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

The effect of aging on urinary kallikrein excretion (UkalV) was investigated in 54 normal subjects, 11-88 yr old, and 37 patients with essential hypertension, 17-82 yr old. Urinary sodium, potassium, and aldosterone excretion (U(Ald)V) were also measured in these subjects. Urinary sodium and potassium excretion in both normal subjects and hypertensive patients did not significantly change with aging. In normal subjects, U(kal)V (r = 0.45; P less than 0.001) and U(Ald)V (r = 0.58; P less than 0.01) significantly decreased with increasing age. U(kal)V was positively correlated with U(Ald)V (r = 0.44; P less than 0.001). In contrast, the hypertensive patients had a significant decrease with age in U(Ald)V (r = -0.36; P less than 0.05), but no significant age-related change in U(kal)V. No significant correlation between U(kal)V and U(Ald)V was observed in the hypertensive patients. In individuals less than 60 yr old, there was no significant difference in U(kal)V values between normal subjects and hypertensive patients. Hypertensive patients more than 60 yr old excreted more urinary kallikrein than normal subjects of the same age group (P less than 0.05). In conclusion, the age-related decrease of U(kal)V in normal subjects may be due to the reduced activity of the renin-angiotensin-aldosterone system. It remains to be elucidated whether the absence of the age-related decrease in U(kal)V in hypertensive patients is related to the pathogenesis or pathophysiology of essential hypertension.
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PMID:The effect of aging on urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension. 690 97

Recently, we established a very sensitive, specific and simple direct radioimmunoassay method for human urinary kallikrein. In this study, in order to clarify whether or not the low or high excretion rate of urinary kallikrein activity in patients with essential hypertension, primary aldosteronism, pheochromocytoma and Bartter's syndrome is caused by changes in enzyme quantity, urinary kallikrein excretion was measured with this direct radioimmunoassay method in normal subjects and in patients with these diseases. Urinary kallikrein excretion measured as enzyme quantity was significantly lower in patients with essential hypertension, and higher in patients with primary aldosteronism and Bartter's syndrome. These results are consistent with other previously reported data and our data measured by means of esterase assay or kininogenase assay. The results also suggest that lowered or elevated excretion of urinary kallikrein activity in these diseases is caused, in part at least, by the lowered or elevated excretion of enzyme quantity.
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PMID:Excretion of human urinary kallikrein quantity measured by a direct radioimmunoassay of human urinary kallikrein in patients with essential hypertension and secondary hypertensive diseases. 691 9

Basal 24 hour urinary kallikrein excretion of 20 patients with uncomplicated essential hypertension did not differ significantly from that of 18 normotensive age-matched control subjects. 4 of the 20 hypertensive patients, however, had low kallikrein excretion. Furosemide (40 mg i.v.) caused an increase of urinary kallikrein excretion in the normotensive subjects and in most of the patients with essential hypertension. The stimulating effect of furosemide was less pronounced or even absent in 7 hypertensives. No circadian rhythm of urinary kallikrein excretion was observed. There were weak correlations between 24 hour kallikrein excretion and urinary volume (r=0.59; p < 0.05), and potassium excretion (r=0.51; p < 0.05) in the normotensives. In the hypertensives correlations were found between 24 hour kallikrein excretion and potassium excretion (r=0.51; p < 0.05), aldosterone excretion (r=0.57; p < 0.01), and creatinine clearance (r=0.59; p < 0.01). Our findings do not support the concept that the renal kallikrein-kinin system might play a primary role in the pathogenesis of essential hypertension.
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PMID:Urinary kallikrein in normotensive subjects and in patients with essential hypertension. 700 Apr 66

The effects of captopril (SQ 14.225), an orally active inhibitor of angiotensin converting enzyme, were investigated in a dose titration study of primary hypertension. In 32 patients 4 weeks titration with captopril gave a mean blood pressure (BP) reduction of 26/16 mmHg supine and 30/16 mmHg standing. No serious side effects were observed. The BP lowering effect was related to pretreatment plasma renin activity and was less in low renin hypertension (p less than 0.05). Captopril reduced angiotensin II (p less than 0.05), plasma (p less than 0.005) and urinary aldosterone (p less than 0.001) as well as urinary kallikrein excretion (p less than 0.005). Captopril (SQ 14.225) is a competitive inhibitor of peptidyl dipeptide hydrolase, also known as angiotensin converting enzyme (ACE) or kininase II, which converts angiotensin I (A I) into angiotensin II (A II), hydrolyzes des-Asp-angiotensin I to angiotensin III (A III) and inactivates bradykinin (BK) (19). Captopril has potent antihypertensive effects when used in human hypertension (review, 3) especially when the renin-angiotensin-aldosterone system (RAAS) is activated. To further investigate the mode of action and the hypotensive effect of captopril, we measured plasma renin activity (PRA), A II, plasma (PA) and urinary aldosterone excretion (UA) and urinary kallikrein excretion (UK) in 32 patients with established primary (essential) hypertension.
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PMID:Captopril in primary hypertension. Effects related to the renin-angiotensin-aldosterone and kallikrein-kinin systems. 701 90

The antihypertensive effect of oral administration of pig pancreatic kallikrein was investigated in a double blind study of 20 patients with essential hypertension. Kallikrein treatment lowered the blood pressure (BP) significantly from 159.5/104.5 to 146.3/92.8 mm Hg in the supine and from 153/106.1 to 136.1/95.6 mm Hg in the standing position. Blood pressure remained unchanged in the placebo group. Urinary kallikrein, sodium excretion, and GFR increased with treatment, but these changes did not reach statistical significance, In the kallikrein-treated patients but not in the placebo group, urinary kallikrein was correlated both to GFR (r = 0.7, p less than 0.001) and sodium excretion (r = 0.5, p less than 0.01). The antihypertensive mechanism of kallikrein treatment remains unknown. It could be speculated that kallikrein may induce changes in local blood flow, mediated by kinin and prostaglandin release.
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PMID:Antihypertensive effect of orally administered glandular kallikrein in essential hypertension. Results of double blind study. 702 12

Plasma levels of kininogen, kallikrein, and prekallikrein were determined in patients with malignant hypertension (MH) and compared to normotensive controls (NC) and patients with mild to moderate essential hypertension (EH). Also, a recently described kinin potentiating factor (KPF) was estimated by dividing the value of kininogen determined by trypsin (Kgn-Try) by that of kininogen determined by human urinary kallikrein (Kgn-HuUk). No significant alterations were detected among plasma values of pre-kallikrein and kallikrein of MH as compared to NC. However, Kgn-HuUK values were significantly lower in MH (1.9 +/- 0.3 micron gLBK/ml) as compared to EH and NC (2.7 +/- 0.1 micron gLBK/ml and 3.0 +/- 0.2 micron gLBK/ml respectively, p less than 0.05). Furthermore, KPF values were also low (p less than 0.05) in MH (1.6 +/- 0.3) when compared with similar values obtained in EH and NC (3.0 +/- 0.2 and 2.8 +/- 0.1, respectively). Adequate control of blood pressure levels for 90 days in MH group caused no significant alterations in plasma levels of kininogen and KPF. It is suggested that diminished kininogen levels as well as a decrease in a kinin potentiation KPF that is generated in plasma by trypsin may be involved in the pathogenesis of human malignant hypertension.
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PMID:Malignant hypertension: a syndrome associated with low plasma kininogen and kinin potentiating factor. 702 21

A 36-year-old female case of normotensive normoreninemic primary aldosteronism with persistent hypokalemia and nephrocalcinosis is reported. She was referred to us for episodes of sudden muscle weakness during 8 years prior to admission. On the first day of admission, her blood pressure was 174/104 mmHg. On the second day of admission blood pressure normalized to 120/80 mmHg. Both of her parents were hypertensive. Arterial blood gas analysis showed metabolic alkalosis. Except an impaired urine concentration ability, renal functions were normal. Intravenous pyelogram showed numerous granular calcifications. Basal plasma renin activity was 1.0 approximately 1.5 ng/ml/hr and increased by sodium depletion. Plasma aldosterone concentration was 70 approximately 80 ng/dl and did not respond to various stimulations. Blood pressure was dependent on sodium balance. It fell on salt restriction and rose on salt loading. Blood pressure responses to vasoactive hormones were normal. Circulating plasma volume was within normal range. After removal of an adrenal adenoma, there was mild fall of blood pressure, serum potassium returned to normal level and plasma renin activity increased slightly. Histologically, there was renal tubular calcifications, and juxtaglomerular apparatus was normal. Blood pressure was elevated to 160/100 mmHg when patient was followed at out-patient clinic after discharge. We concluded that she had essential hypertension associated with primary aldosteronism. Although sodium loss and an increase in urinary kallikrein were found, they did not seem to be the cause of normoreninemic normotensive state of this patient, and the pathogenesis remains to be elucidated.
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PMID:A case of normoreninemic, normotensive primary aldosteronism associated with essential hypertension and nephrocalcinosis. 703 37

The antihypertensive effect of captopril and its mechanism of action were studied in patients with essential and renal hypertension. In mild essential hypertension (n = 12), during monotherapy with captopril (50 to 450 mg, 4 to 12 weeks) blood pressure was normalized in seven, improved in two and remained unchanged in three patients, plasma levels of active and acid-activatable inactive renin significantly increased and angiotensin II decreased, whereas no consistent changes in urinary kallikrein excretion occurred. In severe renal (n = 14) and essential (n = 9) hypertension, blood pressure was normalized in eight (seven with renal hypertension), improved in seven and unchanged in eight patients, when captopril (50 to 450 mg, 3 to 15 months) was added to the antihypertensive medication. In one patient with stenosis in a transplanted renal artery reversible renal failure occurred during captopril therapy possibly because of a steep initial decrease in blood pressure, although a toxic effect of the drug cannot be excluded. In another series of 12 renal and 8 essential hypertensive patients, a significant correlation between the acute effect of captopril (within 90 minutes) an saralasin on blood pressure was demonstrated (r=0.71, p less than 0.001). The change in blood pressure after either drug was significantly related to the initial plasma renin concentration. In conclusion, captopril seems to be an effective antihypertensive agent in essential and renal hypertension. Renal function should be monitored during captopril therapy. Our studies suggest that captopril decreases blood pressure by inhibiting the vasopressor action of the renin-angiotensin system.
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PMID:Antihypertensive effects of captopril and saralasin in essential and renal hypertension. 704 97

We examined the role of dietary electrolytes and humoral factors in causing seasonal changes in blood pressure. Normal subjects had no seasonal difference in blood pressure, although urinary sodium and norepinephrine were significantly higher in winter than in summer. In patients with essential hypertension blood pressure, urinary sodium and norepinephrine excretion and plasma norepinephrine concentration were significantly higher in winter. Plasma renin activity, plasma and urinary aldosterone and urinary kallikrein excretion were not significantly different between the two seasons in both normal subjects and hypertensive patients. In conclusions, the blood pressure of patients with essential hypertension has a seasonal variation with higher pressures in the winter than in the summer. Increased sympathetic nervous activity and an increased load of sodium presented to the kidney for excretion may be contributing factors in the rise in blood pressure in winter in patients with essential hypertension.
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PMID:The seasonal variation of blood pressure in patients with essential hypertension. 707 93

Urinary kallikrein excretion has been reported to be decreased in patients with essential hypertension and elevated in patients with primary aldosteronism as a reflection of mineralocorticoid activity. Low renin essential hypertension (LREH) has been postulated to result from excess production of an unknown mineralocorticoid(s). Urinary kallikrein excretion was compared in outpatients with essential hypertension, mineralocorticoid hypertension (primary aldosteronism and 17alpha-hydroxylase deficiency), and in normal subjects of the same race. No significant difference in urinary kallikrein excretion of patients with LREH vs. normal renin essential hypertension (NREH) was found for either black (4.1+/-0.4 vs. 4.8+/-0.5 esterase units (EU)/24 h, mean+/-SE, for 27 LREH and 38 NREH, respectively) or white patients (12.2+/-2.3 vs. 11.7+/-1.4 EU/24 h for 13 LREH and 25 NREH, respectively). Urinary kallikrein was decreased in black vs. white hypertensive patients and normal subjects. However, in patients with normal renal function (creatinine clearance >/=80 ml/min) urinary kallikrein was not significantly decreased in either black hypertensive vs. black normal subjects (4.3+/-0.3 vs. 5.4+/-0.6 EU/24 h) or in white hypertensive vs. white normal subjects (11.9+/-1.2 vs. 8.4+/-0.9 EU/24 h). In contrast, hypertensive patients with mild renal insufficiency (creatinine clearance of 41.8+/-78.5 ml/min) had reduced (P < 0.05) urinary kallikrein (3.3 EU/24 h with creatinine clearance of 63.6+/-2.0 for 24 black patients and 4.2+/-0.7 EU/24 h with creatinine clearance of 67.0+/-3.5 for 6 white patients). These results suggest that a reduction in urinary kallikrein excretion rate is an early accompaniment of hypertensive renal injury. Urinary kallikrein excretion in response to a 6-d 10-meq sodium diet and a 3-d Florinef (0.5 mg b.i.d.) administration was compared in hypertensive patients with normal renal function vs. race and age-matched normal subjects. Stimulation of urinary kallikrein excretion by Florinef was equal in black and white normal subjects vs. hypertensive patients (black normals = 12.3+/-2.7 [n = 9], NREH = 11.7+/-1.8 [n = 10], LREH = 10.9+/-1.5 [n = 12]; white normals = 21.2+/-2.9 [n = 11], essential hypertension = 20.9+/-3.2 [10 NREH, 5 LREH]). Stimulation of urinary kallikrein excretion with low sodium diet was decreased (P < 0.05) only in black LREH (black normals = 11.2+/-2.4 [n = 10], NREH = 10.1+/-2.7 [n = 10], LREH = 7.4+/-1.1 [n = 13]; white normals = 19.1+/-2.7 [n = 13], essential hypertension = 17.5+/-2.3 [nine NREH, four LREH]). However, during low sodium diet, black patients with LREH had evidence for less sodium depletion as manifested by a decreased rise in urinary aldosterone excretion (16.3+/-2.7 vs. 33.3+/-6.4 mug/24 h for black normals) and a failure to achieve metabolic balance in 11/13 patients. Thus, the lesser kallikrein stimulation appeared to result from these two factors. Black and white hypertensives with creatinine clearance <80 ml/min had little increase in urinary kallikrein excretion with Florinef or low sodium diet.5 of 12 patients with primary aldosteronism or 17alpha-hydroxylase deficiency did not have an elevated urinary kallikrein excretion rate. Mild renal insufficiency may have contributed to this finding in two of these five patients. Nevertheless, this finding illustrates a limitation to the use of urinary kallikrein excretion rate as an index of mineralocorticoid activity. However, it appears that the majority of patients with LREH have no evidence for excess production of an unknown mineralocorticoid. The failure to find a decrease in urinary kallikrein excretion in racially matched patients with essentil hypertension and normal renal function questions the postulate of a role of the kallikrein-kinin system in the initiation of essential hypertension.
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PMID:Urinary kallikrein excretion in essential and mineralocorticoid hypertension. 735 84


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