ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The blood pressure decrease after beta-blockade is delayed and there are little data on the hemodynamic events associated with the initial decrease in blood pressure. The present study measured the hemodynamics of the initial hypotensive action of timolol maleate, a nonselective betaadrenoreceptor blocking agent, in 10 patients with essential hypertension. Frequent measurements were made for the first 30 hours of treatment, and follow-up measurements made at 3 and 6 weeks. Before treatment, mean arterial blood pressure, cardiac output, and arteriovenous oxygen difference were 115.9 ± 9.1 mm Hg, 4.65 ± 1.05 liter/min, and 55.0 ± 9.6 ml/liter, respectively. At 3 hours after the first dose of timolol, blood pressure had fallen 13.5 ± 8.2 mm Hg (p< 0.05). This was preceded by an initial decrease in cardiac output, which was not associated with a simultaneous decrease in blood pressure, and by an increase of arteriovenous oxygen difference. The early, statistically significant, decrease in cardiac output was followed by a return to normal output, which coincided with the onset of blood pressure reduction. The magnitude of the initial decrease of cardiac output and of the initial increase in arteriovenous oxygen difference was significantly correlated to the later decrease in blood pressure (7 hours after first dose). These hemodynamic observations are consistent with the notion that early underperfusions of tissue play a role in the initial hypotensive action of beta-blockers. After 6 weeks, the blood pressure remained lower but the cardiac output was again decreased at that point. As with many antihypertensive agents, there was a difference between the early and late hemodynamic pattern. Only the early pattern was consistent with a peripheral adjustment of circulation to the decreased cardiac output. The early responders tended to remain responsive in the later phase. We speculate that the initial response is important and sets into motion some secondary adjustments that later alter the hemodynamic picture.

ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

If high sodium intake is involved in the pathogenesis of essential hypertension, the effects of changing the sodium intake should be demonstrable in the susceptible part of the nor mot ensive population. Therefore, we have investigated the effects of moderate salt restriction in 52 young normotensive subjects with and without a family history of hypertension; 22 (42%) responded to moderate salt restriction (200 to 50 mmol/day) over 2 weeks, with a significant fall in blood pressure shown by continuous automatic blood pressure recordings. Accordingly, these subjects were classified as salt-sensitive, and the remainder as salt-resistant. Compared to salt-resistant subjects, salt-sensitive subjects showed a 2.5-fold higher incidence of a positive family history of hypertension (p< 0.01), and a significantly higher blood pressure and lower salivary sodium concentration during the usual high sodium diet. Although there were no differences in Na, K-ATPase activity and in Na-K cotransport of erythrocytes, the pressor response to infused norepinephrine in salt-sensitive subjects was double that of salt-resistant subjects independent of the diet and this was linked to indirect evidence for enhanced proximal tubular sodium reabsorption. On the usual high sodium diet, 40% of the normal population may be salt-sensitive and prone to develop hypertension. Hypersensitivity to catecholamines (genetically determined?) may be the cause of salt sensitivity. A low sodium concentration in saliva deserves further study as a simple screening test to identify salt-sensitive subjects.

ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Sodium-lithium countertransport (SLC), sodium-potassium cotransport (CoT), and ouabain binding to sodium-potassium adenosine triphosphatase (Na, K-ATPase) sites were measured on fresh erythrocytes from hypertensive and normotensive Utah subjects with and without a firstdegree relative with hypertension. SLC was measured as Li+efflux into NaCl and MgCI2media from Li+-loaded cells (5–7 mM). CoT was measured by monitoring Na+and K+efflux from cells loaded to 20–30 mM Na+and 20–30 mM K+. Ouabain binding was determined for fresh cells using3H-ouabain. Subjects were selected from pedigrees that showed a prevalence of hypertension. SLC was significantly elevated in 26.5% of the hypertensive subjects (p< 0.001) as well as in 12.8% of the normotensives with a hypertensive first-degree relative (p< 0.05). Although elevated SLC and decreased CoT have previously been associated with hypertension, no hypertensive subject in this study exhibited both abnormalities. All subjects with elevated SLC had normal CoT. A positive correlation between SLC and CoT was observed. Few hypertensive subjects (11.8%) had decreased CoT. In the majority of subjects studied, both SLC and CoT were normal: hypertensives 61.8%, normotensives with a hypertensive first-degree relative 61.7%, and other normotensives 58.7%. The number of ouabainbinding sites was not significantly altered among hypertensives, or their relatives, even though there was a positive correlation between SLC and the number of ouabain-binding sites.

ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The antihypertensive, hemodynamic, and humoral effects of the new convertingenzyme inhibitor enalapril (MK-421) were assessed by sequential studies during 3 months of uninterrupted treatment (20 mg twice daily) in 10 hypertensive patients. Six achieved good blood pressure (mean arterial pressure) control with enalapril alone (from 126 ± 7.0 mm Hg pretreatment to 105 ± 1.6 mm Hg at 3 months,p< 0.05). The other four required the addition of diuretics (hydrochlorothiazide 25 mg orally twice daily) at different stages of follow-up, with resultant blood pressure control (128 ± 9.6 mm Hg pretreatment to 113 ± 1.9 mm Hg at 2 months after the addition of diuretics). Neither the acute nor long-term blood pressure response could be predicted from the pretreatment levels of plasma renin activity. The blood pressure reduction during enalapril therapy was characterized by a decrease in total peripheral resistance (53 ± 2.5 U.M2pretreatment to 38 ± 3.0 U.M2at 3 months,p< 0.05) with no significant change in cardiac output or heart rate. This lack of reflex tachycardia could not be ascribed to baroceptor dysfunction since the response to head-up tilt (the increase in diastolic blood pressure, in heart rate, and in plasma catecholamines) was normal and not significantly different from pretreatment response. Average blood volume did not change (91% ± 4.3% of normal in the pretreatment period to 93% ± 2.9% after 3 months of therapy, p = NS) despite the significant lowering of arterial pressure with enalapril alone (n = 6). This could have been possibly related to the reduction in plasma aldosterone (12.6 ± 2.3 to 8 ± 0.9 ng/dl,p< 9.95) induced by treatment. In conclusion, the hemodynamic consequences of blood pressure reduction by enalapril were similar to those produced by other converting-enzyme inhibitors and angiotensin II antagonists. These findings suggest that the hemodynamic effects of enalapril were related to interference with the generation of angiotensin II rather than a direct action of the drug.

ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Urinary kallikrein excretion during acute water or saline loading was studied in normal and hypertensive humans after chronic Na+depletion and Na+loading to answer the following questions. 1. Is urinary kallikrein a natriuretic or diuretic substance? 2. During acute water or saline loading, does the underlying Na+balance influence (a) the urinary kallikrein response? or (b) the relationship between urinary kallikrein and renal Na+or water handling? 1) Urinary kallikrein did not change during a 1.2 liter water load given to nine white hypertensive and five white normal men. Urinary kallikrein was significantly decreased, however, in five white hypertensive and five white normal subjects during and after 1 hour of isotonic saline infusion (30 ml/kg). In sodiumdepleted hypertensive patients kallikrein excretion was decreased from 19.8 to 9.5 mEU/min, and in Na+-depleted normal subjects it was decreased from 15.7 to 12.6 mEU/min (p = 0.003). The response in hypertensive patients was not different from normal subjects. In all Na+-loaded subjects, kallikrein excretion was also significantly decreased during isotonic saline infusion (p = 0.01). Urinary kallikrein did not change in three other subjects given hypertonic saline. 2(a) The underlying state of Na+balance influenced the baseline level of kallikrein excretion, but not the directional decline in kallikrein during isotonic saline, (b) In Na+-restricted hypertensives given isotonic saline, urinary kallikrein was inversely related to the fractional excretion of Na+(r = -0.54,p< 0.01) and the tubular reabsorption of H2O (TcH2O/GFR; r = - 0.50,p< 0.01). In Na+-loaded hypertensives given isotonic saline, urinary kallikrein was directly related to TcH2O/GFR (r = 0.38,p< 0.05). Prior to infusion, the hypertensives who received isotonic saline showed subnormal renin and aldosterone after dietary Na+restriction, but normal kallikrein excretion. Factors in addition to mineralocorticoids appear to regulate kallikrein excretion. Urinary kallikrein was not a natriuretic or diuretic factor in normal and hypertensive subjects who received acute water or saline loads. In Na+-restricted and -loaded hypertensive and normal subjects, urinary kallikrein was clearly decreased by isotonic saline loading. The state of Na+balance influenced the relationship between urinary kallikrein and renal handling of Na+and H2O.

ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

To clarify the mechanism by which potassium (KCl) protects against the blood pressure rising action of sodium (NaCl), we studied the effects of KCl loading in patients with idiopathic hypertension who, after a period of NaCl restriction, partook of a high NaCl diet. Eleven patients who had taken the KCl supplement (96 mEq/day) during the high NaCl period showed lesser mean blood pressure (MAP) rise with changes in NaCl intake from 25 to 250 mEq/day than 12 patients who had not taken the KCI supplement (p< 0.001). With a high NaCl diet, the KCl-supplemented patients retained less NaCl, gained less weight, and showed a lesser increase in plasma volume and cardiac output than the non-KCl-supplemented ones. Overall, the increase in blood pressure levels during the high Na diet correlated directly either with changes in plasma volume (p< 0.05) or with changes in cardiac output (p< 0.01). The results suggest that KCI may prevent a rise in blood pressure with NaCl loads in hypertensive patients by attenuating the increase in cardiac output, mainly as a result of the natriuresis. Furthermore, plasma norepinephrine was measured to estimate the sympathetic activity, since the sympathetic nervous system is known to control urinary NaCl excretion. From the low NaCl diet to Day 3 of the high NaCl diet, plasma norepinephrine was significantly (p< 0.01) decreased in the KCl-supplemented patients, whereas it remained unchanged in the non-KCl-supplemented ones. Concomitantly, urinary Na excretion was significantly greater in the early period of NaCl loading in the KCl-supplemented group as compared to the other group. Taken together, these results suggest that lower levels of norepinephrine measured in the plasma of the KCl-supplemented patients in the early NaCI-loading phases of the study are indicative of reduced adrenergic neural activity, which might be involved not only in the attenuation of increased cardiac output, but also in the responses of the kidney to shift the pressure-natriuresis relationship toward normal, leading to the natriuresis.

ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The effect on blood pressure (BP) levels of modifying the saturated fat and cholesterol content in the diet was studied in two separate protocols in normotensive volunteers. For 3 months, 19 men and women, aged 14 to 54 years, adhered to a diet that eliminated meat, poultry, eggs, and dairy fat from the subjects' customary nonvegetarian diet, which had included 71 g/day (35%) of dietary fat. The experimental diet reduced the consumption of saturated fat from 21 to 10 g, dietary cholesterol was lowered from 398 to 69 mg per day, but consumption of polyunsaturated fatty acids, carbohydrates, and dietary fiber was unchanged. Body weight and urinary sodium and potassium excretion were not significantly altered. Mean BP before and after the low fat diet was 116/74 and 115/74 mm Hg, respectively. A second double-blind study tested the effect on BP of dietary cholesterol at levels of 155 and 471 mg/day. Seventeen semivegetarian college students consumed one egg per day concealed in desserts for 3 weeks, and identical desserts containing no eggs for an additional 3 weeks. Mean BP at the end of the egg and eggless periods was 108/69 and 107/69 mm Hg, respectively. Thus, in shortterm nutritional studies, dietary saturated fat and cholesterol at low-to-moderate levels of intake have no significant effects on BP in normotensive adults.

ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Vegetarians have relatively low blood pressure (BP) levels and consume less protein than do nonvegetarians, and there have been suggestions that certain proteins may raise BP. To determine whether dietary protein supplements raise the BP of vegetarians, 58 g/per day of a 60:40 mixture of soy and wheat proteins and an isocaloric low protein supplement supplying 7 g/day of rice protein were added for 6-week periods to the diet of 18 vegetarians in a 2-group crossover design. Mean daily protein intake during consumption of the low and high protein supplements was 63 and 119g, respectively. Mean BP was 109/72 mm Hg after the high protein and 108/71 mm Hg after the low protein diet. Consumption of other major nutrients, mean body weight, and sodium and potassium excretion did not change significantly. Thus, protein supplementation of a vegetarian diet that contained a below average but nutritionally adequate amount of protein did not significantly affect BP over 6 weeks.

ISSN:0194-911X    

出版商:OVID    

年代:1984

数据来源: OVID