摘要:

The aim of the present study was to investigate whether plasma concentration of proANP1–30, the N-terminal fragment of the atrial natriuretic peptide prohormone, or 24-hour urinary excretion of urodilatin reflects the degree of salt sensitivity in hypertension-prone individuals. Plasma concentration of proANP1–30and urinary urodilatin excretion were determined at baseline, after 1 week on a low-salt diet (10 mmol/d) and after another week on a high-salt diet (240 mmol/d) in 30 healthy subjects with heredity for hypertension. Salt sensitivity was defined as the difference between mean arterial blood pressure after the high-salt diet and the mean arterial blood pressure after the low-salt diet. High- versus low-salt intake increased proANP1–30(668±330 versus 358±150 pmol/L;P<0.00001) and urodilatin (18.7±5.2 versus 16.0±8.3 pmol/24 h;P<0.05). ProANP1–30correlated with salt sensitivity at baseline (r=0.76,P<0.000001), after the low- (r=0.80,P<0.0000001) and high-salt diets (r=0.85,P<0.00000001). The increase in proANP1–30induced by changing from the low- to the high-salt diet was also directly related to salt sensitivity (r=0.78,P<0.000001). ProANP1–30was not related to urinary sodium excretion. Neither urodilatin nor the sodium-induced change in urodilatin correlated with salt sensitivity. However, urodilatin was related to the urinary sodium excretion at baseline (r=0.58,P<0.01) and after the high-salt diet (r=0.62,P<0.001). In conclusion, the close correlations between proANP1–30and salt sensitivity suggest that proANP1–30may serve as a marker for salt sensitivity and could be useful in identifying subjects who would benefit from dietary salt restriction to prevent development of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Relationships of nutrients, alcohol intake, and change in weight to change in blood pressure over 8 years in 1714 employed middle-aged men from the Chicago Western Electric Study were explored. At first and second annual examinations, 2 in-depth interviews were performed to assess usual intake of foods and beverages during the preceding 28 days. Annual follow-up data through examination year 9 were used to determine change in weight and blood pressure. Averages of nutrients from 2 interviews were related to annual blood pressure change from baseline by use of the Generalized Estimating Equation, with control for confounders. In analyses of dietary variables considered individually, total and animal protein; total, saturated, monounsaturated, and polyunsaturated fatty acids; cholesterol; Keys dietary lipid score; calcium; alcohol; and average annual change in weight were positively and significantly related to average annual change in systolic pressure; vegetable protein, total carbohydrate, beta-carotene, and an antioxidant vitamin score based on vitamin C and beta-carotene were inversely and significantly related to average annual change in systolic pressure. In analyses of combinations of dietary factors, cholesterol, Keys score, and alcohol were positively related to change in systolic pressure (eg, Z-scores 2.21, 2.05, and 2.50); vegetable protein and antioxidant index were inversely related to change in systolic and diastolic pressure. Change in weight was directly related to change in systolic and diastolic pressure. These findings support the concept that multiple macro- and micronutrients, alcohol intake, and calorie imbalance relate prospectively to blood pressure change.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Elements of a renin-angiotensin system expressed along the entire nephron, including angiotensinogen secreted by proximal tubule and renin expressed in connecting tubule, may participate in the regulation of sodium reabsorption at multiple sites of the nephron. The response of this tubular renin-angiotensin system to stepwise changes in dietary sodium was investigated in 2 mouse strains, the sodium-sensitive inbred C57BL/6 and the sodium-resistant CD1 outbred. Plasma angiotensinogen was not affected by sodium regimen, whereas plasma renin increased 2-fold under low sodium. In both strains, the variation in urinary parameters did not parallel the changes observed in plasma. Angiotensinogen and renin excretion were significantly higher under high sodium than under low sodium. Water deprivation, by contrast, induced significant activation in the tubular expression of angiotensinogen and renin. C57BL/6 exhibited significantly higher urinary excretion of angiotensinogen than did CD1 animals under both conditions of sodium intake. The extent to which these urinary parameters reflect systemic or tubular responses to challenges of sodium homeostasis may depend on the relative contribution of sodium restriction and volume depletion.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

We investigated the difference between male and female rats in the increase in blood pressure (BP) when they were fed a lard-enriched diet. We also investigated the effect of a gonadectomy, with or without testosterone treatment, on the dietary lard-induced increase in BP. Wistar-strain male or female rats were bilaterally castrated or ovariectomized. Some of them were implanted subcutaneously with silicon tubes containing crystalline testosterone. Each group was fed either chow alone or chow in which 50% of the energy content was from substituted lard. Systolic blood pressure (SBP) was determined weekly during each 7- or 11-week feeding period. A steady-state plasma glucose method was used to determine the insulin sensitivity. The dietary lard-induced increase in SBP was observed at 5 weeks after the start of the feeding in the sham-operated male rats. In the sham-operated female rats, SBP did not change from the basal values until 11 weeks into the experimental period. Castration eliminated the dietary lard-induced increase in SBP. Ovariectomy had no effect on SBP throughout the experimental period in both diet groups. In castrated males given testosterone, SBP increased in a dose-dependent manner. In ovariectomized females given testosterone, SBP increased significantly in the lard-enriched diet group. The dietary lard developed an insulin resistance in both the sham-operated and gonadectomized rats. However, SBP increased only in the sham-operated male rats. These results suggest that the dietary lard-induced increase in SBP depends on the presence of testosterone. The development of insulin resistance by dietary lard triggers the increase in SBP.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Two distinct subtypes of angiotensin (Ang) II receptors, type 1 (AT1) and type 2 (AT2), have been identified. Vascular smooth muscle cells (VSMCs) usually express AT1receptor. To elucidate the direct effects of the AT2receptor on the AT1receptor in VSMCs, we transfected AT2receptor gene into cultured rat VSMCs. Overexpression of AT2receptor significantly decreased expression of AT1areceptor at both the mRNA and protein levels in the presence and absence of Ang II in VSMCs. Overexpression of AT2receptor increased expression of bradykinin and inducible NO in the presence and absence of Ang II in VSMCs. Bradykinin B2receptor antagonist HOE–140 and NO synthase inhibitorN&ohgr;-nitro-l-arginine methyl ester (L-NAME) inhibited the decreases in AT1areceptor expression by the overexpression of AT2receptor in VSMCs. l-Arginine augmented the decrease in AT1areceptor expression. Overexpression of AT2receptor suppressed basal DNA synthesis and proliferation of VSMCs and abolished response of DNA synthesis to Ang II in VSMCs. Our results demonstrate that overexpression of the AT2receptor downregulates AT1areceptor expression in rat VSMCs in a ligand-independent manner that is mediated by the bradykinin/NO pathway. Downregulation of AT1areceptor is a novel mechanism by which the AT2receptor regulates growth and metabolism of VSMCs.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Although cerebral hypoperfusion caused by cerebral occlusive disease leads to cerebral ischemic events, an effective treatment has not yet been established. Recently, a novel therapeutic strategy for ischemic disease using angiogenic growth factors to expedite and/or augment collateral artery development has been proposed. Therapeutic angiogenesis might be useful for the treatment of cerebral occlusive disease. Hepatocyte growth factor (HGF) is a potent angiogenic factor, in addition to vascular endothelial growth factor (VEGF), whereas in the nervous system HGF also acts as neurotrophic factor. Therefore, we hypothesized that gene transfer of these angiogenic growth factors could induce angiogenesis, thus providing an effective therapy for cerebral hypoperfusion or stroke. In this study, we employed a highly efficient gene transfer method, the viral envelop (Hemagglutinating Virus of Japan [HVJ]-liposome) method, because we previously documented that &bgr;-galactosidasegene could be transfected into the brain by the HVJ-liposome method. Indeed, we confirmed wide distribution of transgene expression using &bgr;-galactosidase via injection into the subarachnoid space. Of importance, transfection ofHGForVEGFgene into the subarachnoid space 7 days before occlusion induced angiogenesis on the brain surface as assessed by alkaline phosphatase staining (P<0.01). In addition, significant improvement of cerebral blood flow (CBF) was observed by laser Doppler imaging (LDI) 7 days after occlusion (P<0.01). Unexpectedly, transfection ofHGForVEGFgene into the subarachnoid space immediately after occlusion of the bilateral carotid arteries also induced angiogenesis on the brain surface and had a significant protective effect on the impairment of CBF by carotid occlusion (P<0.01). Interestingly, coinjection of recombinantHGFwithHGFgene transfer revealed a further increase in CBF (P<0.01). Here, we demonstrated successful therapeutic angiogenesis usingHGForVEGFgene transfer into the subarachnoid space to improve cerebral hypoperfusion, thus providing a new therapeutic strategy for cerebral ischemic disease.

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:2002

数据来源: OVID