ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The aim of the present study was to investigate whether angiotensin II, by increasing extracellular matrix synthesis, contributed to the vascular wall thickening observed in hypertension. Thus, we examined the direct effects of angiotensin II on collagen and fibronectin synthesis in cultured rat vascular smooth muscle cells by measuring3H-proline incorporation. Angiotensin II, in a concentration of 10 μmol/l, increased collagen synthesis in a dose-dependent manner up to 1.8-fold. This increase occurred within 24 h after the addition of angiotensin II and the time required to reach maximum stimulation was approximately 48 h. This increase was receptor-mediated and correlated with an increase in its specific messenger RNA. A closer study of the collagen increase demonstrated a relatively greater increase in type V collagen than type I or type III collagen. Fibronectin synthesis was also increased 1.5-fold with 10 μmol/l angiotensin II. These data suggest that angiotensin II induces vascular wall thickening by acting directly on smooth muscle cells and enhancing the production of extracellular matrix proteins.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Skin fibroblasts from newborn spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were cultured to study their growth rate and their reactivity to various agonists in terms of mitogenic potency and inositol phosphate production. A marked enhancement of nuclear3H-thymidine incorporation, occurring after stimulation of quiescent fibroblasts by fetal calf serum, correlated with the increased growth rate of these cells with regard to WKY ones. Insulin (1 μg/ml) and epidermal growth factor (10 ng/ml) induced two and four times greater DNA synthesis in SHR fibroblasts compared to WKY cells, without activating the phospholipase C pathway. In contrast, angiotensin II, bradykinin, vasopressin which stimulated inositol phosphate production, and phorbol-12 myristate 13-acetate were unable to stimulate DNA synthesis. Higher levels of tritiated inositol phosphates were produced in SHR cells after serum, bradykinin and angiotensin II stimulation, but not in WKY cells after vasopressin. This enhanced mitogenic response of SHR skin fibroblasts is probably due to a genomic alteration and appears to be independent of the hyperactivation of the phospholipase C to some vasoactive agonists.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Rat kidney renin was purified 29000-fold using a nine-step procedure with a 4% recovery. N-terminal sequence analysis of the non-reduced renin revealed two sequences, indicating a two-chain structure. When compared with the amino acid sequence deduced from the rat preprorenin cDNA sequence, the N-termini of the A and B chains were residues 72 and 355, respectively, of preprorenin. The two-chain structure was confirmed by sodium dodecyl sulphate polyacrylamide gel electrophoresis. Rat kidney renin migrated as two broad bands of 35000–36000 and 37000–38000 Da under non-reducing conditions. Under reducing conditions, the size of both bands decreased by approximately 3000 Da and a band migrated at the buffer front (∼5000 Da). The site of cleavage between the two chains of rat renin is analogous to that of mouse submandibular gland renin. However, processing of the prosequence of rat prorenin differs from that of mouse and human prorenin, indicating that the mechanism of activation of prorenin is species-specific.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The extractions of atrial natriuretic factor (EANF) and the glomerular filtration marker51Cr-ethylenediamine tetraacetic acid (EEDTA) were determined before and after intravenous injection of furosemide across each of the two kidneys during renal vein catheterization in hypertensive patients with unilateral or bilateral renovascular disease. Before administration of furosemide, EANFwas approximately 55% across both the more and the less affected kidney while EEDTAwas significantly decreased across the more affected kidney. Significant lateralization of renin secretion to the more affected kidney was found, demonstrating an enhanced ipsilateral formation of renin. Administration of furosemide caused a significant decrease in EEDTAacross the less affected kidney while the ipsilateral EANFdid not change. Furosemide caused no change in EEDTAor EANFacross the more affected kidney. No significant correlations were found between EANFand EEDTA. These results demonstrate that the extraction of ANF is unchanged across the chronic ischemic human kidney. Furthermore, in the single kidney, changes in EEDTA, as induced by furosemide, are not related to changes in ipsilateral EANF. Since the relation between simultaneously determined single kidney extractions of ANF and51Cr-EDTA reflects the relation between the single kidney clearance of ANF and the ipsilateral glomerular filtration rate, our data indicate a dissociation between changes in the single kidney glomerular filtration rate and the ipsilateral total renal clearance of ANF.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

To examine and characterize the vascular renin-angiotensin system in low-renin models of renal hypertension with and without the presence of overt renal insufficiency, we studied the formation and metabolism of angiotensin in isolated perfused rat hindquarter preparations. Rats with 5/6 nephrectomy (5/6NX) and rats with one-kidney, one clip (1K1C) hypertension were compared to sham operated (sham) animals. Angiotensin peptides in plasma or perfusate were characterized by high-performance liquid chromatography and radioimmunoassay (RIA). Plasma angiotensin II was lower, and blood pressure was higher in both experimental groups, compared to sham animals. Plasma angiotensinogen, measured by both direct and indirect RIA, was increased in both experimental groups. The spontaneous release of angiotensin I and angiotensin II from perfused hindquarters did not differ between the groups. Angiotensin I conversion was not different in 5/6NX or 1K1C groups compared with controls. Furthermore, angiotensin conversion was completely inhibited by captopril (1 μmol/l) in all groups. Renin-induced angiotensin release was significantly increased in 5/6NX as compared with sham rats, whereas there was no difference in renin-induced angiotensin release between 1K1C and sham animals. Angiotensin II degradation was significantly attenuated in 5/6NX rats when compared with sham rats (27.6% versus 53.9%, respectively,P< 0.05) but was unaltered in 1K1C rats. Thus, in chronic uremic hypertension, renin-induced angiotensin formation was increased in the face of decreased angiotensin II degradation. These data suggest that vascular angiotensin may contribute to the elevated blood pressure observed in chronic renal failure. In 1K1C rats, vascular angiotensin formation and metabolism was unchanged despite suppressed plasma angiotensin II.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

To investigate the mechanism whereby blood pressure rises with NaCl loading in salt-sensitive essential hypertension, salt-sensitivity index was determined along with sodium and lithium clearances, plasma Na+, K+-ATPase inhibitor and intra-erythrocyte sodium and potassium concentrations. Salt-sensitivity index was defined as the percentage of change in mean blood pressure when NaCl intake was changed from low (34 mmol/day) to high (342 mmol/day). Salt-sensitivity index was inversely correlated with fractional excretion of lithium both on the low and high NaCl diets (r = −0.721,P< 0.01 and r = −0.591,P< 0.02, respectively; n = 16), but not with fractional excretion of sodium. The change of plasma Na+, K+-ATPase inhibition with NaCl loading had a direct correlation with salt-sensitivity index (r = 0.704,P< 0.01; n = 16). Either intra-erythrocyte sodium and potassium concentrations or the ratio of these two values did not change significantly with an increase of dietary NaCl intake. These results suggest that an enhancement of proximal tubular sodium reabsorption stimulates secretion of plasma Na+, K+-ATPase inhibitor which may be involved in a rise in blood pressure with sodium loading. They also suggest that lithium clearance is a determinant which can predict salt sensitivity without actual NaCl loading.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Blood pressure was measured in 864 young people aged 16–24 years, 8 years after both of their parents had their blood pressures measured as part of the screening phase of the Medical Research Council Mild Hypertension Trial. Only 29% of offspring with a conventional ‘family history of hypertension’, defined in terms of having at least one parent with a score in the top 10% of the distribution, had a blood pressure score in the top 20% after 8 years. The positive predictive value was increased to 38% in offspring with two parents in the top 20%, but only 4% of offspring met this definition and only 7% of offspring in the top 20% after 8 years were identified by this method. Sensitivity was increased to 46% in offspring with at least one parent in the top 20%, but 33% of offspring met this definition and 74% of them did not have a blood pressure level in the top 20% after 8 years. It is concluded that parental blood pressure data are of limited value for the prediction of high blood pressure in young people and provide no scientific basis for a high risk strategy of prevention.

ISSN:0263-6352    

出版商:OVID    

年代:1991

数据来源: OVID