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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The extracellular volume (ECV) and plasma volume (PV) were determined simultaneously in nine men with untreated essential hypertension and in nine healthy matched control subjects, using a single injection of inulin and of 131I-labelled human serum albumin, respectively. The average mean arterial blood pressure in the hypertensive group was 178/118 mmHg. ECV was nearly the same in the two groups, viz. 151 ml/kg body weight (SD 17) in the hypertensive group compared to 147 ml/kg (SD 16) in the control group. The corresponding figures for PV were 38.2 ml/kg body weight (SD 4.7) and 43.7 ml/kg (SD 7.9) respectively (P less than 0.1). The calculated interstitial fluid volume (IV) was 113 ml/kg (SD 16) and 103 ml/kg (SD 10) (P less than 0.2). The PV/IV ratio was significantly lower (P less than 0.02) in the hypertensive group (0.34, SD 0.06) than in the normal group (0.42, SD 0.06). The difference might suggest increased transcapillary water filtration in hypertension.
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PMID:Extracellular fluid volume determined by a single injection of inulin in men with untreated essential hypertension. 60 11

The hematocrit, hemoglobin, serum total protein and serum albumin concentration increased significantly following sublingual administration of nifedipine in patients with essential hypertension (p less than 0.05). The mean increase in hematocrit at 60 min after administration was 1.5%. The results suggest a decrease in plasma volume, perhaps due to diuresis and a shift of fluid from the intravascular to the extravascular space.
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PMID:Increase in hematocrit by nifedipine in hypertensive patients. 224 94

Subjects with high renin hypertension tend to be sodium-resistant showing paradoxical blood pressure responses to alterations in sodium intake. Of twenty-five subjects with high renin essential hypertension (ten females, 15 males, mean age 30 years), 14 were noted to have a decrease in mean arterial blood pressure (MAP) when sodium intake was increased from 10 to 100 mmol/d. The percentage response of plasma renin activity was greater in these patients than in those with an increase in MAP (-55.4 +/- 5.4 v -33.6 +/- 6.9, P = .018). Overall, the response of MAP was directly correlated to the percentage response of plasma renin activity (r = .549, P = .005), and inversely related to the change in serum calcium concentration (corrected for changes in serum albumin) (r = -.547, P = .005). No intercorrelation between the changes in plasma renin activity and serum calcium concentration was detected. The blood pressure response to increased sodium intake in high renin hypertension would appear to be divergent and related not only to the suppression of plasma renin activity, but also to changes in circulating calcium.
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PMID:Blood pressure and serum calcium responses to altered sodium intake in high renin hypertension. 264 17

The acute haemodynamic effect of perindoprilat was examined at rest, supine and sitting, and during 100 W bicycle exercise in 12 patients (mean age 42 years) with essential hypertension. Intra-arterial blood pressure and the heart rate were recorded continuously. Cardiac output was measured by dye dilution (Cardiogreen) and blood volume was determined by radio-iodinated (125I) human serum albumin. Two hours after a slow (3 min) intravenous injection of perindoprilat, blood pressure was reduced in all patients (P less than 0.01)--at rest sitting from 175/108 to 153/97 mmHg (11%)--because of reduction in total peripheral resistance index (f = 2.63; P less than 0.05). Only minor changes were seen in the heart rate, stroke index and cardiac output. The fall in blood pressure was significantly (P less than 0.05) correlated with blood volume (r = 0.65) and pretreatment total peripheral resistance index (r = 0.59).
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PMID:Acute haemodynamic effects of perindoprilat in essential hypertension at rest and during exercise. 268 9

The purpose of this study is to evaluate the plasma Na, K-ATPase inhibitor (NKI) in patients with essential hypertension and to compare the mode of its biochemical actions on the Na, K-ATPase with that of ouabain. Plasma NKI was extracted through a reversed-phase cartridge column and its inhibitory action on hog brain Na, K-ATPase was measured in vitro. Plasma NKI activity was significantly greater in patients with essential hypertension (44 +/- 2.8% (S.E.), n = 28, p less than 0.01) than in normotensive controls (25 +/- 2.4%, n = 21). No significant correlation was demonstrated between the values of plasma NKI and mean arterial pressure in either group. Both plasma NKI and ouabain showed a dose-dependent inhibition on the Na, K-ATPase reaction. An action of ouabain was competitively antagonized by increased concentration of potassium in the reaction mixture, while plasma NKI showed a constant inhibition on the Na, K-ATPase independently of potassium concentrations. The action of plasma NKI was of rapid onset and linear with time, while ouabain showed a delayed onset of the reaction over 30 sec, followed by a progressively increasing inhibition on the enzyme reaction. Finally, the inhibitory action of plasma NKI on Na, K-ATPase was completely abolished in the presence of bovine serum albumin even at the concentration of 500 micrograms/ml in the reaction mixture, which did not have any influence on the actions of ouabain. To sum up, the results showed a markedly different nature of plasma NKI from ouabain in the mode of biochemical actions on the Na, K-ATPase in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A plasma inhibitor of sodium and potassium activated adenosine triphosphatase in patients with essential hypertension. 285 Jun 42

The autoregulation theory of essential hypertension states that the characteristic haemodynamic derangement of this disease, i.e. increased vascular resistance, is a homeostatic response to abnormal sodium retention by the kidneys. The postulated relationship between arterial pressure and urinary sodium excretion is disturbed in such a way that a higher than normal pressure is required for sodium excretion to keep up with intake. This will initially expand plasma volume and raise cardiac output. However, hyperperfusion of the tissues will ultimately induce vasoconstriction, presumably by greater than normal wash-out of vasodilator metabolic products. Thus, cardiac output will be restored. Some elements of this theory are not supported by current evidence, but the key element, i.e. the assumption that increased vascular resistance is somehow dependent on abnormal renal sodium handling, is consistent with the following clinical observations: Arterial pressure and urinary sodium excretion are directly correlated over a wide range of pressures in patients with autonomic failure, both acutely during titling and chronically with changes in posture during a 24-h period. The failure to demonstrate pressure-natriuresis in normal subjects may therefore be related to the amplifying effect of the sympathetic nervous system on this mechanism, so that small changes in pressure are capable of inducing large changes in sodium excretion. The pressure-natriuresis curve in patients with autonomic failure is shifted to higher pressures by administration of aldosterone, which is consistent with an important role of renal sodium retention in mineralocorticoid hypertension. Measurements of total extracellular fluid volume, plasma volume/interstitial fluid volume ratio, transcapillary escape rate of serum albumin, cardiac output and arterial pressure at timed intervals during the development of hypertension, in patients exposed to mineralocorticoid excess, or during the reversal of hypertension in nephrectomized patients treated with ultrafiltration haemodialysis, revealed an association of increased total peripheral resistance with a reduced plasma volume/interstitial fluid volume ratio and an increased transcapillary escape rate of serum albumin. This association has also been observed in cross-sectional studies of patients with essential hypertension and suggests that part of the increase in resistance is located at a post-capillary level. It may be related to compression of collapsible venules and veins due to abnormally increased interstitial fluid pressure, not only in sodium-dependent secondary forms of hypertension but also in essential hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The second Sir George Pickering memorial lecture. What regulates whole body autoregulation? Clinical observations. 402 Jan 27

30% of patients with essential hypertension have a decreased adrenal response to angiotensin II (A II) on a low but not a high sodium intake. They also have a compensatory increase in the activity of the renin-angiotensin system best documented in a sodium-restricted state.To assess whether such a mechanism could account for the hypertension in genetically hypertensive rats, adrenal responsiveness to A II was determined in three groups of rats; spontaneously hypertensive rats (SHR), normotensive Wistar rats (WKY), and normotensive Sprague-Dawley rats (SDR). Animals in each group were placed on either a low or high sodium diet for 14 d with balance assessed by sodium excretion. The animals were then decapitated, blood was obtained for plasma renin activity (PRA), A II and aldosterone and adrenals isolated for the preparation of purified glomerulosa cells. The cells were incubated in Krebs-Ringer bicarbonate solution, containing bovine serum albumin, for 60 min in the absence and presence of increasing concentrations of A II. The PRA, basal aldosterone output, and adrenal sensitivity to A II were similar in the three groups of rats on the high sodium diet. On the low sodium diet the SHR had a significantly (P < 0.01) higher PRA (25+/-7 ng/ml per h) than either the WKY (12+/-2 ng/ml per h) or the SDR (7+/-1 ng/ml per h) and lower basal aldosterone output (68+/-17 vs. 154+/-43 and 197+/-21 ng/10(6) cells per h, respectively). In addition, the slope of the A II dose response curve was more shallow (P < 0.01) in the cells from the SHR than those obtained from the WKY and SDR.Thus, the SHR PRA and aldosterone responses to sodium restriction and aldosterone response to A II were similar to that previously described in a subgroup of patients with essential hypertension suggesting that the SHR will serve as a model for exploring the mechanism(s) responsible for the hypertension in these patients.
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PMID:Decreased adrenal responsiveness to angiotensin II: a defect present in spontaneously hypertensive rats. A possible model of human essential hypertension. 627 15

Thirty-five patients with uncomplicated hypertension were observed for blood pressure behaviour after prolonged antihypertensive medication withdrawal. Twenty-three patients (Group 1) remained normotensive (systolic less than 140 mmHg, diastolic less than 95 mmHg) for over 60 weeks compared to 12 patients (Group 2) who became hypertensive again during a 4-week placebo period. Discriminant analysis was performed on 31 clinical and laboratory variables measured before therapy to separate any discriminating factors for the two groups. Four variables maximized the separation of Group 1 from Group 2 patients. In descending order, these were serum sodium (p less than 0.001), mean corpuscular volume (p less than 0.01), serum albumin (p less than 0.01), and body weight (p less than 0.05). Using these four variables 73.9% of patients in Group 1 and 75% of patients in Group 2 were classified correctly into their respective groups. It is suggested that this observation may be useful in the development of new therapeutic regimens for patients with uncomplicated essential hypertension, for example by predicting those patients who may respond favourably to intermittent therapy or even to its withdrawal.
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PMID:Separation of essential hypertensive patients based on blood pressure responses after the withdrawal of antihypertensive agents by step-wise discriminant analysis. 635 5

A total of 1075 relatives of 106 individuals (probands) with treated essential hypertension and heredity for this disease have been investigated concerning the existence of hypertension. The prevalence of hypertension or hypertensive diseases was near 50%. Of the decreased relatives, 77% had a positive history for hypertension. Of the decreased relatives with cerebrovascular diseases, 52% had expired before 65 years of age. We have examined 307 relatives of these probands. They had significantly higher systolic blood pressure, heart rate and serum albumin concentration than age- and sex- matched controls without heredity for hypertension and a screened population. Screening of relatives belonging to families with a high frequency of hypertension seems to have a potential practical value and may furthermore provide information about the etiology of the disease.
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PMID:Blood pressure, heart rate and plasma albumin in relatives of hypertensive patients. 725 62

The urinary aldosterone (ALD) was measured by aldosterone RIA kit and the following results were obtained. (1) We have known that ten percent solution of bovine serum albumin (BSA) instead of free serum LAD is used as the diluent of the urine in aldosterone RIA kit. (2) The upper limits of free ALD, HCl-ALD and beta-glucuronidase ALD in the urine diluted with 10% BSA were 1.6, 9.0 and 9.5 micrograms/dl respectively. (3) The values of urinary conjugated HCl-ALD and beta-glucuronidase ALD were approximately 3.5 times and 4 times as much as that of free ALD respectively. (4) A good correlation was obtained among the results of three methods (HCl-ALD, beta-glucuronidase ALD and free ALD). (5) No difference was found in the values of the urinary ALD in the healthy subjects and the patients with essential hypertension, kidney diseases and acute liver diseases.
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PMID:[Estimation of the urinary aldosterone (author's transl)]. 732 22


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