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

A technique for continuous and quantitative collection of parotid saliva--including salivary flow rate determination--for in vivo experiments in rats is described. Excretion of kallikrein-like activity in parotid saliva of rats with various forms of arterial hypertension (genuine, renovascular and DOCTMA-salt hypertension) was studied. Kallikrein excretion was measured by its esterolytic activity. The levels of kallikrein-like activity in parotid saliva of normotensive control rats ranged between 2.5--4.0 mU/min during salivary flow stimulation with pilocarpine. In all forms of experimental hypertension salivary excretion of kallikrein-like activity was increased 2--4 fold. This increase was not related to the activity of the renin-angiotensin system.
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PMID:Kallikrein excretion in parotid saliva in rats with various forms of arterial hypertension. 26 42

Kallikrein excreted with the urine appears to be formed in the kidney. The kallikrein-kinin system in the kidney is localized in the distal nephron from the juxtaglomerular apparatus to the collecting duct. It has been shown that intrarenal infusion of kinins produces an increase in renal blood flow as well as diuresis and natriuresis. Part of the effect of kinins appears to be mediated by the release of prostaglandins. However, the precise role of the renal kallikrein-kinin system in sodium and volume homeostasis and in blood pressure regulation still remains to be determined. Mineralocorticoids as well as the diuretics furosemide, bumetanide and bendroflumethiazide increase, spironolactone decreases kallikrein excretion. Urinary kallikrein has been shown to increase acid-as well as cryoactivation of prorenin in vitro. It is unclear as yet, however, whether the renal kallikrein-kinin system takes part in converting inactive prorenin into active renin in vivo. There are reports on subnormal, normal as well as increased kallikrein excretion in spontaneously hypertensive rats. In rats susceptible to the hypertensive effect of salt a substantially decreased excretion of kallikrein has been observed. Kallikrein excretion has been described to be increased in primary aldosteronism and to be reduced in a proportion of patients with established essential hypertension. In patients with labile hypertension, however, kallikrein excretion appears to be normal suggesting that decreased urinary kallikrein in essential hypertension is a consequence rather than a cause of hypertension. The renal kallikrein-kinin system does not appear to play a primary role in the pathogenesis of hypertension.
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PMID:[Renal kallikrein-kinin system and control of blood pressure (author's transl)]. 39 77

Renal kallikrein and phospholipase activities were evaluated in a strain of spontaneously hypertensive rats developed by Dr. Bianchi in Milan (MHR). MHR showed lower than normal kallikrein and phospholipase activities before, at 3 weeks of age and following the development of hypertension. Kallikrein and phospholipase activities were directly correlated both in normotensive and spontenously hypertensive rats. The data suggest that MHR have a genetic defect in kallikrein and phospholipase activities, which may play a pathogenetic role in the development of high blood pressure.
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PMID:Kidney kallikrein and phospholipase activities in Milan spontaneously hypertensive rats. 52 75

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

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

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

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

1. Urinary kallikrein, sodium, potassium and water excretion, and plasma renin activity were measured before and during the reversal of experimental hypertension produced by unclamping the renal artery in rats. 2. Kallikrein excretion decreased significantly after unclamping, suggesting that it does not play a significant role in the reversal of hypertension. 3. A decrease in plasma renin activity coupled with a slight increase of sodium excretion was observed, indicating that these might participate in the reversal of hypertension.
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PMID:Urinary kallikrein and plasma renin during the reversal of renovascular hypertension in rats. 107 24

1. The kallikrein content of kidneys from spontaneously hypertensive and normal rats at birth and at age 37 days was determined. 2. Kallikrein values were significantly lower in the hypertensive rats. 3. It is suggested that the lowered kallikrein may be related to the development of hypertension.
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PMID:Renal kallikrein content of spontaneously hypertensive rats. 114 96

Urinary kallikrein excretion was studied in a number of animal models of hypertension. Kallikrein excretion was subnormal in spontaneously hypertensive rats as compared to Wistar/Kyoto rats and in rats made hypertensive by a clip on one renal artery. Kallikrein excretion was supranormal in rats made hypertensive by desoxycorticosterone and salt and in rats receiving desoxycorticosterone alone. It was subnormal after bilateral adrenalectomy. Kallikrein excretion increased in normotensive rats fed a low-sodium diet but was unchanged by a high-sodium diet. Thus, kallikrein excretion responded to changes in activity of sodium-retaining steroids and was not correlated with excretion of salt or water. In studies in dogs with stenosis of one renal artery kallikrein excretion was decreased on the stenoic side and the decrease correlated highly with the reduction in renal blood flow. While the role of the kallikrein-kinin system is still unclear the data indicate that the kidney may modify the initiation or maintenance of hypertension via this potent vasodilator system.
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PMID:Urinary kallikrein in hypertensive animal models. 124 54


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