ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

Purpose:This review addresses the question of renin gene control by examining information from messenger RNA, transgene, transient expression and DNA-protein binding studies.Contents:Although information from messenger RNA studies may be reliable for tissues such as kidney and, in mouse, submandibular gland, which have relatively high expression, more sensitive approaches, e.g. polymerase chain reaction technology, are needed for studies of renin gene regulation in other tissues. Control at the molecular level is particularly uncertain, with conflicting data suggesting that renin promoter activity depends either upon a complex interaction of positive and negative regulatory elements or upon the presence of specific trans-acting factor(s) alone, which act upon putative enhancer(s) in the renin-associated DNA. Only after renin-synthesizing cell lines are studied will a clearer picture emerge. Transgenic work has loosely defined the DNA needed as being less than several kilobases of flanking sequences, with the possibility that sequences in the gene itself, particularly in intron 1, are necessary. Such transgenic work has also shown that the renin gene can cause hypertension.Conclusion:Knowledge of DNA and proteins and the interactions that turn on transcription of the renin gene is still rudimentary and currently represents the major challenge in renin research.

ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

Objective:The purpose of this study was to determine whether the pressor effect of infused calcium is inhibited by increased serum magnesium.Design:Intravenous infusions of calcium, magnesium, and calcium + magnesium were performed in 10 subjects and the effect upon haemodynamic variables was investigated.Methods:Intra-arterial blood pressure and heart rate were recorded during i.v. infusions of magnesium, calcium and calcium + magnesium. Cardiac output and serum concentration of electrolytes were measured before and after the infusions. Total peripheral vascular resistance (TPVR) was calculated from: mean blood pressure/cardiac output.Results:Magnesium infusion increased serum magnesium, but did not change blood pressure, cardiac output, or TPVR. Calcium infusion increased serum calcium and elevated both blood pressure and TPVR with no change in cardiac output. Calcium + magnesium infusion increased both serum magnesium and calcium, showing elevation of blood pressure and TPVR with no change in cardiac output. Changes in haemodynamic variables caused by the calcium + magnesium infusion were similar to those caused by the calcium infusion alone.Conclusions:These results suggest that increased serum calcium elevates blood pressure and TPVR through arterial vasoconstriction by arterial smooth muscle contraction, but increased serum magnesium does not induce arterial vasodilation.

ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

Objectives:(1) To compare urinary guanosine 3',5' cyclic monophosphate (cyclic CMP) excretion between normotensive subjects and essential hypertensive patients; (2) to determine the influence of changes in sodium intake on urinary cyclic GMP excretion in response to the neutral endopeptidase inhibitor candoxatril in essential hypertensives.Design:(1) Twenty-five normotensive subjects and 25 patients with established essential hypertension not on treatment; (2) Single oral dose of candoxatril in eight patients with essential hypertension after equilibration on a low- or high-sodium diet in a placebo-controlled, double-blind, randomized, crossover study.Methods:Blood pressure was measured by ultrasound sphygmomanometry. Atrial natriuretic peptide (ANP) and urinary cyclic GMP were measured by radioimmunoassay. Group comparisons were made using unpaired t-tests and two-way analysis of variance.Results:Plasma ANP was significantly raised in patients with essential hypertension compared with the normotensive group, but there was no difference in urinary cyclic GMP excretion. Plasma ANP increased significantly on the high- compared with low-sodium diet. After candoxatril, there were significant diet-related increases in plasma ANP and urinary sodium excretion up to 6 h after drug administration. There were similar increases in urinary cyclic GMP excretion on both diets, but there were no consistent differences in this excretion between the low- and high-sodium diets.Conclusions:These observations not only point to the importance of ANP-cyclic GMP coupling as a determinant of the natriuretic response to endopeptidase inhibition, but also suggest that the excretion of urinary cyclic GMP can be influenced by other factors in addition to circulating ANP

ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

Objective:To investigate the hemodynamic effects of a moderately low-salt diet in a 9-week, randomized, double-blind, crossover study in 20 hypertensive, ambulatory patients.Methods:All subjects followed a 9-week, low-salt diet. During this period, they received capsules containing either lactose or salt in 4-week treatment periods, separated by a 1-week washout period. Hemodynamic and biological parameters were evaluated on the day of randomization and at the end of weeks 4 and 9. We defined a low-sodium diet (LSD) as a salt-restriction period with lactose capsules, and a normal-sodium diet (NSD) as a salt-restriction period with capsular salt supplementation.Results:Blood pressure was significantly lower during LSD compared with NSD. This fall in blood pressure was associated with a decrease in peripheral resistance in carotid and forearm circulation. Brachial artery diameter was larger during LSD whereas carotid artery diameter remained unchanged. The changes in brachial artery were: (1) not related to blood pressure changes; (2) positively related to age; and (3) negatively correlated with baseline intracellular sodium content.Conclusions:These results suggest that moderate low-salt restriction is capable of decreasing blood pressure and peripheral resistance in carotid and forearm circulation. The increase in brachiai, but not carotid, artery diameter following salt restriction suggests a difference in salt dependence among different arteries.

ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

Objective:Clarification of the role of estrogen in the regulation of angiotensinogen gene expression in multiple tissues.Design:The effect of 17P-estradiol (E2; 10|J.g/100mg body weight) administration in ovariectomized (OVX) rats upon angiotensinogen messenger RNA (mRNA) levels in multiple tissues was assessed. Confounding ovarian factors were thus removed by studying the animals in the castrate state. Controls consisted of OVX and intact female rats.Methods:Adult female Sprague-Dawley rats were ovariectomized and experiments begun 21 days postsurgery. Animals were injected with E2 and studied after 0, 1, 4, and 24 h of treatment. Levels of angiotensinognen mRNA were determined by Northern blot analysis using (3-actin mRNA as an internal standard.Results:A single angiotensinogen mRNA species with molecular size of approximately 1800 bp was observed in rat liver, aorta, kidney, cardiac atria, hypothalamus and whole brain. Little or no angiotensinogen mRNA was identified in the pituitary gland. Angiotensinogen mRNA was most abundant in rat liver, hypothalamus, aorta and progressively less abundant in whole brain, cardiac atria and kidney. A twofold induction of hepatic angiotensinogen mRNA levels in E2-OVX rats was observed by 4h. The angiotensinogen mRNA levels in kidney were threefold higher by 4h compared with OVX control animals. In aorta, the angiotensinogen mRNA level was also threefold higher by 1 h after E2 treatment. No significant effect of estradiol treatment was observed in cardiac atria although the level of angiotensinogen mRNA was higher in intact female rats compared with OVX controls.Conclusion:These results suggest that estrogen modulates angiotensinogen gene expression in a tissue-specific manner.

ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID

摘要:

Objective:To assess the role Na plays in the pathogenesis of pregnancy-induced hypertension (PIH).Methods:We assessed Na and K content, the maximum number of ouabain binding sites, Na+- L i+countertransport and Na+— K+cotransport in erythrocytes from women with untreated PIH, normal pregnant women and healthy non-pregnant women.Results:In normal pregnancy, the Na content of erythrocytes decreased, accompanied by the activation of Na excretion systems. In women with PIH, the Na content of erythrocytes and the Na+-K+cotransport activity significantly increased, whilst erythrocyte K content and the maximum number of ouabain binding sites significantly decreased, compared with observations in normal pregnancy. In both normal pregnancy and PIH, there were no differences in Na+-Li+countertransport.Conclusions:These results suggest that the increase of erythrocyte Na content in women with PIH may be contributed to by a reduction in the number of ouabain binding sites, whilst Na+-K+cotransport and Na+- L i+countertransport may compensate for this effect in women with PIH.

ISSN:0263-6352    

出版商:OVID    

年代:1992

数据来源: OVID