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

1. Urinary kallikrein was measured in 67 patients with essential hypertension and 25 normotensive subjects variously on unrestricted and low sodium diet. Also, the effect of orally applied hog pancreatic kallikrein on elevated blood pressure and kallikrein excretion was evaluated. 2. Urinary kallikrein was reduced in a large subgroup of patients with sustained essential hypertension. 3. With salt restriction, urinary kallikrein rose markedly in normotensive subjects and patients with borderline hypertension but not in those with sustained hypertension. 4. Oral kallikrein normalized reduced kallikrein excretion and lowered elevated blood pressure. 5. The rise in urinary kallikrein with oral kallikrein was due to an increased formation of endogenous enzyme. 6. A defective kallikrein-kinin system may be involved in both the low urinary kallikrein excretion and the hypertension.
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PMID:Low urinary kallikrein excretion and elevated blood pressure normalized by orally kallikrein in essential hypertension. 26 17

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

Hypertension may result from excessive activity of one or more components of the blood pressure-elevating system. These include the adrenergic nervous system, the renin-angiotensin axis, and mineralocorticoids (aldosterone), which potentiate each other, reinforcing their effects on renal hemodynamics and electrolyte transport and thereby affecting extracellular fluid volume, vascular tone, and reactivity. We consider of no less importance in the genesis of hypertension the failure of one or more components of the blood pressure-lowering system: the kallikrein-kinin system, prostaglandin, or one or more lipids associated with the renomedullary interstitial cells. As a corollary of this hypothesis, if one assumes tonic activity of these opposing blood pressure-regulating systems, in the case of a deficiency of the vasodepressor system, hypertension should result. That is, unopposed activity of the pressor system should be sufficient to increase blood pressure without an increase in the "basal level" of its activity. Hypertension, then, may be considered to result from either uncompensated deficiencies or excesses, which may be relative or absolute, of one or more components of the vasodepressor and vasopressor systems.
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PMID:Role of naturally occurring vasoactive principles in hypertension. State of the art. 32 62

The kallikrein-kinin system in the kidney is localized in the distal nephron, where it appears to be linked to processes that control water and electrolyte excretion. Some evidence exists that the effect of the renal kallikrein-kinin system is partially mediated by the release of prostaglandins. It has not yet been determined whether endogenous kinins affect the function of the nephron directly or indirectly by changes in renal blood flow distribution. Further, a number of studies in animals and humans indicates that kallikrein excretion is decreased in most types of hypertension, with the exception of hypertension caused by an excess of mineralocorticoids (where kallikrein is increased). In rats susceptible to the hypertensive effect of salt, kallikrein is conspicuously decreased. In renal diseases, urinary kallikrein excretion is also decreased. Finally, it still needs to be determined whether or not low kallikrein excretion is a pathogenetic factor in hypertension and renal diseases.
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PMID:The renal kallikrein-kinin system in human and in experimental hypertension. 36 76

Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter's syndrome is balanced by high PGE and kallikrein without hypertension.
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PMID:Kallikrein, kininogen and kinins in control of blood pressure. 37 13

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

According to immunohistochemical investigations kallikrein in the majors salivary glands is located predominantly at the apical border of the striated duct cells and as a luminal rim in the main excretory ducts. Comparatively the highest concentrations are observed in the submandibular gland of rats and cats in the cytoplasmic granules of the granular tubules. In normal humans and rats the kallikrein activity of parotid saliva is inversely related to flow rate and sodium concentration. An increased salivary kallikrein concentration is found in human essential hypertension and renoparenchymal hypertension associated with impaired kidney function. Furthermore in rats with various forms of hypertension (genetic hypertension, DOCTMA salt and renovascular hypertension) the salivary kallikrein secretion - as determined by the BAEE-esterase activity - is enhanced. In contrast to the kallikrein secretion the flow dependent sodium concentration of parotid saliva is reduced in human essential and renoparenchymal hypertension as well as in rats with various forms of experimental and genetic hypertension, which indicates an enhanced sodium reabsorption in the glandular duct system. Furthermore in most forms of hypertension, there is a tendency of higher potassium levels in the saliva. The pathogenesis of the enhanced glandular kallikrein secretion in hypertension is discussed with regard to a counterregulatory mechanism in hypertension as well as to a sympathicoadrenergic activation. The enhanced sodium reabsorption in the duct system in the various forms of hypertension could be the cause as well as a consequence of the enhanced kallikrein secretion.
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PMID:Salivary kallikrein excretion in hypertension. 39 78

When rats are submitted to diets with variable sodium, concentration, one may observe a significant increase in the excretion of urinary kallikrein and in the kallikrein activity of the renal tissue in animals in chronic sodium depletion. During experimental renovascular hypertension induced in the rat by stenosis of the renal artery, one may note a significant rise in the excretion of urinary kallikrein; no change in this excretion is observed when the stenosis is associated with nephrectomy on the opposite side. It is possible to consider interrelations between the renin-angiotensin-aldosterone system and the kallikrein-kinin system.
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PMID:[Renal kallikrein: variations in relation to sodium intake and experimental renovascular hypertension (author's transl)]. 44 14

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

Urinary kallikrein is an enzyme, probably originated in the kidney, which acts on plasma kininogen to produce kallidin, the decapeptide precursor of bradykinin, and appears to be implicated in various forms of arterial hypertension. It is significantly decreased in workers exposed to lead showing no hypertension or other clinical signs of lead poisoning. In respect to measurement of ALA or other heme precursors the determination of urinary kallikrein seems to be able to detect a different, and perhaps in certain cases earlier, effect of lead intoxication on enzyme functions.
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PMID:[Urinary kallikrein and risk of lead poisoning]. 60 38


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