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

In essential hypertension, renal dopaminergic activity and PGE2 was suppressed as was the renal kallikrein-kinin system. The suppression of the renal depressor systems may play an important role in the etiology of hypertension through sodium and body fluid retention. At the prehypertensive stage of essential hypertension, renal dopaminergic activity was suppressed, which induced the retention of body fluids and sodium. On the other hand, the renal prostaglandin E2 was augmented, and it seemed to be a compensatory mechanism for sodium retention. We could not confirm the suppression of the renal kallikrein-kinin system at the prehypertensive stage of hypertension. Although all renal depressor systems are suppressed in essential hypertension, the suppression of the renal kallikrein-kinin system and PGE2 seem to be very important in the etiology of hypertension. Further study is necessary to clarify when both systems are suppressed.
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PMID:The renal kallikrein-kinin system at the prehypertensive stage of hypertension. 146 63

A 79-year old man with hypertension, hypokalemic metabolic alkallosis, hyporeninemia and hypoaldosteronemia was studied. Blood pressure fell and serum potassium returned to normal after sodium restriction and the administration of triamterene. Serum DHEA, DOC, corticosterone, 18-OH-corticosterone, 11-deoxy-cortisol, cortisol were within normal range. Adrenal CT scanning did not reveal an adrenal tumor. The excretions of urinary kallikrein and prostaglandin E2 were within the normal range. Although an atrophic juxtaglomerular apparatus and arteriosclerotic change were observed by renal biopsy, there was no evidence of hypokalemic nephropathy. From these results, it is suggested that this patient has a defect in handling sodium and potassium in the distal tubules. This is similar to that observed in Liddle's syndrome.
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PMID:[A 79-year old man with hypertension, hypokalemia, hyporeninemia and hypoaldosteronemia similar to Liddle's syndrome]. 159 40

Epidemiologic surveys, experimental studies in animals, and clinical trials in young and middle-aged patients with hypertension indicate that dietary potassium lowers blood pressure. The mechanism of the antihypertensive effect is not well defined. Variations in serum potassium within the physiologic range may directly affect vascular smooth muscle tone. Potassium may also influence the regulation of blood pressure through effects on sodium handling, aldosterone secretion, the renin/angiotensin system, renal kallikrein, eicosanoids, and atrial natriuretic peptide. This study was undertaken to confirm the blood pressure-lowering effect of potassium in older patients and to determine the mechanism of the antihypertensive effect. Twenty-two patients greater than or equal to 60 yr of age were admitted to a Clinical Research Unit for 8 days after a 2-wk period free of antihypertensive medication. Patients were placed on an isocaloric diet containing 200 mmol/day of Na+, 70 mmol/day of K+, and 500 mg/day of Ca2+ and were treated in a randomized, double-blinded manner with either potassium chloride (120 mmol/day) or placebo. After 4 days, patients were crossed over to the alternate treatment. Systolic blood pressure decreased 8.6 mm Hg (95% confidence interval -14.6, -2.6), and diastolic blood pressure decreased 4.0 mm Hg (-6.9, -1.0) during potassium chloride supplementation. There was no significant change in blood pressure during treatment with placebo. Serum K+ was 3.9 +/- 0.1 mmol/L after 3 days of placebo and 4.3 +/- 0.1 after 4 days of potassium chloride (P less than 0.002). Urinary sodium excretion averaged 192 +/- 11 mmol/day after placebo and 221 +/- 8 after potassium treatment (P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potassium chloride lowers blood pressure and causes natriuresis in older patients with hypertension. 162 56

To prove the effect of aging on the synthesis of renin-angiotensin-aldosterone system, renal kallikrein-kinin system, prostaglandin (PG), and thromboxane (TX) which regulate blood pressure, normotensive subjects and patients with essential hypertension (EH) were investigated in the present study. Although plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were decreased with aging in both groups, there is no significant differences between each groups while compared among each age-groups. Urinary excretion of kallikreins (active, inactive and total) in EH were decreased with aging as similar extent to that of normal subjects. There was no age-related change of kallikrein activation ratio in EH in contrary to normal subjects. In comparison with each age-group, the amount of urinary kallikrein excretion in EH were already small in young age-groups. The amount of urinary PGE2 excretion in female EH group was smaller than that of normal subjects, and there were no age-related changes in both groups. Urinary excretion of TXB2 and 11-dehydro-TXB2, which are the urinary major metabolites of TXA2 which has potent vasoconstrictive action, were increased in the age-group of 80-93 year-old both normal subjects and EH. There were no age-related change in both groups. Although these hypertensive vasoactive substances as renin, aldosterone and TXA2 in EH show the same profile as that in normal subjects, the synthesis of renal antihypertensive vasoactive substances as kallikrein and PGE2 in EH already decrease in younger patients. These results suggest that the lower activities of renal antihypertensive system is a cause of the development of hypertension.
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PMID:[The investigation about age-related changes in vasoactive substances of normal subjects and of patients with essential hypertension]. 163 30

To investigate whether the suppression of the renal dopaminergic system in hypertension is primary or secondary, renal dopaminergic activity was compared between young healthy normotensive subjects without a family history of hypertension [FH(-)] and those with a family history of hypertension [FH(+)]. A significant decrease in urinary dopamine excretion was recognized, and the responses of urine volume, urinary sodium excretion, fractional excretion of sodium, and urinary kallikrein and kinin activity to infused dopamine were significantly augmented in FH(+) subjects. In addition, a normal level of L-dopa delivery into the kidney and at the renal proximal tubules and a significant reduction of the conversion from L-dopa to dopamine in the kidney were found in FH(+) subjects. These findings suggest that renal dopaminergic activity is already suppressed at the prehypertensive stage, and a reduction in the conversion from L-dopa to dopamine in the proximal tubules may contribute to the attenuation of renal dopaminergic activity in FH(+) subjects.
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PMID:Dopaminergic activity and water-sodium handling in the kidneys of essential hypertensive subjects: is renal dopaminergic activity suppressed at the prehypertensive stage? 170 26

Urinary kallikrein (reliable reflexion of its renal excretion) is studied in a large group of diabetic patients with and without nephropathy (again subdivided following Mogensen stages) and in hypertense non-diabetic patients. It is observed that the urinary excretion of kallikrein is independent of the type of diabetes (insulin or non-insulin dependent). There exists a clear difference in the behaviour of this enzyme, in diabetic patients with and without nephropathy, increasing in the former and decreasing in the latter (p less than 0.001). The decrease in urinary kallikrein is parallel to the existence of diabetic nephropathy with arterial hypertension. Urinary kallikrein in hypertense non-diabetic patients who are not treated with diuretics (furosemide) has a behaviour as in normal controls, but it is much higher in patients treated with captopril, being this finding of great importance since it can suggest new therapeutic approaches to diabetic nephropathy.
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PMID:[Renal kallikrein in diabetic nephropathy]. 178 May 9

A genetic influence on the variability of blood pressure in populations has been established. This effect has been demonstrated repeatedly by the presence of familial aggregation of blood pressure; however, a unique bimodal distribution in populations has not been established. About one-third to one-half of the blood pressure variance is explained by heredity with the remainder due to environmental or unknown factors. Direct associations of blood pressure with genetic markers in populations have been described infrequently. However, an association between haptoglobin 1 and increased blood pressure has been reported. This relationship is possibly secondary to increased sodium sensitivity in this genetic subgroup. The familial aggregation of urinary kallikrein as well as sodium-lithium countertransport and hypertension represents a successful attempt by investigators to identify correlates of intermediate phenotypes of hypertension. The association between restriction fragment length polymorphisms and elevated blood pressure represents an unmet potential. It should be emphasized that any genetic predictive factor will be affected by environmental factors. This interaction provides the opportunity for possible modification or prevention of hypertension by hygienic means.
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PMID:Predictors of hypertension. Population studies. 178 36

Epidermal growth factor (EGF) may have a modulatory role in renal growth and function. The aim of the present study was to evaluate whether urinary excretion of EGF is altered in psoriatic patients with or without arterial hypertension. The glomerular filtration rate was similar in psoriatics as compared with age- and sex-matched controls, whereas urinary EGF (microgram/g creatinine) was significantly reduced in psoriatics: normotensive subjects, 29.52 +/- 3.51 (psoriatics) versus 44.31 +/- 1.20 (controls, p less than 0.05); hypertensive subjects, 19.67 +/- 3.96 (psoriatics) versus 30.11 +/- 1.52 (controls, p less than 0.05). The urinary EGF excretion was lower in males than in females, save for hypertensive psoriatics. Urinary EGF correlated inversely with age and directly with urinary kallikrein excretion. Urinary kallikrein activity was reduced and microalbuminuria increased in hypertensive psoriatics. These alterations might suggest that initial deterioration of renal function is present in psoriasis.
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PMID:Depressed urinary excretion of epidermal growth factor in psoriasis. 179 91

The relationships between atrial natriuretic peptide (ANP) and the renal sodium-modulating systems have not yet been completely examined. In particular, the relationships between ANP and the kinins system are almost unknown. We thus examined an extremely selected cohort of normotensive (n = 29, mean age 21 +/- 2 years) and hypertensive subjects (n = 51m mean age 21 +/- 2.9 years), both without hypertensive heredity. After 7 days under normal sodium intake (120 mEq of Na+/day), blood samples were taken in the morning on awaking, for radioimmunoassay of plasma levels of aldosterone, ANP and renin activity. Blood was again drawn after one active hour in orthostatism. We also evaluated urinary kallikrein excretion from urine collected over the previous 24 hours. Our results showed higher plasma levels of ANP in young hypertensives than in normotensives (statistical significance p less than 0.0025). Urinary excretion of kallikrein was markedly reduced (p less than 0.001) in the hypertensive group (0.46 +/- 0.3 U/24 h) compared to youths with normal blood pressure (0.79 +/- 0.24 U/24 h), in which a relationship between plasma ANP and urinary kallikrein was not evident; young hypertensives, on the other hand, showed an inverse correlation (r = -0.72; p less than 0.001). Finally, our investigation, aside from establishing the presence of high circulating ANP levels even at the initial phases of hypertension, points out a new possible means of feedback among sodium-modulating systems. The opposite relationship between ANP and urinary kallikrein excretion in young hypertensives could be attributed to reduced activity of the renal kinins system and a compensatory attempt on the part of ANP.
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PMID:[Correlations between circulation levels of natriuretic atrial peptide and urinary excretion of kallikrein in young normotensive and hypertensive subjects]. 183 37

Twenty-seven male and female black Zimbabweans hypertensive patients were matched by age and sex and compared to 27 normotensive subjects. All subjects were examined after dietary sodium depletion, followed by sodium loading. In addition to renin status and salt-sensitivity, urine aldosterone, renal prostaglandins, plasma atrial natriuretic peptide (ANP) and plasma endothelin were assessed. The following ethnic characteristics for Zimbabwean essential hypertensive patients were found: increased prevalence of salt-sensitive hypertension (66 pc); hyporesponsive renin-angiotensin system after contraction of circulating plasma volume; higher prevalence of low-renin hypertension (59 pc); suppressed renal prostaglandins, especially in low-renin hypertensives, suggesting suppression or deficit of renal kallikrein-kinin system; increased levels of ANP in low-renin hypertensive patients. Plasma endothelin was comparably increased in both normal- and low-renin hypertensive patients.
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PMID:Pathogenesis of systemic (essential) hypertension in Zimbabwean hypertensive patients. I. Humoral factors. 183 14


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