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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary kallikrein was measured in rats bred to be susceptible (S) or resistant (R) to the hypertensive effect of salt. To determine kallikrein, three different methods were used: (1) a new direct radioimmunoassay (RIA) for the enzymic protein: (2) a method based on the capability of kallikrein, when incubated with kininogen, to generate kinins which were then measured by RIA (kininogenase activity); and (3) a method based on the capability of kallikrein to break the ester bond of p-tosyl-L-arginine methyl ester (HCl (TAMe). A significant correlation ( r = 0.90) was found between the direct RIA and the kininogenase method. It was found that urinary kallikrein was significantly decreased in the S as compared to the R rats by the use of these three methods. Urinary kallikrein in the S rats was much lower when measured by the kininogenase method than by direct RIA or esterolytic assay. This difference could be due to excretion of pre-kallikrein and/or kallikrein bound to an inhibitor (inactive kallikrein). It is suggested that the decrease of urinary kallikrein excretion (active and inactive) in the S rats could be a consequence of a genetic defect that may affect the development of hypertension perhaps through the alteration of sodium and water excretion by the kidney.
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PMID:Urinary kallikrein in rats bred for their susceptibility and resistance to the hypertensive effect of salt. A new radioimmunoassay for its direct determination. 63 96

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

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

Previous studies in a population of 721 children aged 2--14 years demonstrated the familial aggregation of blood pressure in children, and a significant regression coefficient (b = 0.25) of follow-up on initial blood pressures over a four-year period. Urinary kallikrein concentration (UKal) also aggregated in families, was lower in black than in white children and was inversely related to blood pressure. Further studies in the same cohort have been conducted. These variables were again measured in 484 children in 129 families seven to eight years after the initial blood pressure and three to four years after the original UKal measurements were made. Familial aggregation again was found for blood pressure and urinary kallikrein. Blood pressure tracking was demonstrated by the finding that blood pressure scores at the third survey were related significantly to those at both previous surveys. Kallikrein concentrations in casual urines at Survey 3 were related to those obtained at Survey 2 (r = 0.499), and were again significantly lower in black than in white children (log = 3.84 +/- 0.8 vs 4.37 +/- 0.7; P less than 0.001). These were significant inverse relations between UKal/creatinine concentration and blood pressure in both white and black children. Thus, familial aggregation of blood pressure, blood pressure rank and concentration of kallikrein in casual urine specimes are relatively stable in children over an eight-year period of observation. This study demonstrates in a free living population of normal children, a stable relation between blood pressure and an enzyme which is involved in the production of potent vasodilator peptides and is related to hypertension in adults.
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PMID:Stability of blood pressure rank and urinary kallikrein concentration in childhood: an eight-year follow-up. 69 59

Young female unilaterally nephrectomized, salt-loaded, Sprague-Dawley rats were treated with 200 microgram or 1 mg 18-hydroxy-deoxycorticosterone-21-acetate (18-OH-DOCA) in oil daily, and a group of kidney-intact animals on a normal salt intake was given 2 mg/day. The hormone was not found to increase saline consumption, increase urinary potassium or kallikrein excretion, or depress serum renin activity or potassium concentration. Slight hypertension did develop at 3 weeks in salt-loaded rats on the lowest dose, but this was neither increased by higher dosage or longer treatment, nor reflected by increased heart or kidney weight. The effect of 40-mg pellet implantation of DOCA and 18-OH-DOCA was then compared in unilaterally nephrectomized, salt-loaded, female Fischer 344 rats. The former caused increased saline consumption, hypertension, hypokalemia, and heart and kidney enlargement, whereas 18-OH-DOCA did not. Thus, the hypertensogenic potency of 18-OH-DOCA is, at best, a reflection of its known, very weak, mineralocorticoid activity.
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PMID:Experimental hypertension and other responses to 18-hydroxy-deoxycorticosterone treatment in the rat. 74 64

We investigated the relationship of the kallikrein-kinin system and the renin-angiotensin system in the regulation of blood pressure, salt and water excretion, and renal blood flow. Normotensive and hypertensive black and white men were studied during unresticted sodium intake as well as on a 10-meq/day sodium intake; potassium intake was held constant throughout the study (80 meq/day). During unrestricted sodium intake, urinary kallikrein activity was greater in white normotensives than white hypertensives or black normotensives. There was no difference (P greater than 0.05) between white and black hypertensives or between black normotensives and black hypertensives. All groups had greater urinary kallikrein activity on low sodium vs. unrestricted sodium intake, but the increase in black hypertensives was small, and they excreted significantly less kallikrein than the ogher groups on the low sodium diet. Plasma renin activity showed similar increments after sodium restriction in all groups. Urinary kallikrein activity correlated with renal blood flow in all groups except the black normotensives on low sodium intake. Renal blood flow could be correlated uniformly with log (urinary kallikrein activity/supine plasma renin activity) in all groups on either diet. Urinary sodium and potassium excretion and urine volume were not different among the groups. We conclude: (a) important racial differences exist in urinary kallikrein activity that are unrelated to sodium or potassium excretion or urine volume; (b) dietary sodium restriction further delineates racial differences and suggests alternative pathophysiologic mechanisms for huma hypertension; (c) urinary kallikrein activity correlates with renal blood flow; and (d) our data support the concept that the kallikrein-kinin system and the renin-angiotensin system contribute to the regulation of renal blood flow and may account for racial differences in renal vascular resistance.
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PMID:Urinary kallikrein and plasma renin activity as determinants of renal blood flow. The influence of race and dietary sodium intake. 87 78

Plasma, blood, and urine volumes, renal kallikrein, and arterial pressure were measured in control and renal hypertensive rats in order to study the role of the renal kallikrein system in regulating arterial pressure and its relation with the alterations in water handling observed in hypertension. A decrease in kallikrein content of the kidney (157 +/- 17 versus 236 +/- 16 ng bradykinin equivalents per gram of tissue in control rats) was associated with an increase in plasma volume (38.0 "/- 1.6 versus 32.0 +/- 0.9 ml/kg body weight in control rats) and an increase in urine volume (45.5 +/- 4.9 versus 20.3 +/- 1.6 ml/kg body weight per 24 hours in control rats). No linear correlation was found between these factors and the arterial pressure of hypertensive animals. These findings support the hypothesis that changes in renal kallikrein are more directly related to water and electrolyte metabolism than to the arterial pressure regulation. Our results also suggest an interaction between the kallikrein-kinin and the renin-angiotensin-aldosterone systems. The possible relations of both enzymatic systems to the regulation of arterial pressure and of water-electrolyte handling are summarized schematically.
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PMID:Renal kallikrein system, volemia, and renal hypertension. 87 70

Urinary kallikrein excretion was studied in rats bred for susceptibility and resistance to the hypertensive effect of salt. The rats were on a regular rat chow diet (0.45% sodium content) and tap water and were not hypertensive at the time of the study. Urinary kallikrein excretion, measured by kinin radioimmunoassay, was 10 to 20 times lower in the susceptible rats than in the resistant rats (4.39 +/- 1.61 microgram/24 hours and 56.4 +/- 5.8 microgram/24 hours, respectively; P less than 0.001). Urinary kallikrein excretion was also measured in New Zealand genetically hypertensive rats and in normotensive Wistar-Otago rats (controls). Kallikrein was found to be significantly lower in the genetically hypertensive rats than in the controls (49.1 +/- 6.2 microgram/24 hours and 76.8 +/- 6.9 microgram/24 hours, respectively); however, when expressed per 100 g of body weight, there was no significant difference. In conclusion, although urinary kallikrein excretion per rat was decreased in the genetically hypertensive rats when compared with the controls, this difference could be caused by the lower body weight of the genetically hypertensive rats. Urinary kallikrein excretion, when expressed per 100 g of body weight, is significantly lower in susceptible than in resistant rats. This could be a consequence of a genetic defect that may play a role in the development of hypertension, perhaps through alteration of renal function.
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PMID:Urinary kallikrein in rats bred for susceptibility and resistance to the hypertensive effect of salt and in New Zealand genetically hypertensive rats. 87 72

In four patients with hypertension and angiographically pronounced unilateral renal artery stenosis, kallikrein activity was estimated in each kidney separately by the determination of kinin output in the renal veins. All patients showed suppression of renin release from the kidney with a non-stenotic artery. Accordingly, plasma flow from the kidney with artery stenosis could be estimated. The ratio of venous output of kinins between the kidney with a non-stenotic artery and the one with artery stenosis was 2.6-6.5. This indicates that renal artery stenosis leads to diminished intrarenal kinin generation. Reduced kinin formation may explain the low diuresis and natriuresis found in the kidney with artery stenosis.
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PMID:Renal venous output of kinins in patients with hypertension and unilateral renal artery stenosis. 91 Jun 36

Urinary and kidney kallikrein were studied in rats with renal clip hypertension. The effect of protease inhibitors on urinary and kidney BAEE esterase activity was similar. Both hypertensive and not hypertensive operated rats excrete significantly less kallikrein than controls; in the ischaemic kidney kallikrein is diminished whereas is not increased in contralateral. Kallikrein is therefore related to renal functional mass but does not seem responsible for a natriuretic effect.
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PMID:Urinary and kidney kallikrein in hypertensive rats. 99 Mar 80


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