ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

&NA;The interaction of angiotensin converting enzyme (ACE) inhibition and atrial natriuretic factor (ANF) was investigated in six supine, sodium‐replete, normal volunteers who received captopril (10 mg i.v. bolus followed by 10 mg/hr constant infusion) or vehicle superimposed on background 3‐hour, constant, low‐dose (1.5 pmol/kg/min) infusions of human ANF (99‐126). Plasma converting enzyme activity was significantly inhibited but this had no effect on endogenous plasma ANF concentrations. ANF infusions, with or without captopril, caused similar increases in plasma ANF concentrations, and calculated metabolic clearance rates for ANF were unchanged. Similarly, blood pressure, heart rate, renal blood flow, glomerular filtration rate, and renal electrolyte excretion, including ANF‐induced natriuresis, were unaffected by captopril. The combination of ANF plus captopril produced a significant increase in plasma aldosterone (79±8 vs. 60±6 pmol/l,p<0.05), cortisol (406±52 vs. 265±29 nmol/l,p<0.01), adrenaline (119±21 vs. 76±10 pg/ml,p<0.05), and noradrenaline (319±49 vs. 215±38 pg/ml,p<0.05) compared with time‐matched placebo data. Converting enzyme inhibition, in the absence of major changes in blood pressure or renal blood flow, has little effect on ANF metabolism or renal bioactivity. However, ACE inhibition and ANF combined may interact to increase activity of the hypothalamo‐pituitary‐adrenal axis and sympathetic nervous system by unknown mechanisms. (Hypertension1989;13:193‐199)

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

&NA;Numerous abnormalities in the renin‐angiotensin system have been described in diabetes mellitus. Plasma renin activity (PRA) has been noted to be low, normal, and high in diabetic patients; these variable results may be explained by differences in patient selection and standardization of study conditions. We evaluated PRA and inactive renin responses in Type II normotensive (n=7) and hypertensive (n=12) diabetic patients specifically selected for no or minimal evidence (background retinopathy) for microvascular complications. Patients were studied in a metabolic ward after 7 days on a constant low sodium (20 meq/day) and 7 days on a high sodium (250 meq/day) diet. Nondiabetic control subjects (n=7) were evaluated under similar conditions. On low sodium intake, mean PRA levels were significantly reduced in the hypertensive diabetic group, but were not different between the control and normotensive diabetic groups. Hypertensive diabetic patients on high sodium intake also had greater reductions in PRA responses compared with the other study groups. In general, diabetic subjects on high sodium intake excreted less sodium and had more cumulative sodium retention than control subjects. Levels of inactive renin were not significantly different between the normotensive and hypertensive diabetic patients and were comparable with the levels in control subjects. Inactive renin levels changed in a similar direction and magnitude as PRA in response to sodium intake and posture in the three study groups. Infusion of angiotensin II led to comparable reductions in PRA in both diabetic groups and in the control group, suggesting an intact short feedback loop control. We conclude that Type II hypertensive diabetic patients with no or minimal complications have abnormalities of renin secretion that are best brought out under conditions of dietary sodium balance. The reduced PRA responses in these patients cannot be explained by defective activation of renin or by abnormalities of the angiotensin II short feedback loop of PRA control. Advanced age and abnormalities in renal sodium excretion in diabetic patients in combination with elevated blood pressure may account for the abnormal PRA responses in Type II diabetic hypertensive subjects. (Hypertension1989;13:200‐205)

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

&NA;To examine the relations between erythrocyte sodium‐lithium countertransport and renal proximal tubular sodium handling, we measured countertransport, and then subjected 30 normal and 32 hypertensive subjects, both white and black, to provocative maneuvers of volume expansion and contraction. The fractional excretions of sodium and lithium were measured simultaneously. In agreement with previous studies, we found that countertransport in erythrocytes was elevated in hypertensive patients compared with normal subjects. We also observed that whites have a higher level of countertransport than blacks. In the basal state, we found that fractional sodium excretion of hypertensive patients was no different than in normal subjects, whereas the fractional lithium excretion of hypertensive persons was increased compared with normotensive values. Volume expansion with 21 0.9% saline administered intravenously during a 4‐hour period provoked an exaggerated natriuresis and a greater increase in fractional lithium clearance in hypertensive patients compared with the control group. With volume expansion and contraction, fractional lithium clearance and countertransport were directly correlated. Our data suggest that hypertensive persons do not have increased proximal tubular sodium reabsorption compared with normal subjects. Further, the exaggerated natriuresis of hypertension is, in part, the result of increased distal solute delivery. The fact that our hypertensive patients were older may partially explain the discrepancies between this report and previous observations. (Hypertension1989;13:206‐212)

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

&NA;The mechanisms by which variations in blood ionized calcium (Ca2+) influence systemic arterial pressures independent of changes in extracellular fluid volume, pH, and electrolytes are unknown. To study this issue, we dialyzed eight stable hemodialysis patients on three separate occasions during 1 week with dialysates differing only in calcium concentration. Ultrafiltration was adjusted to achieve the patient's estimated dry weight. Postdialysis Ca2+was measured, as were arterial blood gases, electrolytes, magnesium, blood urea nitrogen, creatinine, and hematocrit. Blood pressures and two‐dimensional, targeted M‐mode echocardiograms were recorded with the patient in the supine position after 15 minutes of rest. Postdialysis, three different levels of Ca2+were achieved. Other measured biochemical variables and body weight did not differ among the three study periods. Changes in Ca2+correlated directly with changes in systolic, diastolic, and mean blood pressures, left ventricular stroke volume, and cardiac output. In contrast, heart rate, left ventricular end‐diastolic dimension, and total systemic vascular resistance were not altered significantly by changes in Ca2+. Thus, alterations in Ca2+within the physiological range affect systemic blood pressure primarily through changes in left ventricular output rather than in peripheral vascular tone in stable dialysis patients. (Hypertension1989;13:213‐218)

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

&NA;To clarify the mechanism of the antihypertensive effect of oral calcium loading, we studied the effect of low versus high calcium intake on salt‐induced blood pressure elevations in patients with borderline hypertension. After a 7‐day period of dietary salt restriction (50 meq/day), 27 patients were placed on a high salt (300 meq/day), low calcium (250 mg/day) diet for 7 days; 14 of these patients were given 2,160 mg/day of supplementary calcium (Ca group), and 13 patients were given placebo (non‐Ca group). With a high salt intake, the percent increase in mean blood pressure was smaller in the Ca group than in the non‐Ca group (+2.85±1.22% vs. +8.63±1.66%, respectively,p<0.01). The Ca group showed a smaller weight gain (p<0.05) and a greater urinary excretion of sodium (p<0.005) than the non‐Ca group. In the Ca group, but not in the non‐Ca group, high salt intake resulted in an increase in intraerythrocyte magnesium content (p<0.01), which was correlated inversely with the salt‐induced changes in mean blood pressure (r=‐0.54,p<0.05). While the increase in cellular magnesium was greater in the Ca group, the changes in red blood cell sodium and sodium/potassium ratio were not different between the two groups. The results suggest that oral calcium supplementation may prevent a rise in blood pressure in patients on a high salt, low calcium diet by attenuating the sodium retention. The intracellular magnesium level may, in part, be involved in the regulation of salt‐induced blood pressure response, although the pathophysiological mechanism remained unexplored. (Hypertension1989;13:219‐226)

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

&NA;To elucidate the effects of magnesium on high blood pressure, a 4‐week study of oral magnesium supplementation (MgO 1 g/day) was conducted in 21 outpatients with uncomplicated essential hypertension. During the study, blood pressure and intraerythrocyte sodium concentration decreased significantly, and the erythrocyte ouabain‐sensitive22Na efflux rate constant (Kos) and intraerythrocyte magnesium concentration both increased. Serum triglyceride and free fatty acid concentrations were reduced. Furthermore, the elevation inKossignificantly and positively correlated with both the increase in intraerythrocyte magnesium concentration and the decrease in mean blood pressure. There was a significant inverse correlation between the prestudyKosand the decrease in mean blood pressure. In addition, when patients were divided according to their overall decrease in mean blood pressure, the prestudy intraerythrocyte sodium concentration was significantly higher in patients with a mean blood pressure decrease of more than 7 mm Hg than that of patients whose mean blood pressure decrease was less than 7 mm Hg. These results suggest that oral magnesium supplementation may lower blood pressure through the activation of a cell membrane sodium pump and may reduce serum lipid concentration. It also suggests that the lower the prestudyKosor the higher the prestudy intraerythrocyte sodium concentration, the more effective the oral magnesium treatment is in lowering blood pressure. Therefore, we concluded that appropriate oral magnesium intake might be effective as a nonpharmacological treatment for essential hypertension. (Hypertension1989;13:227‐232)

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

&NA;Abnormalities of calcium metabolism and of its two principal regulating hormones, parathyroid hormone and 1,25‐dihydroxyvitamin D3(calcitriol), have been reported in the spontaneously hypertensive rat (SHR). Reports of abnormal calcitriol metabolism in the SHR by several groups have not provided measurements of tissue calcitriol receptors. Similarly, few data are available as to the parathyroid status of the SHR. In the present study, circulating calcitriol levels and intestinal and parathyroid gland calcitriol receptor status were determined in male SHR and in Wistar‐Kyoto (WKY) rats. Parathyroid status was investigated by determination of parathyroid gland mass together with tissue micromorphometry and by quantitative histology of bone as a measure of the biological action of parathyroid hormone. Circulating calcitriol levels were reduced in the 11‐week‐old SHR compared with the WKY rat (165±23 vs. 194±28 pmol/l,p<0.01, mean±SD). Calcitriol‐free ratio was diminished and maximal specific binding capacity for calcitriol was increased in the SHR in parathyroid tissue (172±4.9 vs. 123±6.6 fmol/mg protein,p<0.01) and in intestinal mucosa with no change of receptor affinity. Plasma ionized calcium (1.29±0.05 vs. 1.45±0.35 mmol/l,p<0.05) and phosphate (1.5±0.26 vs. 2.4±0.03 mmol/l,p<0.05) were significantly lower in the SHR. Parathyroid gland mass was increased in the SHR (59±12 vs. 17±7 &mgr;g/100 g body wt,p<0.001) as a result of hyperplasia and not hypertrophy. Higher osteoclast numbers were observed in SHR bone (27.6±0.79 vs. 23.9±0.66 osteoclasts/mm2,p<0.01), suggesting increased parathyroid hormone activity. In summary, in the 11‐week‐old SHR we observed reduced circulating calcitriol levels together with increased tissue calcitriol receptor numbers, increased parathyroid gland mass, and histological evidence of hyperparathyroidism. It is possible that these abnormalities influence the development of hypertension in the SHR. (Hypertension1989;13:233‐242)

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

&NA;The role of sodium retention and consequent changes in cerebrospinal fluid sodium concentration in the genesis of hypertension in Dahl rats was evaluated. Dahl salt‐sensitive (DS,n=7), Dahl salt‐resistant (DR,n=7), and Sprague‐Dawley (n=6) rats were housed in metabolic cages and instrumented with a stainless steel cannula in the cisterna magna and a femoral arterial catheter. A blood sample was drawn daily (200 &mgr;l), and cerebrospinal fluid was collected by continuous 24‐hour withdrawal (200 &mgr;l/day). Daily sodium, potassium, and water balances were also determined. Rats were studied sequentially on 0.4%, 4%, and 8% sodium diets (7 days per sodium level). Mean arterial pressure increased with 4% NaCl from 107 to 120 mm Hg (p<0.05) over 24 hours in DS rats and remained at about that level until the NaCl was increased to 8%, which resulted in a gradual rise of mean arterial pressure over the next 7 days to 135 mm Hg. Cerebrospinal fluid sodium was unchanged in DR and Sprague‐Dawley rats fed 4% or 8% sodium, but in DS rats rose from 152.3 to 155.2±0.6 meq/l on the third day at 4% sodium and remained elevated over the next 2 weeks of study. Blood sodium was unchanged throughout the study in all groups. On the first day only of the 4% and 8% sodium diets, both DS and DR rats exhibited a similar net retention of sodium, which was greater than the Sprague‐Dawley rats (p<0.05). There was no evidence for greater retention of sodium or water, however, in DS rats compared with DR or Sprague‐Dawley rats when subjected to a high sodium diet. In summary, since mean arterial pressure rose in DS rats on the first day of the 4% sodium diet while cerebrospinal fluid sodium did not change until the third or fourth day, we conclude that these central changes were not the stimulus for the initial rise of arterial pressure but might contribute to the maintenance of the hypertension. (Hypertension1989;13:243‐249)

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID