Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has recently been proposed that sequence variation in the gene coding for tissue kallikrein might be involved in the pathogenesis of hypertension. However, molecular evidence of an association between a sequence alteration in the kallikrein gene family and the transmission of increased blood pressure has never been reported. In 32 recombinant inbred (RI) strains derived from the spontaneously hypertensive rat (SHR) and the normotensive Brown Norway rat (BN), we investigated whether a restriction fragment length polymorphism (RFLP) marking the kallikrein gene family cosegregated with blood pressure. In the RI strains that inherited the kallikrein RFLP from the SHR progenitor strain, the median systolic, diastolic, and mean arterial pressures were significantly greater than in the RI strains that inherited the kallikrein RFLP from the BN progenitor strain. These findings suggest that in the rat, sequence variation in the kallikrein gene family, or in closely linked genes, may have the capacity to affect blood pressure.
Hypertension 1991 Feb
PMID:Cosegregation of blood pressure with a kallikrein gene family polymorphism. 167 81

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106 +/- 0.4 mm Hg, n = 7) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c.) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 +/- 6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9, 10, 11, and 12 weeks of age (p less than 0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6- and 4.7-fold by this treatment. Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit. The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment. Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension.
Hypertension 1991 Jun
PMID:Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system. 171 Jun 5

The antihypertensive efficacy of once-daily nitrendipine was studied in 18 patients with severe, resistant, refractory, and complicated hypertension. The dose range was 20-120 mg/day adjusted weekly for a total treatment period of 3 years. Nitrendipine produced a significant reduction in blood pressure compared to pretreatment baseline values with no significant effects on heart rate. Renal function was preserved and there was an increase in urine flow, urinary excretions of Na+, kallikrein, and prostaglandin E2, and plasma renin. Some patients experienced known calcium antagonist side effects but the drug was otherwise well tolerated.
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PMID:Long-term (3 years) sustained antihypertensive and metabolic actions of nitrendipine in severe, complicated, and resistant hypertension. 172 66

The activity of the blood kallikrein-kinin system was evaluated in 18 patients with refractory arterial hypertension who received a combined therapy by using prostaglandin E2 (PGE2) infusions. PGE2 infusions produced a direct effect in modulating the vasoactive peptide system. There was activity mobilization at low baseline values of blood kallikrein and its inhibition at high values. The activating effect of PGE2 remained for further 2 weeks following the infusion. The response of the patients to previously low effective antihypertensive agents could be enhanced.
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PMID:[Activity of the kallikrein-kinin system of blood during combined treatment of patients with high and stable arterial hypertension]. 172 78

Recently, we reported the isolation and identification of a potent vasoconstrictor enzyme from the rat submandibular gland, a member of the rat kallikrein gene family, which we named submandibular enzymatic vasoconstrictor (SEV). We studied whether messenger RNA (mRNA) for SEV is present in the kidney and isolated glomeruli, using the polymerase chain reaction assay with primers specific to the entire rat kallikrein family that would amplify a 430-bp fragment from their mRNA. As a probe we used a phosphorus-32-labeled oligonucleotide specific for SEV mRNA. A fragment of the predicted size was obtained on Southern blot for amplified renal RNA; however, no signal was obtained with glomerular RNA. To further confirm the presence of SEV mRNA in the kidney, polymerase chain reaction was repeated using primers specific to SEV mRNA that would amplify a 372-bp fragment from SEV mRNA alone. Again, a fragment of the predicted size was obtained on Southern blot after amplification of renal RNA but not RNA from the glomeruli. Southern blot of polymerase chain reaction-amplified RNA with primers that amplified the entire kallikrein gene family, using kallikrein complementary DNA that recognizes all members of the kallikrein gene family as a probe, revealed a 430-bp fragment for both renal and glomerular RNA, indicating that glomeruli contain mRNA for a member or members of the kallikrein family other than SEV. When the Southern blots were hybridized with a 32P-labeled oligonucleotide probe specific for glandular kallikrein, a fragment of the predicted size was obtained from amplified renal RNA but not glomerular RNA.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Feb
PMID:Submandibular enzymatic vasoconstrictor messenger RNA in rat kidney. 173 90

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

To investigate pathogenesis of arterial hypertension in diabetes mellitus, the authors measured parameters of central and peripheral hemodynamics, basal renin levels, angiotensin, aldosterone, kallikrein-kinin system. The results were analysed with regard to hypertension type: essential (EH), atherosclerotic (AH) and nephrogenic (NH). Hypokinetic circulation, defected vascular elasticity, activation of renin-angiotensin-aldosterone system and hypoactivity of kallikrein-kinin system were characteristic of EH and AH. Most pronounced changes in peripheral hemodynamics and hypoactivity of depressor kallikrein-kinin system were seen in NH.
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PMID:[Pathogenesis of arterial hypertension in diabetes mellitus]. 178 Jul 71

Several biochemical markers have been reported to be useful in the investigation of patients with hypertension. These markers can be divided into three broad categories: those related to sodium homeostasis (eg, renin, converting enzyme, aldosterone, and the kallikrein-kinin system); those related to sodium homeostasis and vascular reactivity (eg, cytosolic calcium, sodium transporters, insulin resistance, and nonmodulation); those related to vascular reactivity (eg, catecholamines). These biochemical factors may be useful in defining which treatment modality to use, in increasing our understanding of the pathophysiology of the disease, and in evaluating end-organ damage and/or familial risk. Further information, however, is required before one can verify these hypotheses.
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PMID:Biochemical predictors of hypertension. Utility in prevention and treatment. 178 46

To determine the role of sex hormones and sodium intake in hypertension seen in postmenopausal woman, 12 women (aged 50 to 59 years) in whom blood pressure increased for the first time to above 150/90 mmHg after cessation of menstruation were examined in comparison with 7 age-matched postmenopausal normotensive women (118 +/- 2/62 +/- 3 mmHg). All subjects were admitted to the hospital and their sodium intake was maintained at 204 (normal), 306 (high), and 51 (low) mmol/day for 5 days each. In each period, body weight, blood pressure, heart rate, serum levels of sex hormones and vasoactive hormones, and urinary excretions of sodium, kallikrein and dopamine were determined. The plasma levels of prolactin, progesterone, oestrone, and oestradiol in the hypertensive women were all significantly lower than those in the normotensive women in all study periods. With a change in sodium intake from high to low, blood pressure in 8 out of 12 hypertensive patients decreased by more than 10% from 160 +/- 2/100 +/- 2 mmHg to 144 +/- 2/87 +/- 2 mmHg, while in the normotensive women, only 1 out of 7 patients responded to this change in sodium intake. The changes in sodium intake did not alter the plasma levels of sex hormones in the hypertensive and normotensive subjects. Among the hypertensive patients, three had a history of pregnancy-induced hypertension, while none of the normotensive subjects had such a history. The results of the present study suggest that decreases in sex hormones and increased sensitivity to sodium are important factors in the genesis of postmenopausal hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of sex hormones and sodium intake in postmenopausal hypertension. 179 8

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


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