摘要:

BackgroundAn association between serum parathyroid hormone (PTH) levels in normotensive elderly subjects and blood pressure values had been reported.ObjectiveTo examine the relationship between PTH levels and other biochemical markers of calcium metabolism in elderly subjects and 24 h ambulatory blood pressures.MethodsWe performed 24 h ambulatory blood pressure recordings for 123 independent elderly subjects aged 63–88 years using a SpaceLabs 90207 recorder. Mean night-time blood pressures were calculated from the average of readings during sleep; mean daytime blood pressures were calculated from the remaining recordings. Demographic data and details concerning the alcohol consumption and medication usage of the subjects were recorded. Serum PTH, 25-hydroxy-vitamin D, albumin, renin, aldosterone, noradrenaline, creatinine and calcium levels were measured.ResultsFifty-five patients were being administered antihypertensive therapy. Serum PTH levels correlated to the nocturnal systolic blood pressure (SBP; β = 0.29,P= 0.002), nocturnal diastolic blood pressure (DBP), daytime SBP and mean 24 h SBP on univariate and multivariate analysis. Aldosterone levels were related to nocturnal SBP in univariate analysis (β = 0.21,P= 0.02) but the relationship was weakened when PTH levels were included in the analysis (β = 0.16,P= 0.09). Nocturnal, daytime and mean 24 h blood pressures were not significantly related to serum calcium, 25-hydroxy- vitamin D, age, body mass index and alcohol consumption. Sex was a significant predictor of the DBP, men having higher levels than did women (daytime DBP β = 0.29,P= 0.001).ConclusionsSerum PTH levels are related strongly to the blood pressure, particularly the nocturnal blood pressure in the elderly. It is not known whether PTH levels are a consequence or a cause of the elevation in blood pressure.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundChanges in plasma osmolality and arterial pressure can affect the secretion of vasopressin (AVP).ObjectiveTo investigate the effect of a drug-induced lowering of the arterial pressure on the plasma concentration of AVP and on its osmoregulation in moderately severe uncomplicated hypertensives.Design and methodsA group of 33 moderate uncomplicated and untreated essential hypertensives of both sexes (mean age 48 ± 1 years, average arterial pressure 171 ± 3/108 ± 2 mmHg) was studied. We measured AVP and other plasma and urine variables in 21 of them before and after administration of a hypertonic NaCl solution (100 mmol NaCl in 50 ml). Antihypertensive treatment with a single drug or, if necessary, with a combination of drugs was initiated for eight of these subjects and hypertonic saline administration was repeated after 1 month of treatment. The hypertonic stimulus was administered to the other 12 subjects after acute lowering of the arterial pressure by continuous intravenous infusion either of 0.3 mg clonidine in 100 ml (n = 6) or of 50 mg sodium nitroprusside in 250 ml (n = 6).ResultsAdministration of hypertonic saline to untreated hypertensives increased their AVP level from 1.6 ± 0.28 to 5.4 ± 0.7 pg/ml (n = 21,P< 0.01). Their mean arterial pressure was lowered after pharmacological treatment for 1 month (n = 8) from 125 ± 2 to 101 ± 2 mmHg; their baseline AVP level remained unchanged (1.2 ± 0.21 versus 0.9 ± 0.25 pg/ml); after hypertonic saline had been administered to hypertensives with lowered arterial pressures, their AVP level increased to 6.0 ± 1.03 pg/ml (P< 0.01). The AVP level in subjects whose MAP had been lowered acutely by administration of clonidine (n = 6) or of sodium nitroprusside (n = 6; on the average, from 132 ± 3 to 110 ± 4 mmHg) increased concurrently from 1.6 ± 0.63 to 3.4 ± 0.7 pg/ml (P< 0.05); after administration of the hypertonic saline the AVP level increased to 10.8 ± 2.22 pg/ml (P< 0.01). This stimulated value was significantly (P< 0.01) higher than that observed after hypertonic saline had been administered to untreated hypertensives (5.4 ± 0.7 pg/ml).ConclusionsAcute lowering of the arterial pressure in moderate essential hypertension appears to facilitate the secretion and osmoregulation of AVP. On the other hand, during prolonged antihypertensive treatment, baroreflex regulation of the secretion of AVP appears to be set at a lower operating point, thus exerting the same influence on the release of AVP as it did before antihypertensive treatment.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo determine whether chronic treatment with benidipine, a calcium antagonist, leads not only to regression of left ventricular hypertrophy, but also to an improvement in coronary flow reserve and microvascular remodeling.Design and methodsTwo-kidney, one clip Goldblatt hypertensive rats were assigned either to a benidipine-treatment group or to a group without treatment after their kidneys had been clipped for 4 weeks. Benidipine was administered to rats in the treatment group for 6 weeks. At the end of the treatment, the systemic hemodynamics and coronary blood flow were determined in conscious unrestrained rats by using nonradioactive colored microspheres injected through the left atrium. The coronary blood flow was determined in rats of both groups with the rats at rest and after near-maximal vasodilatation induced by carbochrome. For evaluation of the microvascular remodeling capillary density, the wall : lumen ratio of arterioles and perivascular fibrosis were quantified by using an image analyzer after fixation of heart tissue.ResultsBenidipine treatment lowered the blood pressure significantly with a decrease in total peripheral resistance, and the left ventricular mass decreased markedly compared with that of untreated hypertensive rats. The coronary flow reserve of the untreated hypertensive rats was lower than that of the controls, but benidipine treatment improved the coronary flow reserve. We found a significant decrease in capillary density, and significant increases in wall : lumen ratio and perivascular fibrosis in untreated hypertensive rats. These changes in microvasculature were improved by benidipine treatment.ConclusionTaken together, these results suggest that benidipine exerts favorable effects as an antihypertensive drug by reversing cardiac hypertrophy and improving the coronary flow reserve and microvascular remodeling.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundThe clinical usefulness of angiotensin converting enzyme (ACE) inhibitors in preventing the recurrence of myocardial infarction has been investigated in large randomized trials. Results from many studies using animal models have suggested that ACE inhibitors have vasculoprotective effects, which may contribute to the prevention of coronary atherosclerosis.ObjectiveTo examine the association between vascular angiotensin generation and the development of coronary atherosclerosis in humans.MethodsWe used immunocytochemical techniques to examine frozen sections from 44 coronary artery segments from 19 corpses.ResultsThree segments were sites of plaque rupture in patients who had died from acute myocardial infarction. Other specimens of coronary artery segments were characterized histologically to be normal artery segments with diffuse intimal thickening (n = 6), hypercellular lesions composed of smooth muscle cells with or without infiltration of macrophages (n = 11), atheromatous plaque (n = 12), and fibrosclerotic plaque (n = 12). In normal arteries with diffuse intimal thickening, ACE was expressed in endothelial cells. In those with hypercellular lesions and atheromatous plaques, however, enhanced ACE expression was found in macrophages and smooth muscle cells. In contrast, arteries with fibrosclerotic plaques exhibited little or no ACE expression within the plaque. All three ruptured plaques expressed ACE strongly in macrophages accumulated around the attenuated fibrous cap.ConclusionThe strong association of enhanced ACE expression with the histologic characteristics of plaques suggests that ACE in hypercellular lesions, atheromatous plaques, and ruptured plaques contributes greatly to the further progression of atherosclerosis via an increase in vascular angiotensin II formation and inactivation of bradykinin.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundThe urinary isoflavonoid equol inhibits membrane Na–K–Cl cotransporters at similar concentrations to those at which furosemide inhibits them, but the significance of this action is not known.ObjectiveTo investigate the potential salidiuretic and vascular actions of equol in the rat.MethodsRenal functioning was assessedin vitroin the isolated perfused kidney andin vivoin conscious rats. The vascular contractility of isolated aorta was assessed.ResultsIn the isolated perfused kidney equol was concentrated 50- to 70-fold in the urinary fluid, it was 3–4 times less potent than furosemide at increasing diuresis, natriuresis and kaliuresis (the difference was due to its higher protein-binding affinity), and it induced a modest but significant increase in glomerular filtration rate.In vivo, orally administered equol was a modest natriuretic agent, about 8-fold less potent than orally administered furosemide (in molar terms). In isolated aortic rings precontracted by administration of phenylephrine, administration of equol relaxed the contracted aorta at 10-fold lower concentrations (concentration for half-maximal activity 58.9 ± 16 μmol/l, n = 3) than did furosemide (concentration for half-maximal activity 633 ± 145 μmol/l, n = 3).ConclusionsEquol is a modest natriuretic and vasorelaxant agent in the rat. Further studies are required in order to investigate the potential natriuretic and perhaps hypotensive actions of dietary equol precursors (daidzein).

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundThe nature of the relationship between high blood pressure and kidney damage is controversial. There is a view that essential non-malignant hypertension does not cause renal damage in patients with normal renal function and no proteinuria at first presentation. In contrast, patients with malignant hypertension (MHT) not due to underlying renal disease often exhibit progressive renal impairment, although there can be a dissociation between short-term changes in renal function and the long-term renal outcome. It has been established that the association of MHT and renal impairment is associated with a grave prognosis.ObjectiveTo investigate further the changes in renal function after diagnosis of MHT.MethodsWe studied the clinical features, renal function and survival of patients on the West Birmingham MHT Register. Patients presenting with no or only mild-to- moderate renal impairment (defined as an initial serum creatinine level ≤ 300 μmol/L) were categorized as group 1 patients. Patients with severely impaired renal function, defined as a serum creatinine level > 300 μmol/l at presentation, were categorized as group 2 patients. Patients who subsequently suffered a deterioration in renal function were defined as those whose serum creatinine level had risen at follow-up (group A). Patients with an invariant or improving renal function at follow-up were those whose serum creatinine level neither rose nor fell (group B). Clinical characteristics and survival of patients in group 1 were therefore compared with those of patients in group 2; features of patients in group A were compared with those of patients in group B.ResultsWe studied a total of 169 patients with MHT [107 men, aged 49.4 ± 13.3 years (mean ± SD)]. Of these, 136 (80.5%) patients had an initial serum creatinine level < 300 μmol/l (group 1). After a median follow-up of 53 months (interquartile range 15–103), the serum creatinine level of 56.8% (96 of 169) patients had risen (group A). Patients with MHT with only mild-to-moderate renal impairment at presentation (creatinine level < 300 μmol/l, group 1) had lower serum urea, creatinine and blood pressure levels at follow-up compared with those of patients with initially impaired renal function. Although there was no significant change in follow-up serum urea and creatinine levels compared with initial levels in patients in group 2 (paired Wilcoxon test, NS), there was a significant deterioration in renal function in patients in group 1 (P= 0.001). Group 2 patients had a shorter median survival time than did group 1 patients (15 versus 59 months, Lee–Desu statistic 15.4,P= 0.0001). Patients whose serum creatinine level had risen (group A) had significantly higher initial serum urea and creatinine levels and follow-up blood pressures than did those whose renal function had remained invariant or improved (group B). However, there was no significant difference between the median survival times of patients in groups A and B (51 versus 58 months, Lee–Desu statistic 0.377,P= 0.54).ConclusionWe suggest that renal function continues to deteriorate in some patients with MHT, despite a good degree of control of their blood pressures having been achieved at follow-up. However, the renal function of 16 of the 33 patients with severe renal impairment at presentation either remained invariant or was found to have improved at follow-up. There was no evidence that those cases whose renal function remained invariant were confined to those who had presented with less renal impairment. The severity of MHT at presentation and the amount of renal impairment did not predict the outcome. In contrast the quality of control of the blood pressure that had been obtained at follow-up did predict the outcome. Careful monitoring of renal functioning and effective treatment of the blood pressure is mandatory in patients with MHT.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectivesTo study the forearm vascular resistance in patients at rest and during ischaemia and cardiovascular responses to noradrenaline infusions during treatment with a β1-adrenoceptor antagonist, metoprolol, and with an α1-adrenoceptor antagonist, prazosin.PatientsEighteen previously untreated primary hypertension patients were selected for therapy either with 50–250 mg/day metoprolol (n = 11) or with 3–20 mg/day prazosin (n = 8).MethodsThe minimal vascular resistance after ischaemic work was calculated from the forearm blood flow determined by venous occlusion plethysmography before treatment and after two and 16 months of treatment. Arterial and venous plasma noradrenaline levels were determined and systemic pressor responses and forearm vasoconstriction were studied during intravenous infusion of noradrenaline.ResultsThe resting mean arterial pressure was reduced differently by metoprolol and prazosin (by 20% versus by 8%;P< 0.001 for difference). The minimal vascular resistance decreased similarly after 16 months of metoprolol (17% decrease;P< 0.05) and of prazosin (24% decrease;P< 0.05) treatments. Arterial noradrenaline levels increased after 16 months of metoprolol treatment and after 2 and 16 months of prazosin treatment. The forearm noradrenaline spillover was reduced after 16 months on prazosin, but remained unchanged during metoprolol treatment. Pressor responses to intravenous noradrenaline were affected little by either treatment, whereas reflexogenic bradycardia was attenuated by prazosin treatment.ConclusionThe findings suggest that metoprolol and prazosin treatments reduce the minimal vascular resistance similarly, despite different reductions in blood pressure. Prazosin treatment might also reduce the forearm sympathetic nerve activity. Reductions in minimal forearm vascular resistance during antihypertensive therapy need not be related only to the lowering of the blood pressureper se.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo compare two losartan regimens (with and without hydrochlorothiazide) and amlodipine in treating mild-to-moderate hypertension regarding their blood-pressure-lowering effect, drug tolerability and quality of life.DesignA 12-week, randomized, double-blind, parallel- group, multi-centre study. After 4 weeks of placebo, patients with a diastolic blood pressure (DBP) in the range 95–115 mmHg were allocated randomly to be administered 50 mg losartan (increased to 100 mg if the DBP was 90 mmHg or more after 6 weeks), 50 mg losartan (plus 12.5 mg hydrochlorothiazide under the above conditions), or 5 mg amlodipine (increased to 10 mg under the above condition). The tolerability of the treatment and the quality of life were evaluated by spontaneous reporting, active questioning and the Psychological General Well-Being (PGWB) index.Study populationIn total 898 hypertensives, mainly referred from primary health care (mean age 57.8 years) of whom 52% were men.ResultsAdministration of 50 mg losartan (plus 12.5 hydrochlorothiazide if necessary) and of 5 mg amlodipine (or 10 mg if necessary) lowered the blood pressure as well as or better than did 50 mg losartan (or 100 mg if necessary). The incidence of ‘any discomfort’ and ‘swollen ankles’ increased with amlodipine but not with losartan treatment. The opposite was found for ‘dizziness upon standing’. The incidence of drug-related adverse events and the number of patients withdrawn from therapy were higher with amlodipine than they were with losartan treatment. The PGWB index at week 12 indicated that improvements from baseline had occurred in some domains for the losartan groups whereas it remained unchanged for the amlodipine group.ConclusionBoth losartan and amlodipine were effective in lowering the blood pressure and were tolerated well. Administration of 50 mg losartan (plus 12.5 mg hydrochlorothiazide if necessary) and of 5 mg amlodipine (or 10 mg if necessary) lowered the blood pressure equally well or better than did 50 mg losartan (or 100 mg if necessary). Drug-related adverse effects and withdrawal from the study were more common for the amlodipine group. The clinical significance of the improvements in the PGWB index with losartan needs to be studied further.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveThe Verapamil in Hypertension and Atherosclerosis Study (VHAS) is a prospective randomized study the objective of which was to compare the long-term effects of verapamil and chlorthalidone on the blood pressure, clinical safety, and the progression/regression of carotid wall lesions in members of a large population of hypertensive patients.DesignAfter a 3-week placebo run-in period, 1414 hypertensive patients [692 men and 722 women, aged 53.2 ± 7 years, blood pressure 168.9 ± 10.5/ 102.2 ± 5.0 mmHg (means ± SD)] were assigned randomly to be administered either 240 mg sustained- release verapamil (n = 707) or 25 mg chlorthalidone (n = 707) once a day for 2 years. The study design was double blind for the first 6 months and open thereafter. 25–50 mg/day captopril were added to the treatment of non-responding patients; subsequently, patients not responding to combined therapy were switched to any therapy chosen by the treating doctors (free therapy). The blood pressure of the sitting subject, heart rate, and a standard clinical safety profile (electrocardiogram, laboratory tests, adverse events, cardiovascular events, and deaths) were assessed regularly throughout the study.ResultsAfter 2 years the systolic and diastolic blood pressures were reduced significantly in members of both treatment groups (by 16.3/16.6% with verapamil and by 16.9/16.2% with chlorthalidone, both by analysis of variance,P< 0.0001). The patients for whom we added captopril treatment constituted 22.6% of the verapamil and 26.2% of the chlorthalidone group; while 11.6 and 12.2% of patients in these groups, respectively, were administered free therapy. Normalization of the diastolic blood pressure (to ≤ 90 mmHg or to ≤ 95 mmHg with a ≥ 10% decrease) was achieved for 69.3% of the verapamil and 66.9% of the chlorthalidone group. A decrease in heart rate (by 5.8%) occurred in members of the verapamil group only. A decrease in total serum cholesterol (from 223.6 to 216.9 mg/dl,P< 0.01) and in the total cholesterol : high-density lipoprotein cholesterol ratio (from 4.9 to 4.5,P< 0.01) was noted for the verapamil group only, whereas significantly greater rates of hyperuricemia (plasma urate > 7.0 mg/dl; 10.8 versus 3.9%) and hypokalemia (serum K < 3.5 mmol/l; 24.6 versus 4.4%) were observed for the chlorthalidone group (P < 0.01, versus verapamil for both). Adverse events were reported by 32.5% of patients treated with verapamil and by 33.4% of those treated with chlorthalidone. The most frequent adverse events were constipation in members of the verapamil group (13.7%) and asthenia in members of the chlorthalidone group (8.5%). In total 315 dropped out (153 from the verapamil and 162 from the chlorthalidone group). The occurrence of cardiovascular events was similar for both treatments (42 events for verapamil and 43 for chlorthalidone, NS).ConclusionSimilar antihypertensive efficacies, tolerabilities and cardiovascular event rates were observed with verapamil and with chlorthalidone. However, treatment with chlorthalidone was associated with significantly higher incidences of hyperuricemia and hypokalemia than was treatment with verapamil.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID