Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies of the renal kallikrein-kinin system in chronic renal failure (CRF) have given conflicting results. We have assessed activity of this vasoactive hormone system in CRF and investigated a possible relationship to hypertension in patients with CRF: 24-hour urinary kallikrein excretion (UKa) was measured in 22 patients with CRF (9 normotensive and 13 hypertensive) and 11 healthy controls. Age, sex, urine volume, and urinary sodium excretion were similar in each group. Compared with controls, UKa was reduced in both normotensive and hypertensive patients with CRF, with no difference between CRF groups. The reduction in UKa in CRF was less than the reduction in glomerular filtration rate (GFR), as assessed by endogenous creatinine clearance (CCr). When UKa was divided by CCr, UKa/mL CCr was therefore increased, to a similar extent, in both normotensive and hypertensive patients with CRF. This suggests that release of renal kallikrein from functioning nephrons is increased in CRF. The results do not support a role for deficient kallikrein release in the genesis of hypertension in CRF, as previously suggested; however, these abnormalities could be relevant to other aspects of renal function in CRF. The converting-enzyme inhibitor, captopril, was given to 5 patients with CRF, hypertension, and low UKa. Introduction of captopril was followed by a further reduction in UKa in all subjects. Captopril is known to inhibit kininase II, the principal enzyme involved in degradation of kinins; this potentiating effect may be counteracted by a reduction in renal kallikrein release and hence in kinin generation.
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PMID:Urinary kallikrein excretion in chronic renal failure: relationship to blood pressure and the acute effect of captopril. 333 25

Whether to determine the urinary kallikrein (UKK) level in the second trimester of pregnancy is valuable or not for the prediction of gestosis, especially of hypertension in the third trimester of pregnancy, was studied on 700 cases of pregnant women including 50 cases of gestosis. The main results obtained were as follows. Sixty cases of 610 non-gestotic women were low in UKK, and 17 of these cases later resulted in gestosis or preterm delivery. When a patient with mild gestosis and/or hypertension was admitted, the UKK level was elevated significantly in general by bed rest and a low-salt diet. The UKK level was more significantly lowered in threatened preterm delivery than in normal pregnant women (p less than 0.001). A close positive correlation was seen between UKK levels and prostaglandin E2 in urine in pregnant women (n = 30, r = 0.528). A relatively close correlation was seen between UKK levels and roll-over test results (n = 30). From these results, the authors reached the conclusion that to determine UKK in the second trimester of pregnancy is quite valuable in predicting not only gestosis and/or hypertension in the third trimester of pregnancy but also preterm delivery.
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PMID:[Clinical value of urinary kallikrein determination in obstetrics]. 345 88

The mechanisms causing high blood pressure in patients with Cushing's syndrome were investigated by measurements of humoral factors and pharmacological maneuvers. Twelve patients with adrenal adenomas were studied. The mean systolic and diastolic pressures of the patients were 171 +/- 28 and 109 +/- 15 mm Hg (+/- SEM), respectively, which were significantly higher than those of normal subjects. PRA, plasma renin concentration, plasma renin substrate, plasma cortisol, plasma aldosterone, urinary kallikrein, and urinary prostaglandin E2 were measured as the humoral factors. PC values were markedly elevated in patients with Cushing's syndrome. Among the components of the renin-angiotensin system, only plasma renin substrate was increased. Urinary kallikrein and prostaglandin E2 were decreased in patients with Cushing's syndrome. Oral administration of captopril lowered blood pressure, but infusion of an angiotensin II analog did not. Furthermore, the pressor responses to infusion of both norepinephrine and angiotensin II were increased. We conclude that blood pressure is elevated in patients with Cushing's syndrome because they have enhanced pressor responses to vasoactive substances, suppression of depressor systems, and some abnormalities of the renin-angiotensin system.
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PMID:Multiple factors contribute to the pathogenesis of hypertension in Cushing's syndrome. 351 Feb 23

In order to clarify the mechanism of the hypotensive action of captopril, the acute and chronic effects of this drug on the kallikrein-kinin and renin-angiotensin systems were investigated respectively in 14 and 19 patients with hypertension. To determine the acute effect, a dose of 50 mg of captopril was administered once orally. For the chronic effect, 75-300 mg of the drug was administered daily for 14 days. In observations of the acute effect, blood pressure decreased significantly at 30 min. and maximally at 60-180 min. after administration with no change in heart rate. Significant increases in blood kinin levels and plasma renin activity (PRA), and a decrease in plasma angiotensin II levels were also observed. A marked augmentation was also found in urinary kinin excretion, but not in urinary kallikrein excretion. Moreover, the changes in blood pressure significantly correlated negatively with basal PRA, basal plasma angiotensin II and the changes in blood kinin levels, and positively with the changes in plasma angiotensin II. In our study of the chronic effect of captopril, similar changes in blood kinin levels, PRA, plasma angiotensin II levels, blood pressure and heart rate to the acute effect study were observed. Significant correlations of the changes in blood pressure were found negatively with basal PRA, basal plasma angiotensin II levels and the changes in blood kinin levels and positively with the changes in plasma angiotensin II levels. In addition, significant increases in urine volume and urinary sodium excretion occurred following administration of captopril for 14 days, and both increases negatively correlated with the changes in blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of the hypotensive effect of captopril (converting enzyme inhibitor) with special reference to the kallikrein-kinin and renin-angiotensin systems. 352 64

Evidence indicates that an alteration in kidney function has a causal role in the pathogenesis of hypertension in the Milan hypertensive strain (MHS) rat. At the prehypertensive stage, these animals have increased glomerular filtration rate and 24-hour urinary output, whereas plasma renin activity and urinary kallikrein are lower. After transplantation, the MHS kidney increases the blood pressure of a normotensive recipient. Micropuncture experiments, where single nephron filtration rate, tubuloglomerular feedback, proximal tubular reabsorption, micro-pressures in tubuli, and interstitium and interstitial oncotic pressure were measured, suggest that the intrinsic ability of MHS proximal tubular epithelium to reabsorb solute and water is greater in prehypertensive MHS rats than in Milan normotensive strain (MNS) rats. Also rheogenic Na transport across the brush-border vesicles isolated from proximal tubular cells is faster. When erythrocytes and proximal tubular cells of MHS rats are compared to those of MNS rats, the former have smaller volume and Na content, whereas the Na transport is faster and the Ca ATPase at Vmax is lower. This indicates that the genetic cellular abnormality responsible for the renal functional abnormality and hypertension is also present in erythrocytes. Moreover, MHS erythrocyte abnormalities are genetically determined within the stem cells and are genetically associated with hypertension. Because a correlation was also found in human hypertension between erythrocyte Na transport abnormality and renal function, it is proposed that the erythrocyte may be used for studying the genetic molecular mechanisms of hypertension.
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PMID:Cell membrane abnormalities and genetic hypertension. 353 12

Many similarities in kidney-function abnormalities were found between hypertensive rats of the Milan strain (MHS) and young normotensive human subjects with hypertensive parents, compared with the appropriate controls. These similarities included an increased glomerular filtration rate, increased pressor effect of the kidney after transplantation, increased 24-h urinary output and lower plasma renin activity and urinary kallikrein. The isolated MHS kidney perfused in vitro with an artificial medium had a higher glomerular filtration rate, a higher urinary output, higher tubular sodium reabsorption and higher oxygen consumption than the kidney of control Milan normotensive rats (MNS). Further, reogenic sodium transport across brush border vesicles isolated from proximal tubular cells is faster in MHS than in MNS. Erythrocytes and proximal tubular cells of MHS have a lower volume and sodium content than those of MNS, while sodium transport is faster and the Ca2+-ATPase at Vmax is lower. This indicates that the 'genetic' cellular abnormality responsible for the renal-function abnormality and the hypertension is also present in erythrocytes. Thus these cells may be used to study the genetic cellular mechanisms of hypertension. Experiments with bone marrow transplantation and with F2 hybrids obtained by crossing the F1 (MHS X MNS) hybrids showed that the MHS erythrocyte abnormalities are genetically determined within the stem cells and are genetically associated with the hypertension. Since, in human hypertensives, there was a correlation between abnormal erythrocyte sodium transport and renal function, it is proposed that erythrocytes may be used in studying the cellular molecular mechanisms of hypertension.
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PMID:A renal abnormality in the Milan hypertensive strain of rats and in humans predisposed to essential hypertension. 353 35

The activity of basal 24-hour urinary kallikrein activity (UKA), prostaglandin E2 (U. PGE2) and thromboxane B2 (U. TxB2) and their relationship to natriuresis (U. Sodium), urinary aldosterone (U. Aldosterone) and plasma renin activity (in supine position: PRA1; in standing position: PRA2) were evaluated in 20 patients with early-moderate hemodynamically defined (first pass and gate blood pool radionuclide angiocardiography) essential hypertension (H) and in 13 age-matched normotensive patients (N). In basal conditions, UKA and PRA2 were significantly reduced (p less than 0.005 and p less than 0.05, respectively) in H compared with N. However, no differences between N and H were found for U. TxB2, U. PGE2, U. Aldosterone, U. Sodium, and PRA1. All parameters were also evaluated both in H and N before and after the administration of furosemide (40 mg i.v.). In H, but not in N, furosemide induced an increase of UKA (p less than 0.05), U. TxB2 (p less than 0.05) and U. Sodium (p less than 0.001). In both H and N furosemide caused a significant rise of PRA1 (p less than 0.001 in H and p less than 0.01 in N) and PRA2 (p less than 0.001 in H and p less than 0.05 in N). In H a significant correlation was found between percent increases of U. Sodium and U. Kallikrein (r = 0.54, p less than 0.01) and between percent differences of PGE2 and TxB2 (r = 0.59, p less than 0.01). It is proposed that reduction of basal UKA may be an early evidence of the first stages of hypertension, i.e., in absence of renal and cardiovascular alteration. The finding is not accompanied by significant changes in urinary excretion of arachidonic acid metabolites and aldosterone. Finally, any relation between UKA values and systemic hemodynamics is lacking.
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PMID:Acute effect of furosemide on renal kallikrein and prostaglandin systems in mild to moderate essential hypertension. 354 80

In this study, urinary kallikrein quantity and activity were measured by the kallikrein direct RIA and kininogenase activity with human low molecular weight kininogen in 32 non pregnant healthy women, 20 normal 3rd trimester pregnant women and 18 3rd trimester hypertension type toxemia patients. There was no significant difference in urinary kallikrein quantity between non pregnant women (n = 32, 64.0 +/- 6.3 micrograms/day, mean +/- SE) and normal pregnant women (n = 20, 68.1 +/- 10.1 micrograms/day). There was a significant difference (p less than 0.001) between non pregnant women and toxemia patients (n = 18, 22.5 +/- 3.3 micrograms/day). There was a significant difference (p less than 0.001) between toxemia patients and normal pregnant women. There was a significant difference (p less than 0.05) in urinary kallikrein activity between non pregnant women (n = 32, 496.2 +/- 57.2 micrograms kinin/day) and normal pregnant women (n = 20, 319.5 +/- 48.1 micrograms kinin/day). There was a significant difference (p less than 0.0001) between non pregnant women and toxemia patients (n = 18, 82.6 +/- 13.6 micrograms kinin/day). There was a significant difference (p less than 0.01) between normal pregnant women and toxemia patients. There were no correlation in both urinary kallikrein quantity and activity between severe type toxemia patients (systolic blood pressure greater than or equal to 160mmHg or diastolic blood pressure greater than or equal to 110mmHg) and mild type toxemia patients (160mmHg greater than systolic blood pressure greater than or equal to 140mmHg and 110mmHg greater than diastolic blood pressure greater than or equal to 90mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Urinary kallikrein quantity and activity of normal pregnant women and toxemia patients in third trimester]. 363 50

In investigating the role of urinary kallikrein in the pathophysiology of hypertension, we measured 12-hour kallikrein excretion in 1,100 persons in 68 Utah kindreds. The kallikrein excretion was statistically adjusted to account for variations in body size and urine output. Adjusted kallikrein excretion was greater in youths than in adults and correlated with potassium excretion and sodium excretion in persons with normal blood pressure. It was decreased in normotensive subjects with strong family histories of stroke and hypertension, but was not significantly different in adults with hypertension. Adjusted kallikrein excretion was correlated between pairs of siblings, parent-offspring pairs and spouses. Our results indicate that kallikrein excretion is a familial variable, with the familiality due more to shared environmental than genetic factors.
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PMID:Evidence for environmental familiality of kallikrein excretion in Utah kindreds. 363 40

On the basis of both clinical observations and experimental studies it has been proposed that renal kallikrein is a mineralocorticoid regulated protein. In other studies, changes in renal kallikrein activity have been implicated in the genesis of, and/or response to, hypertension. Using a cloned complementary DNA (cDNA) to rat pancreatic kallikrein (pcXP39) for hybridization histochemistry, and both Northern and dot blot analysis, we studied expression of the kallikrein gene in steroid-treated control animals, and in three strains of genetically hypertensive rats. No differences in renal kallikrein messenger RNA (mRNA) levels were found between adrenalectomized rats and those treated for 5-14 days with 9 alpha-fludrocortisone, corticosterone or dexamethasone, or between hypertensive rats and their appropriate controls. Since mRNA levels appear essentially invariant under such circumstances, the change in renal kallikrein activity/immunoreactivity after chronic mineralocorticoid elevation, or in hypertensive rats, presumably reflects modulation at the post-transcriptional level.
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PMID:Expression of the renal kallikrein gene in mineralocorticoid-treated and genetically hypertensive rats. 363 7


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