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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute effects of 25 mg captopril on blood pressure, heart rate, components of the renin-angiotensin system and blood concentration of bradykinin were followed in a single-blind placebo study of untreated (group A, n = 15) and thiazide-treated (group B, n = 13) patients with mild or moderate essential hypertension. A drug-related fall in blood pressure was seen in both groups. The blood pressure reduction was more marked in group B than in group A. Heart rate remained unchanged. Plasma concentrations of angiotensin II decreased significantly with concurrent increases in plasma concentrations of renin and angiotensin I, indicating the in vivo inhibition of converting enzyme. Blood concentrations of bradykinin showed no systemic changes. The magnitude of blood pressure reduction was correlated both with the pretreatment levels and the concurrent decreases in plasma angiotensin II. Inhibition of angiotensin II formation can explain a large part of the acute hypotensive pharmacological action of captopril. Other vasoactive systems may be involved. The kallikrein-kinin system does not appear to participate as indicated by the unchanged concentrations of kinin in blood.
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PMID:Converting enzyme inhibition in mild and moderate essential hypertension. I. Acute effects on blood pressure, the renin-angiotensin system and blood bradykinin after a single dose of captopril. 300 13

Enalapril maleate is a new angiotensin converting enzyme inhibitor marketed in the U.S. by Merck Sharp and Dohme. It has been demonstrated to actively interfere with the renin-angiotensin-aldosterone system. This is reflected by both hemodynamic (decreased blood pressure) and humoral (increased plasma renin, angiotensin I, and decreased angiotensin II) responses to enalapril therapy. Activity in the kallikrein-bradykinin system is still controversial. Enalapril maleate is a prodrug which is quickly absorbed, hydrolyzed by the liver to the active metabolite enalaprilic acid, and excreted 33 percent in the bile and 61 percent in the urine. The therapeutic dosage range is 10-40 mg/d, maximum of 40 mg, given once or twice daily. The onset and duration of action are dose related. Vertigo and headache have been the most commonly reported side effects. Clinical comparison of enalapril to hydrochlorothiazide, beta-adrenergic blockers, and captopril find it efficacious in the treatment of essential hypertension. Efficacy in treating congestive heart failure and hypertension secondary to renal artery stenosis has also been demonstrated for both angiotensin converting enzyme inhibitors. The overall efficacy and safety of enalapril and captopril appear equivalent when used at low doses in patients with uncomplicated hypertension.
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PMID:Enalapril: a new angiotensin converting enzyme inhibitor. 300 62

In order to investigate the role of the renal kallikrein-kinin (K-K) system in normal (NRH) and low renin (LRH) subgroups of essential hypertension (EHT), daily urinary excretions of renal K-K system components including kallikrein (KAL), total KAL, pre-KAL, kinin (KIN) and kininase (total, I and II), were measured in 21 normotensives (NT) and 45 patients with EHT (NRH: 29, LRH: 16). Urinary KAL and KIN quantities, KAL activity, total and pre-KAL, and kininase (total, I and II) were measured by direct RIA, kininogenase assay, direct RIA of KAL after trypsin treatment, and KIN destroying capacity, respectively. The daily excretions of KAL quantity and activity, total and pre-KAL, and KIN were significantly lower in EHT than in NT. That of total kininase and kininase I were significantly higher in EHT than in NT while no significant difference was found in kininase I between EHT and NT. In comparing NRH and LRH, the urinary KAL activity and KIN were lower in LRH than in NRH, and kininase I was higher in LRH than in NRH. No significant difference, however, was found in total and pre-KAL, KAL quantity and kininase II between NRH and LRH. The ratio of KAL quantity/total KAL which reflects the conversion rate from pre-KAL in the kidney, did not show any significant difference among NT, NRH and LRH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comprehensive studies on the renal kallikrein-kinin system in essential hypertension. 302 78

Captopril effects were studied in 27 patients with second-stage essential hypertension following administration of a single 25 mg oral dose of the drug. Blood pressure (BP), blood angiotensin-1-converting enzyme (ACE) activity, active (APR) and inactive (IPR) plasma renin levels were measured every 30 minutes for 3 hours. Before and near the end of the acute test, urinary kallikrein and catecholamine excretions were measured, and systemic and regional hemodynamic changes assessed. BP decreased in 21 patients: 11 of those had low basal APR (group 1), and 10 had normal or moderately elevated APR (group 2). The greatest hypotensive effect was observed within 1.5 hours after the administration, coinciding with the most marked ACE inhibition. There was no significant intergroup difference with respect to the extent of the hypotensive effect. No correlation was found between the hypotensive effect and the degree of ACE inhibition. All patients showed significantly decreased arteriolar tone, increased venous distensibility, decreased total peripheral resistance, and expanded end diastolic volume, while their cardiac output and heart rate remained unaffected. Hypertensive patients with low APR gave no evidence of renin-angiotensin inhibition or kallikrein-kinin activation that might have accounted for the hemodynamic effect of captopril.
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PMID:[Mechanisms of the hypotensive action of captopril in essential hypertension]. 303 55

The magnitude of captopril hypotensive effect, and variation in renin-angiotensin-aldosterone and kallikrein-kinin parameters were examined in patients with advanced essential hypertension in the presence of normal and low plasma renin activity. The demonstrated differences in the patterns of arterial BP, renin-angiotensin and kallikrein-kinin change have suggested that low-renin essential hypertension is resistant to captopril in most cases.
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PMID:[Changes in the indicators of the renin-angiotensin-aldosterone system, kallikrein-kinin system and arterial blood pressure in elderly patients with essential hypertension treated with captopril]. 307 45

Possible differences in structure-function relationship of urinary kallikrein between normotensive and hypertensive individuals were analysed using two different assay systems which detect two distinct entities of the enzyme. A monospecific goat anti-human urinary kallikrein antibody was characterized by inhibition studies with the purified active enzyme and by trypsin activation of endogenous urinary prokallikrein. Analysis of the data revealed that the antibody is directed against active kallikrein by recognizing an epitope which is different from the catalytic site of the enzyme but which is being exposed together with the active site during trypsin activation of the proenzyme. A direct radioimmunoassay for urinary kallikrein was developed and correlated with the kinin generating activity of the enzyme by assessing endogenous active and trypsin activated kallikrein in the urine of normotensive and hypertensive subjects. Significant positive correlations were found between the two assays for both active and total kallikrein in normotensive and hypertensive subjects and the slopes of the respective regression lines were identical. These data do not provide evidence for a defective enzyme, a defective activation of the proenzyme or for the presence of an inhibitor of urinary kallikrein in essential hypertension.
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PMID:Correlation of two different assays for urinary kallikrein in normotensive and hypertensive subjects. 324 81

In order to clarify the relationship and the pathophysiological role of renal dopamine, kallikrein-kinin and prostaglandin systems in essential hypertensives, the effects of dopamine on these systems and renal sodium handling were investigated. Basal levels of kallikrein, kinin and prostaglandin E2 in essential hypertensives were significantly lower than those in normotensives. Those of kallikrein and kinin were obviously more suppressed in the low renin group than in the normal renin group, but no significant difference in prostaglandin E2 was found in either subgroup. Urinary dopamine excretion was significantly lower in the low renin essential hypertensives, while no significant difference was found between normotensives and normal renin essential hypertensives. Kallikrein activity and prostaglandin E2 were significantly increased in essential hypertensives by dopamine infusion, and no significant difference was found in kallikrein-quantity and kinin between normotensives and essential hypertensives after the infusion. These increases of kallikrein and kinin were significantly higher in the low renin group than in normal renin group, but those of prostaglandin E2 were not. Urine volume, urinary sodium excretion and fractional excretions of sodium and inorganic phosphorus were all increased in both normotensives and essential hypertensives after dopamine infusion. The increases of these were significantly greater in essential hypertensives than in normotensives, and greater in the low renin group than the normal renin group. From these results, it was suggested that the dopamine, kallikrein-kinin and prostaglandin E2 system have a close relationship with each other, and the suppression of these systems may contribute to the pathophysiology of essential hypertension, especially in the low renin group.
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PMID:The pathophysiological role of renal dopamine, kallikrein kinin and prostaglandin systems in essential hypertension. 332 11

Different levels of water-salt metabolism control were studied in patients with stable essential hypertension (SEH). The sample was found to be highly heterogeneous in terms of the magnitude of the body's water-filled spaces in relation to plasma renin activity (PRA) and the cooking salt gustatory sensitivity threshold, examined in the presence of various salt diets and diuretic treatments. Three patterns of response to salt loads were identified in SEH patients with respect to sodium and water elimination by the kidneys: the first was identical to that of normal subjects, while the second one featured increased, and the third one, decreased, diuresis and natriuresis. Prostaglandin E2 and kallikrein were shown to be involved in the formation of the second- and third-type renal response to excessive salt. Differential treatment of EH patients with diuretics alone or, where necessary, in combinations with small-dose beta-blockers or vasodilators provides effective BP control for some 1.5 to 2 years in 65% of patients.
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PMID:[Characteristics of the water-electrolyte metabolism of hypertension patients with stable hypertension and the principles of diuretic therapy]. 351 96

The most important risk factors that may predict the transition from borderline to established hypertension are revised, focusing on those pathological changes that have been investigated for their value as predictors of established hypertension. A patient commonly is diagnosed as a borderline hypertensive if several pressure values are somewhere above as well as below 140/90 mm Hg. Patients in this category generally are regarded as hypertensive when they are younger than age 40. Studies largely favor the hypothesis of polygenic inheritance of essential hypertension, yet the detailed nature of heredity continues to be disputed. Several biochemical markers reflect the hereditary etiology of established hypertension, e.g., a variation in the electrophoretic pattern of plasma proteins, urinary concentration of kallikrein, and an alteration of cell membrane transport of cations. In Western populations, arterial pressure increases throughout life. About 40% of the white population and over 50% of the black population over age 65 have hypertension (blood pressure of 160/95 mm Hg or greater) or isolated systolic hypertension (systolic blood pressure greater than 160 mmHg and diastolic blood pressure less than 95 mm Hg). Essential hypertension is more prevalent and vascular disease more severe in blacks than in whites. There is a well-documented association between obesity and hypertension; obesity increases the prevalence of hypertension 3 to 8 times. Numerous studies have been published about the relationship between arterial hypertension and excessive dietary salt intake, but the results continue to be controversial. In a cross-cultural analysis, a strong relationship was observed between salt intake and the prevalence of hypertension. Also noted was the modifying impact of sodium intake on the increasing prevalence of hypertension with age. Premenopausal women have a lower prevalence of essential hypertension and its risk factors than men of the same age because of the influence of estrogen, but if these women take oral contraceptives, arterial pressure increases and transient hypertension, often severe or even malignant, can be induced. Some behavioral patterns and personality traits appear to be associated with borderline hypertension, but evidence that these factors determine the transition from borderline to established hypertension in later life has not been demonstrated thus far. Measurements of resting heart rate and responses to dynamic exercise have some predictive value in predicting the development of hypertension. Ambulatory monitoring of blood pressure might allow for differentiation of patients with transient elevated blood pressure from those with more sustained hypertension.
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PMID:Risks for arterial hypertension. 351 34

The hypotensive response the thiazide diuretics was studied in 15 males with moderate essential hypertension and correlated with serial changes in plasma volume, weight, plasma renin activity, urinary aldosterone, and urinary kallikrein, both total and activity. A greater than 10 mmHg fall in mean arterial pressure after four weeks of treatment defined the responders to therapy (n = 10) while all others were considered non-responders (n = 5). In responders, the fall in mean arterial pressure was accompanied by sustained reduction in plasma volume and weight. No sustained fall in plasma volume was noted in non-responders. Plasma renin activity and urinary aldosterone excretion increased in responders but not in non-responders. Urinary kallikrein, both total and active, increased in the responders but remained unchanged in the non-responders. The results are consistent with the hypothesis that a sustained reduction in plasma volume is necessary for the maintenance of a hypotensive response to thiazides. Stimulation of the renal kallikrein-kinin system may be necessary to balance the antinatriuretic and pressor effects of the renin-angiotensin-aldosterone system. If unopposed, this system would return plasma volume and blood pressure to pretreatment levels.
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PMID:Thiazide induced hypotension: the role of plasma volume reduction and the urinary kallikrein system. 354 27


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