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

Abnormalities in the kallikrein-kinin system have been found in human and animal models of essential hypertension. The purpose of this study is to assess the kallikrein-kinin system in normotensive Dahl salt sensitive (S) and salt resistant (R) rats on a zero sodium diet. Urinary kallikrein was measured at 7 and 12 wk of age by different techniques. When kallikrein activity was assessed, by a kininogenase assay, S rats excreted 66% (P less than 0.001) and 75% (P less than 0.01) as much kallikrein as R rats at 7 and 12 wk of age. Using an artificial substrate method (Kabi S-2266), S rats excreted 30% (P less than 0.001) and 56% (P less than 0.05) as much kallikrein as R rats at 7 and 12 weeks, respectively. Using a technique to measure total kallikrein, S rats excreted 53% (P less than 0.001) and 65% (P less than 0.05) as much kallikrein as R rats at 7 and 12 wk of age. Normotensive S rats failed to increase maximally kallikrein activity or total kallikrein when the diet was switched from a .4% to a .0064% sodium chloride diet. There was no difference in inhibitors, as measured by the recovery of purified kallikrein added to S and R urine (56 +/- 21% vs. 53 +/- 13%). Km values for S and R urinary kallikrein were similar (3.1 +/- .5 X 10(-5) vs. 2.6 +/- .5 X 10(-5) M/liter). Trypsin-activatable kallikrein was equivalent in the S and R rats on the .0064% and .4% sodium chloride diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased total and active urinary kallikrein in normotensive Dahl salt susceptible rats. 385 74

This study investigated the mechanism underlying the exaggerated natriuresis seen in patients with essential hypertension. The study used the lithium clearance method, which permits accurate determination of both proximal and distal sodium reabsorption in man. One litre of isotonic sodium chloride, intravenously (i.v.), produced a significant increase in sodium excretion in patients with essential hypertension, both during and after the infusion. This increase in sodium excretion was accompanied by a significant increase in the clearance of lithium, indicating an increased output of isotonic fluid from the proximal tubules. The calculated distal reabsorption of sodium increased during the natriuresis. In the normotensive controls, sodium excretion increased only after the infusion of 1 l isotonic saline. This was accompanied by a modest increase in absolute distal sodium reabsorption. However, when the amount of saline was increased to 2 l, similar changes to those seen in hypertensives given 1 l of saline occurred in normotensive subjects. Furthermore, chronic antihypertensive treatment abolished the phenomenon of exaggerated natriuresis. It is concluded that the exaggerated natriuresis represents the normal response to sodium loading being reset to a lower level. This resetting may be a secondary consequence of the high blood pressure, since lowering the pressure abolishes the phenomenon.
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PMID:Effects of acute volume loading on kidney function in patients with essential hypertension, as estimated by the lithium clearance method. 406 7

Bovine hypothalamus contains a stable, low molecular weight substance with ouabain-like properties. To further study its mechanism of action and potential physiological importance we examined its effects on purified Na+-K+-ATPase in a kinetic coupled-enzyme assay. Under optimal conditions up to 95% of Na+-K+-ATPase activity could be inhibited by the factor. Mg2+ is required for maximal inhibitory activity, but ligand requirements for optimal activity are otherwise distinct from those of both ouabain and vanadate. Inhibition is reversed by high concentrations of sodium chloride plus EDTA. Kinetic analysis yielded a Ki = 1.4 nM. The hypothalamic factor is a high-affinity reversible inhibitor of Na+-K+-ATPase, being at least as potent as the cardiac glycoside ouabain and may be a circulating inhibitor of sodium transport, which appears to be associated with experimental volume-expanded hypertension and human essential hypertension.
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PMID:Hypothalamic sodium-transport inhibitor is a high-affinity reversible inhibitor of Na+-K+-ATPase. 609 82

The effects of somatostatin on plasma renin activity (PRA) and blood pressure were evaluated in patients with essential hypertension (EH) and in normotensive subjects. All subjects examined were hospitalized and placed on a diet containing 7-8 g/day sodium chloride and received an intravenous infusion of somatostatin (500 microgram/20 ml of saline, for 60 min) in the basal condition. During somatostatin infusion, the mean blood pressure (MBP) remained unaffected in all patients with EH and the normotensive subjects, while the PRA decreased slightly in the EH group. When the patients with EH were classified according to their renin levels (low, normal and high), parallel significant decreases in MBP and PRA were found only in the high renin group during the somatostatin infusion. No significant change in MBP and PRA was observed in the other groups including the normotensive subjects. To assess the activity of synthetic somatostatin, the plasma levels of growth hormone (GH) and cyclic AMP were measured. These levels were lowered significantly during the infusion and the GH levels showed a rebound 15 min after cessation of the infusion. The cyclic AMP returned to the basal levels, but no rebound was observed. The above data indicate that the fall in blood pressure in the high renin group in the basal condition was probably due in part to reduced renin release by somatostatin, and the maintenance of high blood pressure especially in high renin EH.
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PMID:Effect of somatostatin on plasma renin activity and blood pressure in patients with essential hypertension. 610 26

Prompt and exaggerated natriuresis and diuresis were seen one to two hours after the starting of an infusion of 300 ml of 3% saline for one hour in patients with essential hypertension on a high sodium chloride intake. There were no significant differences in urinary volume and sodium excretion after the saline load in patients with normal and low plasma renin activity. The inhibition of angiotensin converting enzyme with SQ 14225 in patients with normal plasma renin activity did not produce additional natriuresis and diuresis after the saline load. Mean arterial blood pressure and/or changes in mean arterial blood pressure after the saline load showed a positive correlation with urinary volume and sodium excretion in each collection period in hypertensive subjects. Free water reabsorption in hypertensives was lower at high levels of osmolar clearance than that in control subjects. These results suggest that "exaggerated natriuresis" in essential hypertension is due to a decrease in tubular sodium reabsorption, which may be the result of intrarenal hemodynamic changes related to high blood pressure per se. The decreased medullary osmolar gradient is a possible contributing factor in the enhanced sodium and water excretion, while the renin-angiotensin-aldosterone system does not seem to play an important role.
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PMID:Studies on the mechanism of "exaggerated natriuresis" in essential hypertension. 625 57

In 116 patients with coronary heart disease, essential hypertension, acute and chronic glomerulonephritis and pyelonephritis, the authors observed differences in the excretion of the ions of 42K, stable potassium, 24Na, stable sodium, chlorine as well as in the value of diuresis during the administration of equimolar solutions of potassium hydrocarbonate and potassium chloride, sodium hydrocarbonate and sodium chloride labeled with 42K and 24Na respectively. These differences depended on the expression of the basic (alkaline) characteristics of the anions of the administered solutions of potassium and sodium and the osmolarity of the administered amount of liquid. Pronounced ion exchange reactions were observed during the administration of KHCO3 solution only, the multiplicity factor of the excretion of sodium and chlorine ions with urine significantly exceeding that of diuresis. During the administration of KCl solutions in the isotonic NaCl solution and 5% glucose, the excretion of sodium and chlorine ions changed strictly in accordance with the changes of diuresis. Similar changes were noted in the administration of the solutions of sodium hydrocarbonate and sodium chloride.
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PMID:[Metabolism of potassium and sodium when administered with different anions to patients with ischemic heart disease and arterial hypertension]. 632 82

To evaluate sodium susceptibility in subjects with borderline hypertension at increased risk of developing essential hypertension, the effect of salt loading after sodium deprivation with a diuretic was studied in 21 young patients with borderline hypertension and 12 age-matched normal subjects. Treatment with a diuretic caused significant decreases in mean blood pressure (MBP) in subjects with borderline hypertension but not in normotensive subjects. In borderline hypertensives, the subsequent sodium loads resulted in a significant rise in MBP (5.8 +/- 1.7%; p less than .01), but sodium did not change MBP in normotensives. There is a good correlation between the increments in MBP with sodium loads and the decrements in MBP with a diuretic for each patient (r = -.759, p less than .001). After diuretics, cardiac index (CI) as measured echocardiographically fell significantly but calculated total peripheral resistance (TPR) remained unchanged in subjects with borderline hypertension. After 180 meq sodium chloride each day was added for 7 days, CI (9.1 +/- 2.1%; p less than .01) and stroke index (21.0 +/- 3.4%; p less than .01) rose significantly but TPR remained unchanged. Overall, the increments of MBP with sodium loads did not correlate with the changes in CI but did correlate with the changes in TPR (r = .567, p less than .01). In these young patients with borderline hypertension, plasma norepinephrine and epinephrine concentrations and plasma renin activity (PRA) were significantly higher than in normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sodium susceptibility and potassium effects in young patients with borderline hypertension. 636 6

103 patients with mild or moderately severe essential hypertension and 35 healthy normotensive subjects were examined. In all patients examined plasma osmolality, plasma renin activity and plasma level of vasopressin and aldosterone were estimated twice: first after administration of a diet with a sodium chloride content of 100 to 120 mmol/a day and 8 hours recumbency and a second time after 3 days of dietary sodium chloride restriction (20 mmol/a day) and 3-4 hours upright position. In hypertensives independent of the behaviour of the plasma renin activity similar values of the plasma osmolality, the plasma level of vasopressin and the aldosterone level could be established as in healthy persons. In contrast to normals in hypertensive subjects no significant correlation between plasma osmolality or plasma renin activity and plasma level of vasopressin and aldosterone was stated. In spite of normal levels of vasopressin and aldosterone a significant correlation between the plasma level of vasopressin and aldosterone and the systolic blood pressure was found in hypertensive patients. From the results obtained in this study follows that in hypertensive patients the plasma osmolality is only of secondary importance for the secretion of vasopressin and aldosterone and for the plasma renin activity. The importance of plasma vasopressin and aldosterone in the pathogenesis of hypertension seems to be probable but not yet unanimously proved.
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PMID:[Is there a relation between the renin-angiotensin-aldosterone system and vasopressin secretion in essential hypertension?]. 639 82

Intrarenal sodium handling was studied in 8 patients with essential hypertension before spironolactone treatment (200 mg/day), on the 4th day of treatment, and after 3 months of treatment. The results were compared with similar studies with chlorthalidone (50 mg/day). Renal sodium handling was assessed by simultaneous determination of the glomerular filtration rate, sodium, and potassium excretion, and maximal free-water clearance (CH2O). We took CH2O as an index of 'distal' sodium chloride reabsorption from which the proximal sodium reabsorption was calculated. During the first days of spironolactone treatment a natriuresis and increase in urinary flow rate was found. It resulted in a decrease of the extracellular fluid volume amounting to 0.9 liters and a 2.5-fold increase in the plasma renin activity. Potassium excretion showed a small but significant rise. After 3 months, virtually the same degree of volume depletion was found, which was comparable to that obtained after 3 months of chlorthalidone treatment. CH2O, as a fraction of glomerular filtration rate, decreased by 24% both after 3 days and 3 months, whereas proximal sodium reabsorption increased from 87.8 to 90.4% of the filtered load. CH2O, corrected for the 'distal' delivery of sodium, decreased from 85.3 to 80.7%. These changes were nearly the same as those found after 3 months of chlorthalidone treatment. It is concluded from these calculated values that spironolactone inhibits sodium chloride reabsorption in the diluting segment of the nephron and that the resulting increase in sodium delivery or urinary flow to the potassium excretory site partly counteracts the blocking effect of spironolactone on this part of the nephron, thus increasing potassium excretion during the acute administration of this drug.
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PMID:Intrarenal sodium handling during chronic spironolactone treatment. 651 71

Regulation of aldosterone secretion by sodium chloride is impaired in a group of essential hypertensives: high-salt diet fails to suppress aldosterone in these patients despite low renin values. The mechanism of this impaired regulation of aldosterone has not been clarified so far. We tested the sensitivity of aldosterone secretion and blood pressure to A II in 20 normotensive controls (aged 20-60, MAP 92 +/- 3 mm Hg), in ten normotensives with one or two parents with hypertension, and in 21 patients with essential hypertension (aged 17-65, MAP 119 +/- 4 mm Hg). After a period of 6 days on high-salt intake (300-320 mEq Na+/day), A II (0.1, 0.5, 1.0 and 2.0 ng/kg/min) was infused, each concentration for 30 min. According to aldosterone excretion during sodium loading, patients were divided into group A with complete suppression (n = 12, aldosterone excretion 3.6 +/- 0.4 microgram/day) and in group B with insufficient suppression (n = 9, aldosterone excretion 15.5 +/- 2.3 micrograms/day). Despite similarly low plasma renins, rise of serum aldosterone levels during A II infusion was significantly higher in group B patients than in group A patients and normotensive controls. Rise in mean arterial blood pressure, however, brought about by graded A II infusion was similar in both groups of hypertensives and in normotensive controls. The results demonstrate an increased adrenal sensitivity to A II in a subgroup of essential hypertensives only. A similar adrenal hypersensitivity to A II found by others in patients with hyperaldosteronism due to adrenal hyperplasia supports the hypothesis that the same mechanism underlies both disorders.
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PMID:Cardiovascular and adrenal sensitivity to angiotensin II in essential hypertension. 652 58


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