Mitral flow responses to two-week salt loading in elderly hypertensive patients

The effects of a two-week high sodium diet on mitral flow pattern were assessed in 29 patients with essential hypertension (81.9 +/- 6.9 years). Transmitral flow was recorded during different rates of salt intake; 7 g/day for 8 weeks and 20 g/day for 2 weeks. With sodium loading, 25 patients whose mean blood pressure (MBP) increased by 10 percent or more were termed salt-sensitive (SS) group, and 4 patients whose MBP did not change or increased by less than 10 percent were termed non-salt-sensitive (NSS) group with mitral flow velocity integral, cardiac output (CO) and total peripheral resistance (TPR) were calculated. Thirteen of the SS patients were defined as "SST" in which an increase in TPR was greater than that in CO with sodium repletion. In the remaining 12 SS patients termed "SSc", the increase in CO was greater than that in TPR with salt loading. CO increased significantly in the SSc patients, but did not change in the SST or NSS group with sodium loading. TPR increased significantly in the SST and NSS subjects, and decreased significantly in the SSc patients. Peak velocity of transmitral flow in the rapid filling phase (R) decreased significantly in the SST and NSS patients, and increased significantly in the SSc group. On the other hand peak velocity of transmitral flow in the atrial contraction phase (A) increased significantly in the SST and SSc groups, but remained unchanged in the NSS patients. There was a significant increase in A/R in the SSt group and a significant decrease in A/R in the SSc patients with sodium loading.     

Hemodynamic response to dietary sodium loading in essential hypertension studied with Doppler echocardiography

The cardiac response to dietary salt loading was assessed by Doppler echocardiography during various sodium intakes (52-345 mEg per day) in 30 patients with essential hypertension. The Mitral flow velocity integral in the rapid filling phase (IntR) and the atrial contraction phase (IntA) was measured from the transmitral flow pattern, and the sum of IntR and IntA (IntR + IntA), the ratio of IntA to IntR (IntA/IntR), cardiac output (CO) and total peripheral resistance (TPR) were calculated. With salt loading, the mitral flow pattern remained almost unchanged in the nonsalt-sensitive (NSS) patients. Fourteen of the 19 salt-sensitive (SS) patients showed significant increases in IntR + IntA and CO with salt loading (IntR + IntA, from 13.9 +/- 2.8 to 17.9 +/- 3.6 cm, p less than 0.01; CO, from 6021 +/- 2130 to 8305 +/- 1699 ml/min, p less than 0.01), and were termed "salt-sensitive CO-dependent" (SS [COdep]), suggesting that the apparent pressor response to sodium loading was mediated by an increased CO. In the remaining five SS patients termed "salt-sensitive CO-independent" (SS [COindep]), IntA/IntR increased significantly with sodium repletion (from 0.66 +/- 0.23 to 0.90 +/- 0.31, p less than 0.01), without a significant change in IntR + IntA. Increments in IntA/IntR observed in the SS [COindep] patients were considered to be due to an elevation of total peripheral resistance (TPR), since changes in IntA/IntR were significantly correlated with those in TPR in all subjects (r = 0.617, p less than 0.01).     

Hemodynamic changes during dietary salt loading in elderly patients with essential hypertension

Hemodynamic changes with dietary salt loading were assessed by Doppler echocardiography during different sodium intake (7 g/day for 8 weeks, 20 g/day for 1 week) in 29 elderly patients with essential hypertension (81.6 +/- 6.7 years, 4 men, 25 women). With salt loading, 24 patients whose mean blood pressure (MBP) increased by 10% or more were defined as salt sensitive (SS) group, and 5 patients whose MBP did not change, or increased by less than 10% were defined as non-salt sensitive (NSS) group. Based on the mitral flow velocity integral, cardiac output (CO) was calculated, and total peripheral resistance (TPR) was calculated as MBP divided by CO. Nine of the 24 SS patients were termed "SS (COdep)" whose CO increased significantly with salt loading. In the remaining 15 SS patients termed "SS (TPRdep)", TPR increased significantly with sodium repletion. Blood flow in the common carotid, superior mesenteric, or terminal aorta was calculated from each flow velocity integral. The percent change in peripheral resistance calculated by dividing MBP by each blood flow was obtained. There were no significant percent changes in the common carotid resistance in SS (COdep), SS (TPRdep) or NSS groups. The superior mesenteric resistance increased significantly in all three groups. The terminal aortic resistance increased in the SS (TPRdep) group, but decreased in the SS (COdep) or NSS group. These results indicate that salt sensitivity is ascribable to changes in regional vascular resistances.     

Time course of hemodynamic responses to sodium in elderly hypertensive patients

Thirty-one patients with essential hypertension (81.6 +/- 6.9 years old) were studied during two different regimens of sodium intake: 120 meq/day for 8 weeks and 344 meq/day for 2 weeks. Systemic hemodynamic data were measured with Doppler echocardiography from which the mitral flow velocity integral, cardiac index, and total peripheral resistance were calculated. The salt-sensitive patients in whom the increase in total peripheral resistance was greater than the increase in cardiac index with salt loading were termed SST. In the salt-sensitive patients termed SSC, the increase in cardiac index was greater than the increase in total peripheral resistance with increased sodium intake. All SST patients on day 7 of the high sodium diet remained in the SST group on day 14. Nine of 13 patients in the SSC group on day 7 remained in the SSC group on day 14, and the remaining four patients in the SSC group on day 7 fell into the SST group on day 14. Four of eight non-salt-sensitive (NSS) patients on day 7 of the high salt regimen remained in the NSS group on day 14, whereas the remaining four patients in the NSS group on day 7 fell into the SSC group on day 14. Our data suggest a changing pattern with sodium loading of initially high cardiac index followed by a persistently raised total peripheral resistance. The celiac, superior mesenteric, and renal arteries vasoconstricted with sodium repletion in both SST and SSC patients. With salt loading, the terminal aortic vascular bed vasodilated in the SSC patients and vasoconstricted in the SST patients.     

Terminal aortic response to sodium intake is the major determinant of total peripheral resistance in elderly hypertensives.

Thirty-four elderly patients were studied using a Doppler flowmeter during different sodium intakes. Salt increased mean blood pressure and cardiac output (CO), while total peripheral resistance (TPR) remained unchanged. Neither carotid nor terminal aortic resistance changed, while coeliac, superior mesenteric or renal resistance increased. There was a significant and direct correlation (r = 0.82) between the change in TPR and that in terminal aortic resistance. Salt-sensitive patients were divided into two subgroups; the SST group in which sodium loading increased TPR more than CO, and the SSC group in which salt loading increased CO more than TPR. Terminal aortic resistance increased in the SST, decreased in the SSC, and remained unchanged in the non-salt-sensitive group with salt loading. The terminal aortic vascular bed received much of the increase of CO in the SSC patients. In the SST group, the contribution of the individual vascular area to increased TPR was assessed, which revealed that terminal aortic response to sodium loading was the major determinant of increased TPR. We concluded that the responses of terminal aortic vascular bed to sodium loading contributed to the changes in TPR.     

Plasma norepinephrine is a major determinant of hemodynamic alterations with sodium loading.

OBJECTIVE: To assess hemodynamic responses to 3 weeks of sodium loading and to evaluate factors which contribute to hemodynamic alterations. DESIGN: Analysis of patients' central hemodynamic and laboratory variables before and after sodium loading. SETTING: A referral centre. PATIENTS: Thirty-one elderly hypertensives. INTERVENTIONS: Doppler flowmetry and laboratory examinations were performed during different sodium intake; 120 mmol/day for 8 weeks and 344 mmol/day for 3 weeks. RESULTS: Patients were divided into three groups; those in whom sodium loading increased total peripheral resistance (SST); those in whom salt repletion increased cardiac index (SCC); a non-salt-sensitive group (NSS). The overwhelming reaction to salt loading is that, with time, the NSS and SSC groups became part of the SST group. When the SSC patients became SST with sodium loading, serum sodium and plasma arginine vasopressin decreased and haematocrit increased, suggesting that the excretion of sodium and water accompanied with a decrease in circulating plasma volume may be responsible for the hemodynamic alteration from SSC to SST. In those who remained in the SSC group throughout the 3 weeks of salt repletion, plasma norepinephrine decreased on all of days 7, 14 and 21 of the high-sodium diet compared with the regular-sodium regimen, whilst in patients in the SST group on day 21 of the high-sodium diet plasma norepinephrine remained unchanged throughout the 3 weeks of salt loading. CONCLUSIONS: We confirmed a changing pattern of initially high cardiac index giving way to a persistently elevated total peripheral resistance with sodium loading. Plasma norepinephrine proved to be the best predictor of which subjects were or became SST.     

Effects of salt, prostaglandin, and captopril on vascular responsiveness in essential hypertension

To examine the influence of dietary sodium, prostaglandin, and captopril on vascular reactivity, 12 patients with essential hypertension (EH) and seven normotensive subjects (NT) were given a high sodium diet and thereafter a low sodium diet, each for ten days. Indomethacin (IND) (150 mg/d) was administered during the last three days of each dietary period. Blood pressure and cardiac output (CO) (by impedance cardiography) were measured during the angiotensin II (Ang II) infusion before and after the IND treatment of each dietary period. In eight patients with EH, captopril 100 mg was given before Ang II infusion. EH patients were classified as either salt sensitive (SS) or nonsalt sensitive (NSS). The mean blood pressure (MBP) response to Ang II was significantly higher on high sodium intake than on low sodium intake in NSS and NT, but not in SS. IND significantly increased the MBP response to Ang II on low sodium intake in NSS and NT, but not in SS. IND significantly increased the TPR response to Ang II on low sodium intake, remarkably in NSS and NT compared with SS. Salt sensitivity (% decrease in MBP from high to low sodium intake) highly correlated with the increase in the TPR response to Ang II by IND on low sodium intake (r = -0.90). After captopril administration, IND still increased the MBP and TPR response to Ang II on low sodium intake. These results suggest that the modulation of the vascular responsiveness to Ang II by prostaglandins is altered by sodium balance and salt sensitivity in EH.     

Salt-induced exacerbation of morning surge in blood pressure in patients with essential hypertension

The morning surge in blood pressure (BP) is related to the morning occurrence of lethal cardiovascular events. We tested the hypothesis that salt intake may be associated with the morning surge in BP in essential hypertension. Seventy-six patients were admitted and placed on a low salt diet (2 g/day) for 7 days followed by a high salt diet (20-23 g/day) for another 7 days. At the end of each salt diet, 24-h ambulatory BP and heart rate monitorings and head-up tilt (HUT) test were performed. Patients whose average mean BP (MBP) was increased by more than 10% by salt loading were assigned to the salt-sensitive (SS) group (n = 37); the remaining patients, whose MBP was increased by less than 10%, were assigned to the non-salt-sensitive (NSS) group (n = 39). The increase in ambulatory MBP during 6.30-8.00 am above the baseline (2.00-4.00 am) was significantly enhanced by salt loading in the NSS group (P < 0.05), but not in the SS group. The coefficient of variation of 24-h MBP and heart rate was increased by salt loading only in the NSS group. The significant elevation of plasma noradrenaline concentration after awakening, which was noted during the low salt diet period, was unchanged during the high salt diet period in the NSS group, but abolished in the SS group. Salt loading enhanced HUT-induced decrease in systolic BP without affecting the heart rate response only in the NSS group. We conclude that the morning surge in BP is enhanced by salt loading in the NSS type of essential hyper- tension, presumably by the excessive activation of the sympathetic nervous system. Journal of Human Hypertension (2000) 14, 57-64.     

Systemic and regional hemodynamics in patients with salt-sensitive hypertension

Twenty-two patients with normal plasma renin and essential hypertension were classified as "salt-sensitive" (SS) (n = 9) or "non-salt-sensitive" (NSS) (n = 13) from an increase in mean blood pressure with changes in sodium intake from 25 to 250 meq/day. With the high sodium diet, the SS patients gained more weight (p less than 0.05), retained more sodium (p less than 0.05), and had a greater increase in cardiac output (p less than 0.05). Despite the markedly increased cardiac output, systemic vascular resistance did not change with sodium loads in the SS patients, whereas the NSS patients had a significant decrease in systemic vascular resistance. Thus, the greater increase in blood pressure with sodium loads in SS patients can be attributed not only to an increase in cardiac output, possibly resulting from greater sodium retention, but also to inappropriately elevated systemic vascular resistance. Concomitant with a greater increase in cardiac output, the SS patients had a greater increase in forearm blood flow with sodium loading than the NSS patients (p less than 0.02). In contrast, blood flow to the kidney and the liver was not significantly changed in either group; renal (p less than 0.05) and hepatic (p less than 0.01) vascular resistance increased significantly in SS patients but remained unchanged in NSS patients. Thus, evidence presented suggests that the greater increase in blood pressure with sodium loads seems to be characterized by a very inhomogenous distribution of local flow and resistance in SS patients; renal and hepatic blood flow remains essentially unchanged and skeletal muscle blood flow receives almost all of the increase in cardiac output. Moreover, systemic vascular resistance changes did not reflect the resistance of individual beds because vasoconstriction appeared in the kidney and the splanchnic area but was masked by prominent vasodilation in the skeletal muscle. Because this hemodynamic pattern is similar to the pattern evoked during defense reaction, it is suggested that sympathetic overactivity on a selective basis might be involved in the impaired renal function for sodium excretion and the increase in blood pressure with sodium loads in SS patients.     

Attenuated release of atrial natriuretic factor due to sodium loading in salt-sensitive essential hypertension.

Forty-one patients with essential hypertension were classified as salt-sensitive (SS) or non-salt-sensitive (NSS) from the changes in mean blood pressure (MBP) with alterations in sodium intake from 35 mmol (low-sodium) to 250 mmol/day (high-sodium). Whereas there was no difference in plasma levels of atrial natriuretic factor (ANF) on a normal-sodium diet (120 mmol) between the 2 groups, the degree of increase in the plasma ANF level between the low- and high-sodium intake was significantly greater in NSS than in SS (p less than 0.001). In addition, the urinary sodium excretion on a high-sodium diet was smaller in SS than in NSS. There was a significant positive correlation between the plasma ANF and MBP after the high-sodium intake in both SS (r = 0.67, p less than 0.01) and NSS (r = 0.60, p less than 0.01); however, the relation of plasma ANF to MBP shifted apparently to a lower level in SS compared with NSS. These findings not only indicate that there exists a hyporesponsiveness of ANF release by the heart of SS patients in response to high-sodium loading, but also imply that such a response contributes to blood pressure-elevating mechanisms due to sodium loading in this type of human hypertension.     

盐敏感性高血压患者昼夜血压变异性与尿钠排泄节律的关系

目的观察盐敏感性高血压患者24 h血压昼夜节律变化,探讨昼夜尿钠排泄改变与血压变异性的关系。方法选取住院的1²级原发性高血压患者58例,进行24 h动态血压监测,收集测量昼、夜尿钠排泄量。采用快速静脉输注生理盐水与呋塞米排钠缩容相结合的方法,测定盐敏感性。结果 58例受试者共检出盐敏感者25例(43.1%)。24 h动态血压监测结果显示,盐敏感(SS)组与盐不敏感(NSS)组白天血压比较,差异无统计学意义,但SS组收缩压夜间下降百分比(4.0%±2.0%比11.0%±3.0%)、舒张压夜间下降百分比(7.0%±4.0%比13.0%±4.0%)均显著小于NSS组(均为P<0.05)。SS组与NSS组24 h尿钠排泄量差异无统计学意义,但SS组夜间尿钠排泄量显著大于NSS组[(108.2±39.2)mmol比(70.6±35.0)mmol,P<0.01];SS组夜尿钠占全天百分比高于NSS组(48.0%±23.0%比35.0%±22.0%,P<0.05)。结论盐敏感性高血压患者夜间尿钠排泄量增加,致夜间血压代偿性升高,呈"非杓型"改变。     

Salt sensitivity and central dopaminergic activity in patients with essential hypertension

The pathophysiological role of the central dopaminergic mechanism in human essential hypertension (EH) is still unknown. We studied on the relationship between the dopaminergic activity and the salt-sensitivity. Twenty three hospitalized patients with EH were divided into the salt-sensitive group (SS, n = 12) or non salt-sensitive group (NSS, n = 11) by their responses whether they caused more than 8% increase in mean blood pressure (MBP) when the dietary salt was increased from 2g/day to 20g/day for 7 days of each. The change of central dopaminergic activity by the salt load was evaluated by the decrement of plasma prolactin (PRL) response to small dosage (25 micrograms) of thyrotropin releasing hormone. The mean percent change of PRL response by the salt load in the SS group was -6.5 +/- 8.3% (mean +/- SEM), which was significantly lower than 26.8 +/- 5.5% in the NSS group (p less than 0.01). There was a significant negative correlation between the percent changes of PRL response and the percent changes of MBP by the salt load (r = -0.448, p less than 0.05). These results suggested that the rise in blood pressure by salt load in SS patients with EH might be due to a reduced activity of the central dopaminergic mechanism.     

Significance of sympathetic nervous system in sodium-induced nocturnal hypertension.

OBJECTIVE: The purpose of this study was to investigate the effects of salt loading on circadian patterns of blood pressure (BP) and sympathetic nervous activity. SUBJECTS AND METHODS: Seventy-six patients with essential hypertension were hospitalized and placed on a low-salt diet (2 g/day) for 7 days followed by a high-salt diet (20-23 g/day) for another 7 days. On the last day of each salt diet, 24 h ambulatory BP, plasma noradrenaline concentrations, urinary noradrenaline excretion, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured. Patients whose average mean BP was increased by more than 10% by salt loading were assigned to the salt-sensitive (SS) group (n = 44); the remaining patients, whose mean BP was increased by less than 10%, were assigned to the non-salt-sensitive (NSS) group (n = 32). RESULTS: Salt loading converted the circadian pattern of BP from dippers, whose mean BP during the night-time was decreased by more than 10% from the daytime BP, to non-dippers in the SS group but not in the NSS group. A nocturnal decrease in plasma noradrenaline concentration was unaffected after salt loading in the NSS group but dampened in the SS group. The night-time/daytime ratio of urinary noradrenaline excretion, which was increased after salt loading in the SS group only, was greater in the SS group than in the NSS group under the high-salt diet. The salt-induced suppression rate of PRA and PAC was similar between the SS and NSS groups. CONCLUSION: BP fails to fall during the night under the high-salt diet in patients with the SS type of essential hypertension. This may be related to the lack of nocturnal decrease in sympathetic nervous activity.     

盐敏感性高血压病患者血浆心钠素、血管紧张素Ⅱ和醛固酮水平测定及苯那普利治疗的初步观察

目的探讨心钠素(ANP)和肾素-血管紧张素-醛固酮系统(RAAS)在盐敏感性高血压病发病中的作用及苯那普利的降压作用和ANP的关系.方法采用改良的Sullivan急性口服盐水负荷试验的方法将64例高血压病患者分为盐敏感性(SS, 30例)和非盐敏感性(NSS,34例)高血压病组,测定盐负荷前与盐负荷期间血浆ANP、血管紧张素Ⅱ(AⅡ)和醛固酮(ALD)水平.30例正常人为对照组.SS组患者采用自身对照的方法予以口服安慰剂和苯那普利(10 mg/d～20 mg/d),观察治疗前后血压及血浆ANP水平的变化.结果 (1)基础血浆ANP水平,SS组显著低于NSS组,NSS组显著低于正常组[分别为SS(110.28±15.40)pmol/L,NSS(145.52±26.53)pmol/L和对照组(197.74±26.20)pmol/L, P均<0.01].盐负荷期SS组和NSS组血浆ANP水平均明显增高[分别为(133.56±34.03)pmol/L和(169.20±35.91)pmol/L,P均<0.05].增高的百分数两组间无显著性差异(P>0.05).但SS组血浆ANP仍低于正常水平.(2)基础血浆AⅡ和ALD水平在SS组与NSS组间无明显差异(P均>0.05).盐负荷期SS组和NSS组血浆AⅡ和ALD水平无明显改变(P均>0.05).(3)SS组于苯那普利治疗后血压明显降低(P<0.01),血浆ANP水平显著增高[(146.74±31.86)pmol/L,P<0.01].(4)基础血浆ANP水平与盐负荷引起的平均动脉压增高的幅值呈显著负相关( b=-0.06,P<0.05).结论循环内源性ANP的不足可能是SS高血压病的一个重要发生机制.苯那普利显著升高血浆ANP水平,能够有效降低SS高血压病患者的血压.     

Physiological significance of atrial natriuretic peptides in essential hypertension

To investigate the significance of atrial natriuretic peptides (ANP) in essential hypertension, plasma ANP concentrations in 43 essential hypertensives, 16 borderline hypertensives and 17 normotensive controls were measured. Furthermore, effects of high-sodium and low-sodium intakes on plasma ANP concentration were examined in "salt-sensitive" [SS] and "nonsalt-sensitive" [NSS] patients with essential hypertension. Plasma ANP concentration was significantly higher in hypertensives than in borderline hypertensives and in normotensive controls. No significant difference in plasma ANP concentration was observed between borderline hypertensives and normotensive controls. Plasma ANP concentration increased with the high-sodium diet in both the SS and NSS patients, but the mean increment was significantly greater in the SS than the NSS patients. Urinary excretion of sodium was lower in the SS patients taking the high-sodium diet than the corresponding value in the NSS patients. These findings suggest that an increased level of circulating ANP in hypertensive patients represents a compensatory mechanism to offset further elevation of blood pressure and sodium retention.     

Abnormal renal hemodynamics in salt-sensitive patients with essential hypertension

Thirty hypertensive patients were studied during a low-sodium diet for three days and a high-sodium diet for six days. They were classified as "salt-sensitive" (SS) (n = 10) or "non-salt-sensitive" (NSS) (n = 20) based on the increase in mean blood pressure (BP) with changes in sodium intake from 25 mEq/day to 250 mEq/day (14.7 +/- 1.3% versus 4.0 +/- 0.8%, p less than 0.001). With the high-sodium diet, the SS patients had a greater increase in cardiac output (p less than 0.001), and the increment in mean BP with the salt loading significantly correlated to that in cardiac output (r = 0.672, p less than 0.01). Thus, the increase in BP during short-term salt loading may be attributed to the increase in cardiac output. The role of renal hemodynamics in the increment of BP with salt loading after sodium restriction was evaluated in six SS and 14 NSS patients. Although the glomerular filtration rate was not different in the two groups, the renal vascular resistance was greater (p less than 0.05) in the SS patients than in the NSS ones. Moreover, renal vascular resistance positively correlated to the increment in mean BP with salt loading (r = 0.612, p less than 0.01). Thus, it is suggested that renal vasoconstriction may be an important factor influencing "salt-sensitivity" in essential hypertension, possibly via the impaired renal sodium excretion.     

Factors influencing blood pressure in salt-sensitive patients with hypertension

Eighteen patients with hypertension in whom all known causes of elevated blood pressure levels had been ruled out were studied during a low-sodium diet for seven days, a high-sodium diet for seven days and after the oral administration of furosemide. They were classified as “salt-sensitive” (SS) or “nonsalt-sensitive” (NSS) from the increase in 24-hour averages of mean blood pressure with changes in sodium intake from 9 meq to 249 meq/day (15.1 ± 1.2 (SE) mm Hg (SS) versus 2.7 ± 0.9 mm Hg (NSS), (p < 0.001)). With a highsodium diet, SS patients gained more weight (p < 0.001), retained more sodium (p < 0.05), had a greater increase in cardiac output (p < 0.05), showed higher plasma norepinephrine levels on day 4 (p < 0.05), showed lesser decrements in PRA and plasma aldosterone concentration than the NSS patients, and showed no change in urinary prostaglandin E₂ (PGE₂) which decreased (p < 0.01) in the NSS patients. With furosemide, SS patients showed greater decrements in cardiac output (p < 0.05) and showed no change in urinary PGE₂, whereas NSS patients showed increases (p < 0.01). Results suggest that the greater increase in blood pressure in SS patients with sodium loading can be attributed to greater sodium retention, leading in turn to an increase in cardiac output. The persistence of autonomic “drive” in the SS patients may contribute to the relative sodium retention with sodium loads and the increase in blood pressure.     

原发性高血压患者盐敏感性与血管重构的探讨

目的探讨原发性高血压患者盐敏感性与血管重构的关系。方法选择原发性高血压患者204例(高血压组),高血压组又分为:盐敏感性组96例和盐不敏感性组108例,另选46例健康体检者作为对照组。采用ELISA法测定血清血管内皮生长因子(VEGF)、碱性成纤维细胞生长因子(bFGF),超声测试肱动脉血流介导的血管舒张功能(FMD)和颈动脉内膜中层厚度(IMT)。结果高血压组患者尿酸、体重指数较对照组明显升高(P0.01)。与盐不敏感性组比较,盐敏感性组患者LDL-C、尿酸明显升高,HDL-C明显下降(P0.01)。高血压组患者VEGF、bFGF、IMT较对照组明显升高,FMD明显下降(P0.01)。盐敏感性组患者VEGF、bFGF、IMT较盐不敏感性组进一步升高,FMD进一步下降(P0.01)。回归分析显示,盐敏感性、TC、TG、lgVEGF是IMT独立预测指标,盐敏感性与IMT独立相关(r=0.534,P0.01)。结论盐敏感性是高血压患者血管重构、靶器官损害的独立预测因素。     

Salt sensitivity and central dopaminergic activity in patients with essential hypertension.

The pathophysiological role of the central dopaminergic mechanism in human essential hypertension (EHT) is still unknown, so we investigated a possible relationship between the central dopaminergic activity and salt sensitivity to blood pressure in patients with EHT. We divided 22 inpatients with EHT into salt-sensitive (SS, n = 11) and non-salt-sensitive (NSS, n = 11) groups according to an 8% increase of mean blood pressure (MBP) when dietary salt intake was increased from 2 g/day to 20 g/day for two periods of 7 days each. The change of central dopaminergic activity by salt load was evaluated as the percentage change of plasma prolactin (PRL) response to a small dose (25 micrograms) of thyrotropin-releasing hormone (TRH) administered intravenously. The mean percentage change of PRL response by salt load in the SS group was -9.4 +/- 8.5% (mean +/- SEM), which was remarkably lower than the 26.8 +/- 5.5% in the NSS group (P less than .01). There was a significant negative correlation between the percentage change of PRL response and that of MBP by salt load (r = -0.456, P less than .05). These results suggest that a lack of activation of the central dopaminergic system by salt load may contribute in part to a rise in blood pressure in SS patients with EHT.     

Different patterns of left ventricular filling in arterial hypertension

To determine whether left ventricular (LV) filling dynamics may be influenced by the type of LV morphological adaptation to arterial hypertension, pulsed Doppler mitral flow velocity recordings were performed in 30 hypertensive patients and in 18 normotensive subjects matched for age, body surface and heart rate. Peak early (E) and late (A) mitral flow velocity, A/E ratio (A/E), time to peak E (TP), acceleration (AHT) and deceleration half-time (DHT) of early mitral flow and isovolumic relaxation time (IRT) were measured. Compared with the control group, hypertensive patients showed prolonged IRT and DHT, increased A and A/E, whereas TP, AHT and E were unchanged. Hypertensive patients were classified into two subgroups on the basis of h/r ratio (h/r). Subgroup 1: 16 patients with normal h/r, less than 0.42, (five patients with increased LV mass index, greater than 129.2 g m-2, and 11 patients with normal LV mass index, less than 129.2 g m-2). Subgroup 2: 14 patients with increased h/r, greater than 0.42, (nine patients with increased LV mass index, greater than 129.2 g m-2 and five patients with normal LV mass index, less than 129.2 g m-2). In Subgroup 1 the cardiac output (CO) was increased and the total peripheral resistance (TPR) was unchanged in comparison with the control group. In Subgroup 2 the opposite haemodynamic profile was detected: normal CO and increased TPR.(ABSTRACT TRUNCATED AT 250 WORDS)