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)

The pathogenesis of hypertension in autosomal-dominant polycystic kidney disease (ADPKD) is unclear, but increased activity of the renin-angiotension system may contribute. The renal and systemic hemodynamic response to lisinopril, an angiotension converting enzyme (ACE) inhibitor, in patients with ADPKD without renal failure was compared with the response in matched unaffected family members. Mean blood pressure and renal vascular resistance decreased in the affected group after lisinopril, with no significant change in the unaffected group. Glomerular filtration rate (GFR) was unchanged and therefore filtration fraction fell significantly. Changes in urinary excretion of 6-keto-PGF1 alpha and kallikrein suggested that increased renal synthesis of PGI2 or activation of the renal kallikrein-kinin system were not likely to be responsible for the hemodynamic effects. The acute decrease in renal vascular resistance without change in GFR suggests that ACE inhibition may have a particular value in the treatment of hypertension associated with ADPKD which should be assessed by further long-term studies.
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PMID:Effects of angiotensin converting enzyme inhibition in adult polycystic kidney disease. 131 77

In the rat, the results of genetic linkage studies by "candidate" gene or "positional mapping" approaches have suggested that DNA sequences that regulate blood pressure may be located in the vicinity of the kallikrein gene family on chromosome 1, the gene for angiotensin-converting enzyme on chromosome 10, the renin gene on chromosome 13, and the major histocompatibility complex on chromosome 20. Some studies have also suggested that blood pressure regulatory genes may be located on the sex chromosomes. Pending the results of confirmatory studies, these experiments should be interpreted with caution. However, with confirmation of these studies, it should be possible to create a variety of new animal models that will provide excellent opportunities for investigating the molecular, biochemical, and physiologic determinants of high blood pressure. In addition, in genetic studies in humans with essential hypertension, it may be worthwhile to target chromosome regions that are homologous to those implicated in linkage studies of hypertension in rodents. By narrowing the focus on selected areas of the genome, experimental linkage studies in the rat may also be used to guide the detailed molecular approaches ultimately required to identify the specific DNA sequence alterations that give rise to increased blood pressure.
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PMID:Gene mapping in experimental hypertension. 132 57

Urinary kallikrein and kallikrein activity significantly decreased in cases of preeclampsia (u-kall./CRE.index 42.39 +/- 9.66 ng/mg, u-kall. act./CRE.index 0.26 +/- 0.06 ng/min/mg), and urinary kininase II and kininase activity significantly increased (u-kininase/CRE.index 10.91 +/- 1.26 x 10(-3) IU/min/mg, u-kininase act./CRE.index 506.37 +/- 178.45 pg/min/mg) when compared with those of normal gravidas from 28 weeks to 42 weeks of gestation (u-kall./CRE.index 189.31 +/- 14.17 ng/mg, u-kall. act./CRE index 1.08 +/- 0.10 ng/min/mg, u-kininase/CRE.index 6.24 +/- 0.31 x 10(-3) IU/min/mg, u-kininase act./CRE.index 15.64 +/- 0.10 pg/min/mg). Urinary FPA, B beta 5-42, alpha 2-PI, and alpha 2PI-plasmin-complex (PIC) significantly increased in preeclampsia (u-FPA/CRE.index 23.59 +/- 8.47 ng/mg, u-B beta/CRE.index 105.26 +/- 29.30 ng/mg, u-alpha 2PI/CRE.index 121.53 +/- 43.57 ng/mg, u-PIC/CRE index 278.39 +/- 60.50 ng/mg) when compared with those of normal control group (u-FPA/CRE.index 0.92 +/- 0.04 ng/mg, u-B beta/CRE.index 12.15 +/- 0.44 ng/mg, u-alpha 2PI/CRE.index 4.18 +/- 0.33 ng/mg, u-PIC/CRE.index 5.98 +/- 1.15 ng/mg). Urinary urokinase markedly increased and urinary D-dimer was detected in severe cases of preeclampsia (u-UK/CRE.index 58.20 +/- 43.69 ng/mg, u-D-dimer 54.76 +/- 9.89 ng/ml) when compared with those of normal control group. These findings suggest that deficiency in urinary kinin excretion may induce hypertension in addition to the changes of urinary coagulation-fibrinolysis system that represents the occurrence of either the endothelial cell injury in the glomerulus or the renal tulbular damage in mild cases of preeclampsia, eventually resulting in the intra-renal vascular coagulation.
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PMID:Urinary coagulation-fibrinolysis, kallirein-kinin systems and kininase in cases of preclampsia. 133 34

The behavior of plasma atrial natriuretic factor (ANF) and digoxin-like substance (DLS), and the daily urinary excretion of kallikrein (uKK) were evaluated in young hypertensives and in young normotensives with or without a family history of essential hypertension. Each group was also evaluated, separating those with low plasma renin activity from the total sample. The sample group was made up of 75 young males; 31 hypertensives (mean age 22.7 +/- 2.5 years), 28 normotensives with hypertensive heredity (normotensives F+) (mean age 22.2 +/- 1.9 years) and 16 normotensives (mean age 22.0 +/- 2.1 years). An inverse correlation between ANF and PRA was shown in all groups. In hypertensives, ANF was inversely correlated with uKK (r = -0.664, P less than .0001). Plasma ANF (P less than .012) and DLS (P less than .0001) were higher in hypertensives than in normotensives, while uKK excretion was lower (P less than .0001). Plasma levels of DLS were higher in F+ normotensives than in normotensives (P less than .003). Low renin hypertensives showed the lowest uKK excretion (P less than .0001 v normal-high renin hypertensives). Furthermore, low renin hypertensives showed the highest plasma levels of ANF (P less than .0001 v normal high renin hypertensives) and DLS (P less than .012 v normal-high renin hypertensives). Plasma ANF (P less than .0001) was higher, while uKK was lower (P less than .045) in low renin F+ normotensives than in normal-high renin ones. In conclusion, our data indicate that plasma ANF and DLS are elevated since the early phase of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Natriuretic hormones in young hypertensives and in young normotensives with or without a family history of hypertension. 141 48

Sodium balance plays a primary role in blood pressure regulation. Atrial natriuretic peptide, a recently discovered natriuretic substance, seems to participate in renal sodium handling, but its behavior in essential hypertension has not been fully defined. In our study, to avoid the "contamination" of factors other than hypertension, we evaluated the plasma levels of atrial natriuretic peptide in young men at military draft age. Our main results showed that plasma atrial natriuretic peptide levels are higher in young hypertensives with low plasma renin activity and low urinary excretion of active kallikrein. The influence of a positive genetic background for essential hypertension on plasma atrial natriuretic peptide levels was also investigated. Our data showed slightly elevated levels of the atrial hormone in young normotensives with a family history of hypertension.
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PMID:[Cardiac and renal sodium-modulating hormones in juvenile arterial hypertension. The physiopathological aspects and therapeutic results of a trial at the Policlinico Militare Celio in Rome]. 149 65

To evaluate the antihypertensive effect of magnesium lithospermate B isolated from Salviae miltiorrhizae radix, determinations of blood pressure and urinary excretions of sodium, potassium, prostaglandin E2 (PGE2) and kallikrein, which have been proposed to play an important role in the regulation of blood pressure, were made in rats with sodium-induced hypertension and renal failure. In rats given magnesium lithospermate B, blood pressure was significantly decreased, whereas urinary excretion of electrolytes was significantly increased. Urinary PGE2 excretion following administration of magnesium lithospermate B increased as the dose of the compound was stepped up. The activity of kallikrein in urine was also increased by the treatment. From these results, the blood pressure-lowering action of magnesium lithospermate B may be due in part to enhancement of the kallikrein-prostaglandin system.
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PMID:Effect of magnesium lithospermate B in rats with sodium-induced hypertension and renal failure. 158 22

Essential hypertension is a complex clinical disorder in which multiple environmental and genetic factors interact to increase blood pressure. To search for chromosome regions that contain genes regulating blood pressure, some investigators have begun to conduct linkage studies in rodent models of spontaneous hypertension. Preliminary results suggest that in the rat, blood pressure regulatory genes may be located in the vicinity of the kallikrein gene family on chromosome 1, the gene for angiotensin converting enzyme on chromosome 10, the renin gene on chromosome 13, and the major histocompatibility complex on chromosome 20. Some studies have also suggested that blood pressure regulatory loci may be located on the sex chromosomes. Although comparisons between humans and animals should be made with caution, it is hoped that the identification of genes regulating blood pressure in the rat might shed light on the pathogenesis of hypertension in humans.
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PMID:Genetic approaches to hypertension. 161 May 44

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

Sinoaortic denervation SAD in dog induces a permanent rise in blood pressure and heart rate leading to an experimental model of arterial hypertension. This model is associated with a marked increase in plasma catecholamine levels during the two first months. The present study investigates the changes in some renal vasoactive systems (renin activity, aldosterone and kallikrein) and cortical renal beta adrenoceptors during the development of this experimental neurogenic hypertension in dogs. SAD dogs exhibited a biphasic change in plasma renin activity and catecholamines: 1 month after SAD, plasma noradrenaline rose and renin activity decreased. These parameters return to normal values 18 months after SAD whereas blood pressure remained elevated. In contrast, plasma aldosterone levels decreased and urinary sodium increased. Urinary kallikrein was enhanced 1 month after SAD and showed a marked decrease 18 months later when compared with pre-SAD values. Cortical renal beta adrenoceptors (evaluated by 125I-cyanopindolol) exhibited a permanent decrease (Bmax) whatever the duration of arterial hypertension. These results show that SAD-induced hypertension in dog is associated with changes in renal vasoactive system involving urinary excretion of kallikrein and cortical renal beta adrenoceptors. These alterations could be involved in the maintenance of arterial hypertension in this experimental model.
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PMID:[Renal adrenergic beta receptors and experimental neurogenic hypertension]. 165 44

Fifty-four patients with vasorenal arterial hypertension were examined for the activity of kallikrein, prekallikrein, carboxycatepsin and renin in the blood of renal veins. In patients with an appreciable stenosing of one of renal arteries, asymmetry of kallikrein excretion due to its activity reduction was discovered on the side of the ischemized kidney. In patients with unilateral insignificant stenosis of the renal artery and bilateral stenosing of renal arteries, no consistent asymmetry in the activity of the enzymes under study was revealed.
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PMID:[The activity of the components of the kinin system in renal vein blood in vasorenal arterial hypertension]. 166 61


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