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

The effect of furosemide on urinary kallikrein excretion was studied in 10 patients with essential hypertension and 9 normal volunteer subjects. After intravenous administration of furosemide and 2 hours of upright posture, urine volume (UV), urinary sodium (UNaV) and potassium (UKV) excretion, plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary kallikrein markedly increased. However, the augmentation of urinary kallikrein in patients with essential hypertension (1.50 +/- 0.19 EU/2 hr) was less remarkable than that in normal subjects (2.33 +/- 0.24 EU/2 hr), although the same degrees of response were observed in PRA and PAC. The increments of UV, UNaV and UKV in patients with essential hypertension were also significantly lower than in normal subjects. Significant positive relations were found between urinary kallikrein and UV or UNaV in both hypertensive and normotensive groups, but there was no such correlation before fursemide administration. It is likely that diuresis and natriuresis induced by furosemide are somehow associated with an increase in urinary kallikrein excretion. Blunted response of urinary kallikrein in essential hypertension may suggest an abnormality in the renal kallikrein-kinin system in this disease.
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PMID:Effect of furosemide on urinary kallikrein excretion in patients with essential hypertension. 63 97

To learn more about the regulation of blood pressure in renal parenchymal disease, 57 subjects (18 normal controls, 25 patients with essential hypertension and 14 with renal parenchymal disease and hypertension) were evaluated for peripheral renin activity, 24-hour urinary kallikrein activity and whole-blood volume. Blood volumes were significantly lower in patients with essential hypertension (P less than 0.001) and those with renal disease and hypertension (P less than 0.001) than in normotensive subjects. Renin activities (measured after the subjects were standing) were also lower in patients with essential hypertension and hypertension due to renal disease (P less than 0.01 and P less than 0.02, respectively). Kallikrein activity was similar in subjects with renal disease and those with hypertension (P less than 0.05) but markedly diminished in both groups as compared with normotensive subjects (P less than 0.001 and P less than 0.01, respectively) when glomerular filtration rates were taken into account. The kallikrein-kinin system may be involved in the hypertension associated with renal parenchymal disease.
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PMID:Urinary kallikrein activity in the hypertension of renal parenchymal disease. 66 89

The effect of tilting on the release of renal kallikrein as compared to renin was studied by the determination of kinin concentration and plasma renin activity (PRA) in the renal veins in supine position and after 15 min of 45 degrees upright tilting in 10 patients with essential hypertension. Kinin concentration decreased from 0.62 +/- 0.05 microgram/1 (mean +/- S.E.M.) in supine position to 0.51 +/- 0.05 after tilting (p less than 0.01), while PRA increased from 2.84 +/- 0.39 microgram/1/3 h tpo 4.87 +/- 0.66 (p less than 0.001). These results indicate that tilting diminishes the release of renal kallikrein. It is suggested that decreased intrarenal generation of kinins may be of importance for the reduction of diuresis and natriuresis induced by tilting.
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PMID:Effect of upright tilting on kinins as compared to renin activity in the renal venous blood from patients with essential hypertension. 66 8

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroup: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients beta-adreno-receptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.
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PMID:Urinary kallikrein excretion and plasma renin activity in patients with essential hypertension and primary aldosteronism. 66 67

Urinary kallikrein excretion was measured before and after administration of spironolactone in 12 patients with essential hypertension (including 7 patients with low renin and 5 patients with normal renin) and 6 patients with primary aldosteronism. In low renin essential hypertension, two types of urinary kallikrein excretion were observed. In one type, urinary kallikrein decreased from 6.2+/-2.1 (S.E.) EU/day to 2.7+/-0.3 EU/day after the treatment. In another type, urinary kallikrein increased from 3.1+/-0.5 EU/day to 6.4+/-1.0 EU/day. In the former, plasma aldosteron showed high levels (12.3+/-2.1 ng/100 ml), while in the latter, it was normal (3.2+/-0.5 ng/100 ml). In normal renin essential hypertension, urinary kallikrein excretion did not alter after the treatment. In primary aldosteronism, urinary kallikrein showed moderate decrease after the spironolactone treatment from 8.5+/-1.6 EU/day to 4.2+/-1.6 EU/day. Spironolactone is said to compete directly with the effect of aldosterone at renal distal tubules. The present investigation suggests that urinary kalikrein excretion is related to the effective levels of aldosterone at renal distal tubules, and alteration of aldosterone levels mediates the release of kallikrein, and that there are different mechanisms in the renal handling of sodium and kallikrein in low renin essential hypertension, in normal renin essential hypertension, and in primary aldosteronism.
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PMID:Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism. 84 38

The relationship between urinary kallikrein, urinary aldosterone, and plasma renin activity (PRA) was studied in hypertensive patients and normal subjects. Kallikrein was measured by a radiochemical esterolytic assay. Nine white males with normal renin, mild essential hypertension (25 +/- 5 [SD] yr; blood pressure [BP] 143 +/- 7 / 95 +/- 5 mm Hg) and six white normal males (23 +/- 3 yr; BP 115 +/- 15 / 70 +/- 6 mm Hg) were placed on a one-week diet consisting of 400 mEq Na+, 80 mEq K+ diet and a one week diet of a 10 mEq Na+, 80 mEq K+ diet. During salt restriction, PRA, urinary aldosterone, and urinary kallikrein progressively rose. (Urinary kallikrein on day 7: normals 18.3 +/- 13.7 esterase units [EU] per 24 hr; hypertensives 22.7 +/- 12.5 EU/24 hrs). There were no significant differences between the normals and hypertensives in PRA, aldosterone, or kallikrein excretion. After sodium balance was achieved, during salt loading, the PRA, aldosterone and kallikrein values were similar in both normals and hypertensives. (Urinary kallikrein on day 7: normals 5.0 +/- 5.2; hypertensives 7.9 +/- 4.4 EU/24 hrs.) Abnormalities in urinary kallikrein in hypertensives were not found when young white males with normal renin essential hypertension were compared to age-matched white male normal subjects. PRA appears related to urinary kallikrein excretion in this type of patient.
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PMID:Urinary kallikrein in normal renin essential hypertension. 91 48

Urinary kallikrein was measured in normal pregnant women stages of gestation and in women who developed hypertension in late pregnancy. Mean urinary kallikrein was highest in the first trimester and fell significantly in the third trimester to nonpregnosterone system. A negative correlation was observed between urinary kallikrein and the length of gestation in normal pregnancy. Urinary kallikrein fell significantly below nonpregnant levels in patients with hypertension while the renal excretion of sodium and water was not different from that in normal pregnancy of the same dy is discussed in the light of factors known to increase kallikrein excretion. It is considered unlikely that this elevation is due to the escape from the sodium-retaining effect of the high aldosterone of pregnancy. It may be due in part to the stimulating effect of raised angiotensin II levels but it is considered most likely to be the effect of a circulating renal vasodilator. The reduced kallikrein in hypertension of pregnancy may play a part in the development of the hypertension and resembles the reduced kallikrein excretion in essential hypertension.
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PMID:Urinary kallikrein in normal and hypertensive pregnancies. 100 45

Urinary kallikrein excretion was measured in 21 healthy subjects and 44 patients with various types of hypertension. The kallikrein activity was determined by the method of esterolytic assay. The excretion rates in normal subjects were 112.9 +/- 11.1 (S.E.) EU/day. The kallikrein excretion was decreased in patients with essential hypertension, the mean estimated values were 75.2 +/- 10.0 EU/day. In this disease, however, an enhancement of urinary kallikrein was observed after sodium depletion. An obvious increase in kallikrein excretion was found in the primary aldosteronism. In primary aldosteronism and renovascular hypertension, one of the secondary aldosteronisms, there was a good correlation between the urinary kallikrein output and the urinary sodium excretion. The present data indicate that the renal kallikrein-kinin system, one of the renal antihypertensive factors, is suppressed in essential hypertension and is under the influence of mineralocorticoid levels.
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PMID:Urinary kallikrein excretion and sodium metabolism in hypertensive patients. 118 19

Urinary kallikrein excretion is reduced in patients with hypertension of unknown etiology. In addition, the excretion of this renal, kinin-forming enzyme was found to be elevated in hypertensive patients with primary aldosteronism. Aldosterone regulates kallikrein excretion, as normal subjects show increased kallikrein excretion in response to a low sodium intake, high potassium intake, or the synthetic mineralocorticoid, fludrocortisone, whereas kallikrein excretion falls during treatment with spironolactone. The relationship between kallikrein excretion and aldosterone activity may directly reflect the intrarenal activity of the kallikrein-kinin system, as determined by studies of kallikrein levels from isolated renal cells or of plasma kinin levels in man in response to postural changes or saline loads. Some patients with essential hypertension do not show a normal increase in kallikrein excretion in response to low dietary sodium intake despite an apparently normal aldosterone response, suggesting that there may be a defect in the renal kallikrein-kinin system in these patients. Whether these findings are of pathogenetic significance in human hypertensive disease remains to be determined.
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PMID:Relationships among urinary kallikrein, mineralocorticoids and human hypertensive disease. 124 55

In essential hypertension, renal dopaminergic activity and PGE2 was suppressed as was the renal kallikrein-kinin system. The suppression of the renal depressor systems may play an important role in the etiology of hypertension through sodium and body fluid retention. At the prehypertensive stage of essential hypertension, renal dopaminergic activity was suppressed, which induced the retention of body fluids and sodium. On the other hand, the renal prostaglandin E2 was augmented, and it seemed to be a compensatory mechanism for sodium retention. We could not confirm the suppression of the renal kallikrein-kinin system at the prehypertensive stage of hypertension. Although all renal depressor systems are suppressed in essential hypertension, the suppression of the renal kallikrein-kinin system and PGE2 seem to be very important in the etiology of hypertension. Further study is necessary to clarify when both systems are suppressed.
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PMID:The renal kallikrein-kinin system at the prehypertensive stage of hypertension. 146 63


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