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

The function of the endothelium is impaired in hypertension. In spontaneously hypertensive rats (SHR), acetylcholine-induced relaxation is decreased and serotonin-induced constriction is increased. The goal of our study was to evaluate the effect of a long-term treatment with cilazapril, a new angiotensin converting enzyme inhibitor, or hydralazine, a vasodilator, on the endothelium-dependent responses in aorta of SHR. Wistar-Kyoto rats were used as normotensive reference. Isolated aortic rings with or without endothelium were suspended in organ chambers. The rings with intact endothelium were contracted with norepinephrine. Acetylcholine-induced relaxation was markedly enhanced by cilazapril treatment. The tension achieved at maximal relaxation was 8 +/- 4% of norepinephrine contraction in the cilazapril-treated SHR versus 55 +/- 5% in the untreated SHR (p less than 0.001). Hydralazine had no significant effect. The effect of serotonin was also markedly modified by cilazapril. In untreated SHR, serotonin induced the release of a vasoconstrictor substance by the endothelium as assessed by the ratio of maximal tension induced by serotonin in rings with endothelium over maximal tension in rings without endothelium, which was greater than 1. This ratio was reversed in cilazapril-treated SHR but not in hydralazine-treated SHR. Captopril had effects similar to cilazapril. Finally, evaluation of carotid arteries showed that cilazapril also prevented morphological changes of the intima in SHR (i.e., infiltration by mononuclear cells). We conclude that angiotensin converting enzyme inhibitors prevent the functional and morphological alterations in endothelium that are found in hypertension and speculate that this action might participate in their antihypertensive effect.
Hypertension 1990 Nov
PMID:Effects of angiotensin converting enzyme inhibitors and of hydralazine on endothelial function in hypertensive rats. 222 54

Twenty-three children were admitted to a pediatric intensive care unit for scorpion envenomation with severe hypertension. The hypertension responded to analgesics and sedatives in 15 (65 percent) of the 23. The remaining eight children required specific antihypertensive therapy, and their condition promptly responded to intravenous hydralazine and sublingual nifedipine; rebound hypertension was observed in one. Hypertension is a frequent complication of a scorpion's sting in children, and specific antihypertensive therapy is indicated in severe cases. Hydralazine and nifedipine are effective and safe in such instances.
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PMID:Vasodilators and hypertensive encephalopathy following scorpion envenomation in children. 229 29

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. The purpose of this study was to investigate the effect of calcium antagonists on hypertension and diabetes in hypertensive diabetic rats, which were newly established by neonatal injection of streptozotocin in spontaneously hypertensive rats. At the age of 6 months, hypertensive diabetic rats and control hypertensive nondiabetic rats were treated with hydralazine, diltiazem, or nifedipine for 2 months. In diabetics, antihypertensive therapy not only prevented the progression of nephropathy but also improved glucose metabolism by increasing insulin secretion. Calcium antagonists in this study reduced urinary protein excretion, and nifedipine relieved hypoalbuminemia. Hydralazine had no beneficial effect on urinary protein excretion. Calcium antagonists as compared to hydralazine decreased the heart weight. Calcium antagonists have a beneficial effect on cardiac hypertrophy. Good correlations have been found between kidney weight and blood pressure in hypertensive diabetic rats. It is suggested that blood pressure reflects increase in kidney weight in diabetic patients.
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PMID:Effect of calcium antagonists on hypertension and diabetes in new hypertensive diabetic models. 245 31

This study measured the time course of the development and reversal of structural change in resistance vessels during deoxycorticosterone acetate (DOCA) hypertension and after cessation of DOCA in Wistar rats by hindquarter perfusion. The relationship of structural change to blood pressure was further assessed by preventing hypertension during DOCA treatment with hydralazine. Blood pressure rose progressively during DOCA treatment reaching 198.6 +/- 2.0 (s.e.) mmHg at 10 weeks. Five weeks after the cessation of DOCA, when it had been given for 2 weeks, hypertension reversed completely but after 4, 8 and 10 weeks of treatment, post-DOCA reversal of hypertension was only partial. Hindquarter perfusion pressure at maximum vasodilatation and maximum vasoconstriction increased with increasing duration of DOCA treatment and reversed 5 weeks post-DOCA to a similar degree to the blood pressure with only partial reversal of both perfusion pressures and hypertension when DOCA had been given for 8 and 10 weeks. Hydralazine did not completely prevent heart hypertrophy in the DOCA rats and caused some cardiac hypertrophy in the control ('vehicle' only) rats, although it both prevented hypertension and evidence of vascular structural change in DOCA rats.
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PMID:Structural change in the rat hindlimb during deoxycorticosterone acetate hypertension; its reversibility and prevention. 252 77

The purpose of these studies was to evaluate cardiovascular structural and functional changes in a model of hypertension-induced myocardial hypertrophy in which vasodilator therapy decreased blood pressure to normal levels. Thus, we determined the separate contributions of hypertension and hypertrophy on myocardial and coronary vascular function and structure. Twelve-month-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) with and without 12 weeks of vasodilator antihypertensive treatment (hydralazine) were studied using an isolated perfused rat heart model. Hydralazine treatment normalized blood pressure in SHR but did not cause regression of cardiac hypertrophy (heart weight to body weight ratio of SHR + hydralazine 4.33 +/- 0.098 vs. SHR 4.66 +/- 0.091; WKY 3.21 +/- 0.092 and WKY + hydralazine 3.38 +/- 0.152; mean +/- SEM). Coronary flow reserve, elicited by adenosine vasodilation in the perfused heart, was decreased in SHR (29%) compared with WKY (105%) and WKY + hydralazine (100%) and was significantly improved in SHR + hydralazine (75%). Morphometric evaluation of perfusion-fixed coronary arteries and arterioles (30-400 microns diameter) demonstrated a significant increase in the slope of the regression line comparing the square root of medial area versus outer diameter in SHR (0.444) compared with WKY (0.335) and WKY + hydralazine (0.336, p less than 0.05). Blood vessels from SHR + hydralazine were not different from control (0.338). Cardiac oxygen consumption was decreased in SHR (10.9 +/- 0.74 mumols oxygen/min/g/60 mm Hg left ventricular pressure) compared with WKY (22.4 +/- 1.47) and WKY + hydralazine (23.4 +/- 1.90; p less than 0.01), while SHR + hydralazine was intermediate (16.0 +/- 1.60). These studies suggest that significant alterations in myocardial and coronary vascular structure and function occur in hypertension-induced cardiac hypertrophy. The coronary vasculature is responsive to blood pressure, independent of cardiac hypertrophy, although moderate coronary deficits do remain after chronic antihypertensive therapy.
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PMID:Vascular remodeling and improvement of coronary reserve after hydralazine treatment in spontaneously hypertensive rats. 252 90

This study was initiated to test the hypothesis that attenuation of long-term hypertension with or without regression of left ventricular hypertrophy (LVH) will lower minimal coronary vascular resistance (MCVR). Six-month-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were treated with captopril or hydralazine for a period of 3 mo. Myocardial perfusion, measured with microspheres, and hemodynamic data were obtained in awake, unrestrained rats aged 9 mo. MCVR was calculated from the quotient of mean/myocardial perfusion. Both drugs significantly lowered arterial systolic pressure in both strains of rats, but only captopril was effective in reducing heart mass. Left ventricular MCVR per 100 g was lower in captopril-treated WKY (0.064 +/- 0.012) and SHR (0.079 +/- 0.006) than the untreated controls (SHR: 0.124 +/- 0.006; WKY: 0.098 +/- 0.009), whereas total LV MCVR was unaltered by treatment. Hydralazine tended to lower LV MCVR per 100 g in both strains despite its tendency to increase ventricular mass. Captopril, but not hydralazine, treatment was associated with a significant increase in capillary density in both WKY and SHR. We conclude that the improvement in MCVR is related to both the regression of LVH and to the consequences of lowering arterial systolic pressure. In contrast, the increase in capillary density appears to be related to the decrease in ventricular mass after captopril treatment.
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PMID:Role of lowering arterial pressure on maximal coronary flow with and without regression of cardiac hypertrophy. 2773 36

The prevalence of hypertension in adult Nigerians is about 20% and hypertension remains a significant risk factor in cardiovascular morbidity and mortality. In Africans, hypertension carries a dismal prognosis, has a late clinical presentation and certain antihypertensives may be less effective. We therefore conducted a therapeutic audit in order to assess the initial cardiovascular risk profile of Nigerian patients as well as the safety and efficacy of different antihypertensive agents. A cross-sectional survey of 367 patients (M:F:2:1) modal age 25-44 years, mostly WHO II, enrolled in our clinic was undertaken. 56% had been on treatment for up to one year and 2% for longer than ten years. 12.5% had concomitant diabetes mellitus. Statistical analyses of drug efficacy were done by Spearman correlation and Analysis of Variance (ANOVA). The rank order of hypertensive efficacy was as follows: Thiazides (T) (r = 0.57, P less than 0.05), T + Methyldopa (M) (r = 0.91, P less than 0.001) T + M + Hydralazine (r = 0.92, P less than 0.001). Neither propranolol, nor frusemide showed significant overall efficacy. However, propranolol appeared efficacious in hypertensives with renal impairment. Postural dizziness was occasionally reported. Total mortality was 6% occurring mostly in the modal age group. Diabetic hypertensives had a 5 fold enhanced risk of a fatal outcome (X2 P less than 0.001). Our findings support a rational stepped care approach to pharmacotherapy of hypertension in black Africans, a cost-effectiveness analysis of common antihypertensives; it elucidates the associated adverse effects to patients, and draws attention to the lethality of concomitant hypertension and diabetes. Prospective large scale studies of the treatment of hypertension in Africans are required.
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PMID:A therapeutic audit in the management of hypertension in Nigerians. 260 27

Hydralazine (1-hydrazinophthalazine) has been used extensively in the treatment of hypertension and congestive heart failure and produces arteriolar vasodilation, in part, mediated by prostaglandins. Its associated reflex baroreceptor-mediated responses of tachycardia and increased ejection velocity are attenuated in congestive heart failure. A direct inotropic effect has been attributed to the drug. Pharmacokinetic data indicate hydralazine is absorbed well from the gastrointestinal tract, and has an extensive and complex metabolism depending on acetylator status: slow acetylators undergo primary oxidative metabolism, while rapid acetylators are acetylated. Half-lives, clearances and bioavailability of the drug are not significantly altered in congestive heart failure compared with hypertensive patients. A wide range of dosages in heart failure has been noted (150 to 3000 mg/24h), and may related to a saturation of the first-pass effect. Hydralazine improves haemodynamics in the short term in patients with increased peripheral vascular resistance, and has variable effects on pulmonary capillary wedge and left ventricular filling pressures. Prediction of the short term clinical response is difficult and appears to be independent of pharmacokinetics. A meta analysis did not demonstrate long term efficacy of hydralazine alone in heart failure, but combination therapy with nitrates has been shown to improve survival and exercise performance in patients with mild to moderate heart failure. Side effects are common and are dependent on dose, duration and acetylator status.
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PMID:Clinical pharmacokinetics and therapeutic use of hydralazine in congestive heart failure. 265 46

Antihypertensive treatment may, for the same effect on hypertension, have a very different influence on the cerebral blood flow and the autoregulation curve. For instance, sodium nitroprusside, a potent vasodilator, risks to be poorly tolerated from the cerebral standpoint, when the sympathetic system is not inhibited. Diazoxide has no direct vasodilating effect on the cerebral vessels but, because of its marked hypotensive action must be used in divided doses. Hydralazine, a strong vasodilator, must be avoided in case of cerebral edema and hypertensive encephalopathy. Diuretics and beta-blockers, on a long-term basis, do not significantly modify the cerebral blood flow while alpha-methyl-dopa would increase it and facilitate a return to normal of the autoregulation curve. Captopril has demonstrated experimentally, interesting properties: in anaesthetized rats, it shifts the autoregulation curve to the left, i.e. toward lower pressures and it reduces the autoregulation curve to the left, i.e. toward lower pressures and it reduces the autoregulation limits; in awaken subjects, the decreased lower limit is also observed, explaining the good central tolerance of marked blood pressure reductions; on the contrary, its effects on the upper limit of the plateau are, unquestionably, counterbalanced by the effects of sympathetic stimulation concomitant with sudden blood pressure rises. As for calcium inhibitor, they do not seem to influence the long-term autoregulation of the cerebral flow.
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PMID:[The brain and arterial hypertension. 2. Effects of antihypertensive treatment on cerebral circulation]. 266 Jul 36

It is now well established that structural changes in resistance vessels contribute to the long-term maintenance of many forms of hypertension. This study measured the time course of structural change in smaller resistance vessels during the development of deoxycorticosterone acetates (DOCA) hypertension and after cessation of DOCA in Wistar rats by histometric assessment of cross-sections of renal arterioles. The relationship of structural change to blood pressure was assessed by preventing hypertension during DOCA treatment with hydralazine. Blood pressure rose progressively during DOCA treatment reaching 192 +/- 3 mmHg compared with 132 +/- 2 mmHg in controls after 10 weeks. Five and 10 weeks after cessation of DOCA, following 10 weeks of DOCA treatment, post-DOCA reversal of hypertension was only partial. Medial area to internal elastic lamina (IEL) radius ratio, wall to lumen ratio and intimal area to IEL radius ratio of renal arterioles increased progressively during 10 weeks of DOCA treatment with partial reversal of the increased medial area and wall to lumen ratio 5 weeks post-DOCA. Hydralazine completely prevented hypertension in DOCA rats and also largely prevented structural change.
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PMID:Histometric assessment of renal arterioles during DOCA and post-DOCA hypertension and hydralazine treatment in rats. 270 16


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