistinguishable from those of S rats on low salt. (3) Chlorothiazide significantly increased urinary 24Na excretion only in S rats on high salt (P less than 0.01). (4) Chlorothiazide significantly increased PRA and urinary aldosterone excretion in both strains on low or high salt diets (P less than 0.001). (5) Morbidity and mortality of salt hypertension were alleviated by chlorothiazide treatment. The unique aspect of this study is the finding that chlorothiazide did not abolish the hypertensiogenic action of salt in S rats.
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PMID:Influence of thiazide on salt hypertension. 85 74

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
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PMID:Hypertension and insulin resistance. 128 47

The incidence of hypertension is increased in obesity, a state associated with an insulin resistance syndrome. By using an euglycemic clamp method, Ferrannini et al. demonstrated the existence of an insulin resistance state in patients with essential hypertension. However, the body mass index of the subjects studied appeared to be slightly excessive. This abnormality has not been observed in patients with secondary hypertension. Insulin resistance is probably localized to peripheral tissues such as muscles and may be associated with other cellular abnormalities. Can insulin resistance, characterized by a raised circulating insulin concentration in the presence of normal blood glucose, be responsible for certain "modifications" associated with essential hypertension? Insulin induces sodium retention and increases the aldosterone-secreting effect of angiotensin II. These effects are likely to promote a rise in blood pressure and an increase in the sensitivity of vessels to endogenous substances. Moreover, insulin is a known growth factor and is involved in lipoprotein metabolism. If insulin resistance plays an important role in the maintenance of complications of essential hypertension, it is important that the treatments used tend to correct this anomaly. Thiazide diuretics and beta-blockers aggravate insulin resistance while angiotensin converting-enzyme inhibitors correct this condition.
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PMID:[Arterial hypertension, hyperinsulinism and insulin resistance]. 143

The only drugs which commonly cause diabetes during therapeutic use are the anti-hypertensive vasodilator diazoxide, and corticosteroids in high doses such as those used to palliate intracranial tumours. Thiazide diuretics have in the past been used in higher doses than necessary to treat hypertension, and the lower doses now used probably carry only a slight risk of inducing diabetes. The risk from beta-blockers is also quite small, but there is some evidence that thiazides combined with beta-blockers may be more likely to cause diabetes than either drug alone. The combination is probably best avoided in patients with a family history of non-insulin-dependent diabetes. The effect of the low-oestrogen combined oral contraceptive pill seems to be slight, and it presents a risk only to women who have had gestational diabetes. Bodybuilders who take enormous doses of anabolic-androgens can develop impaired glucose tolerance. Several drugs, including theophylline, aspirin, isoniazid and nalidixic acid can cause transient hyperglycaemia in overdosage, but only streptozotocin, alloxan and the rodenticide Vacor are likely to cause permanent diabetes.
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PMID:Drug-induced diabetes. 144 73

Thiazide diuretics are efficacious, either as monotherapy or in combination with other antihypertensive drugs. They reduce blood pressure in a high percentage of hypertensive patients with minimal subjective side effects. There is increasing evidence that the use of diuretics, singly or in combination, will reduce morbidity and mortality associated with essential hypertension in both young and elderly subjects. Although diuretics may induce some changes in the plasma lipid profile, serum uric acid concentration and glucose metabolism, there is little evidence that these changes are of clinical significance. The increase in serum cholesterol concentration has rarely persisted in any trial beyond the first year of treatment. The incidence of diabetes mellitus in diuretic treated subjects is only about 1%, even when large doses are used. Gout may be precipitated in susceptible subjects, but is uncommon. For these reasons, diuretics should remain a preferred first-step drug of choice in the management of hypertension.
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PMID:Diuretics and cardiovascular risk factors. 148 10

Diuretics have long been used in the treatment of hypertension and are outstandingly efficacious when used either alone or in combination with other antihypertensive compounds. Blood pressure is controlled with diuretics alone in over 50% of patients and in over 80% in combination with other drugs. Thiazide diuretics were used singly and in combination in the early VA Co-operative studies that demonstrated decrease in cardiovascular morbidity with blood pressure control. Subsequent studies have confirmed these early findings and clearly demonstrated that the thiazide diuretics are as effective in lowering blood pressure as other currently available antihypertensive compounds. Diuretics, like all other antihypertensives, have side effects, of which the most important ones are hypokalaemia, alterations of the plasma lipid profile, hyperuricaemia and glucose intolerance. Diuretic-induced hypokalaemia may be hazardous in the presence of digitalis, but does not appear to have any inherent propensity to induce life-threatening arrhythmias. Diuretics remain amongst first-line drugs in the treatment of high blood pressure due to their efficacy, especially in blacks and the elderly, the potentiation of the antihypertensive efficacy of other compounds, their low side effect profile and their low cost.
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PMID:Diuretics in hypertension: clinical experiences. 148 13

Antihypertensive agents may modify the renal effects of angiotensin converting enzyme inhibition (ACEI). This potential interaction, which is important in the diagnosis of renovascular hypertension was studied in two rat models with and without diuretic treatment prior to ACEI. Acute intravenous administration of furosemide or hydrochlorothiazide in one-kidney, one-clamp animals (1K1C) did not change glomerular filtration rate (GFR) or effective renal plasma flow (ERPF). ACEI administration after furosemide and hydrochlorothiazide decreased GFR (p less than 0.001, p less than 0.01) but not ERPF. Chlorothiazide administered to 1K1C prior to ACEI, decreased GFR (p less than 0.02) but not ERPF captopril administration to 1K1C which received hydrochlorothiazide intraperitoneally for 7-10 days decreased GFR (p less than 0.007) and ERPF (p less than 0.02), while two-kidney, one-clamp animals (2K1C) decreased GFR only in the clamped kidney (p less than 0.005). ERPF in 2K1C increased only in the contralateral kidney (p less than 0.01). Without diuretic 1K1C animals decreased GFR and ERPF after ACEI (p less than 0.005, P less than 0.001). In the clamped kidney of 2K1C rats, GFR and ERPF decreased significantly (p less than 0.0005, p less than 0.004) and contralateral kidney ERPF increased (p less than 0.001), but GFR did not. The consequences of ACEI on GFR are similar with or without diuretic. These data suggest that diuretic therapy may not significantly interfere with ACEI evaluation of renovascular hypertension.
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PMID:Renal functional response to captopril during diuretic therapy. 156 84

Several antihypertensive agents have been found to influence serum lipid profiles. Thiazide diuretics increase total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels and slightly reduce high-density lipoprotein (HDL) cholesterol. Most beta-blockers substantially increase triglycerides and lower HDL cholesterol. Angiotensin-converting enzyme inhibitors, calcium channel antagonists, alpha- and beta-blockers, and beta-blockers with intrinsic sympathomimetic activity are lipid neutral. alpha 1-Antagonists (e.g., terazosin and prazosin) lower total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels and improve total cholesterol/HDL ratios. Observational epidemiologic studies indicate that the lipid effects of antihypertensive agents are large enough to account for substantial differences in the predicted incidence of coronary heart disease. Combination therapy with the alpha 1-antagonist terazosin plus either thiazides or beta-blockers also ameliorates the adverse lipid effects of these agents used alone. A reasonable approach to managing the lipid problems often associated with hypertension is to advise a cholesterol-lowering, low-sodium diet and weight reduction and to select drugs that alone or in combination do not adversely affect lipid profiles.
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PMID:Antihypertensive therapy: taking lipids into consideration. 167 22


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