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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 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

Maintenance of normotension rests upon the overall salt and water balance, which, in the event of disequilibrium, modifies body fluid, cardiac output and total peripheral resistance. The kidneys play a central role in this hydro-saline regulation. The central and autonomous nervous systems, the renin-angiotensin system, the mineralocorticoids, the antidiuretic hormone and the kallikrein-bradykinin-prostaglandin system all affect this regulation and are closely interrelated. The role of each of these nervous and endocrine systems in hypertension, and their close interrelationship, is briefly reviewed.
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PMID:[Physiopathology of arterial hypertension. Role of the nervous system and of the hormones]. 101

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

The state of the kinin system of blood was studied in terms of its content of kininogen, prekallikrein, kallikrein inhibitor and the spontaneous esterase activity. The examination was conducted in 10 normal individuals and in 81 hypertensive patients with labile and stable arterial pressure and an uncomplicated course. The studies were conducted at rest, during the transfer into an orthostatic position, and after 15 or 60 minutes of walking. The normals demonstrated an activation of the kinin system that ensued in orthostasis, but was more distinct at walking. A significant correlation was noted between the content of prekallikrein and kininogen in all the states under examination. In cases of labile arterial hypertension an increased activation of the blood kinin system was observed at rest, a lack of its activation at walking, and disorders in the correlation between the content of prekallikrein and kininogen. The observed changes in the kinin system may affect the central haemodynamics and the formation of the hyperkinetic type of circulation.
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PMID:[Characteristics of changes in the kinin system of blood in hypertensive disease]. 108 40

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 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 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

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

We investigated the effect of two oral (p.o.) doses of cicletanine (5 and 30 mg/kg/day) for 4 weeks on urinary excretion (UKE), renal concentration (RKC) of kallikrein, and prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha urinary excretion of stroke-prone (SP) spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) rats submitted to a high sodium intake (1%). Both doses of cicletanine induced a significant antihypertensive effect in treated SHR as compared with hypertensive untreated controls (HC). After 4-week treatment, a significant difference in mortality was observed between normotensive controls (NC) (0%) and HC (84%). Both doses of cicletanine reduced the mortality of hypertensive animals (8% SHR with 5 mg and 24% SHR with 30 mg vs. 84% in HC). Whereas UKE and RKC were decreased in HC during the progression of untreated hypertension from week 1 to week 4, both doses of cicletanine administration significantly prevented this decrease. Consistently with maintenance of UKE during the course of hypertension, the level of tissue kallikrein was higher in hypertensive cicletanine-treated than in untreated SHR. This increased RKC was associated with a significantly higher rate of kallikrein biosynthesis. The increased level of the urinary excretion and tissue concentration of PGE2 and 6-keto-PGF1 alpha in cicletanine-treated SHR as compared with untreated animals was also of interest. This protective effect on PG excretion correlated with that on kallikrein excretion. The results confirm the efficiency of cicletatine as an antihypertensive treatment. The antihypertensive action includes protective effects on potential vasodepressor kallikrein-kinin and prostaglandin systems.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of cicletanine on hypertension-induced decreases in the renal kallikrein-kinin and prostaglandin systems in stroke-prone spontaneously hypertensive rats. 128 Jul 17

Deoxycorticosterone acetate (DOCA)-salt hypertension was induced in Brown Norway (BN) kininogen-deficient rats (BN-Ka) and normal rats from the same strain (BN-Ki) after nephrectomy. Systolic blood pressure, which was determined by the tail-cuff method, of BN-Ki increased gradually during this treatment. In contrast, the blood pressure of mutant BN-Ka increased rapidly 2 weeks after the onset of the treatment. Urinary excretion of active kallikrein and prokallikrein increased at the same degree in rats of both strains during this treatment. Significant increase in urinary sodium excretion was observed with a tendency to increase in urine volume during the treatment in normal BN-Ki rats, whereas both parameters were essentially not increased in mutant BN-Ka rats, which could not generate urinary kinin. Aprotinin infusion by osmotic minipump to normal BN-Ki rats during the DOCA-salt treatment resulted in significant further increase in the systolic blood pressure.
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PMID:Essential role of kallikrein-kinin system in suppression of blood pressure rise during the developmental stage of hypertension induced by deoxycorticosterone acetate-salt in rats. 128 79


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