Effects of hormone replacement therapy on office and ambulatory blood pressure in Japanese hypertensive postmenopausal women.

No study has demonstrated that hormone replacement therapy (HRT) affects blood pressure (BP) measured by 24-h ambulatory blood pressure monitoring (ABPM) in Japanese postmenopausal women (PMW) with normotension or mild-to-moderate essential hypertension. In the present study, we examined the effects of HRT on office BP and 24-h ambulatory blood pressure (ABP) in Japanese hypertensive or normotensive PMW. Thirty-one hypertensive (HT-HRT group) and 17 normotensive PMW (NT-HRT group) received HRT (0.625 mg of conjugated equine estrogen combined with 2.5 mg of medroxyprogesterone acetate) orally for 12 months, and 30 hypertensive (HT-Control group) and 19 normotensive PMW (NT-Control group) did not receive HRT. In all of the hypertensive PMW, BP was controlled by a variety of antihypertensive drugs before starting HRT. The hypertensive PMW were divided into two groups according to the results of ABP before HRT: nondippers (those without a diurnal change in BP) and dippers (those with a diurnal change in BP). In all patients, office BP measurements and 24-h ABPM were performed before and 12 months after the start of HRT. HRT did not change either the office or the 24-h ambulatory systolic, diastolic, or mean BP in any of the groups. Therefore, HRT did not significantly alter the proportion of nondippers. We conclude that with respect to BP, HRT might not be harmful in hypertensive PMW whose BP has been well-controlled prior to the initiation of HRT, as well as in normotensive PMW.     

Hormone replacement therapy increases plasma level of angiotensin II in postmenopausal hypertensive women

The renin-angiotensin-aldosterone system plays a major role in the pathogenesis of hypertension by enhancing the production or the activity of angiotensin II (ANG II). We evaluated the effects of hormone replacement therapy (HRT) on the renin-angiotensin-aldosterone system and on bradykinin in postmenopausal women (PMW) who were hypertensive or normotensive. Subjects included 28 PMW whose elevated blood pressure (BP) was well controlled on antihypertensive agents excluding diuretics, angiotensin-converting enzyme (ACE) inhibitors, and ANG II receptor antagonists. As controls, we evaluated 16 normotensive PMW. All subjects received oral HRT daily for 6 months. The plasma levels of angiotensin I (ANG I), ANG II, and bradykinin as well as plasma renin activity (PRA) showed a significant increase in HRT in the hypertensive group, but not in the normotensive group. The serum ACE activity showed a significant decrease in both groups, but the plasma level of aldosterone was unchanged. Despite the decrease in serum ACE activity, there was an increase in the plasma ANG II level. Hormone replacement therapy increased the level of ANG II in the hypertensive women, but their BP was unaffected. The increase in plasma bradykinin level may maintain homeostasis in the presence of an increase in plasma ANG II, which is a risk factor for cardiovascular disease. Hormone replacement therapy was associated with a decrease in serum ACE and an increase in plasma bradykinin in hypertensive PMW. Accordingly, the protective effect of HRT against cardiovascular disease in PMW can be provided by a decrease in ACE activity and an increase in bradykinin.     

Effects of hormone replacement therapy on left ventricular hypertrophy and growth-promoting factors in hypertensive postmenopausal women.

We investigated the effects of hormone replacement therapy (HRT) on left ventricular hypertrophy (LVH) and growth-promoting factors in hypertensive postmenopausal women (PMW) with LVH. Twenty-one Japanese hypertensive PMW (age 55.3+/-0.8 years) with LVH who had never received HRT volunteered to participate in this study. Eleven subjects received a daily dose of HRT (0.625 mg conjugated equine estrogen, 2.5 mg medroxyprogesterone acetate) orally for 12 months. Ten PMW who refused HRT were enrolled as controls. Blood pressure and serum angiotensin-converting enzyme (ACE) activity, plasma aldosterone, and insulin resistance were measured. M-mode echocardiography and blood pressure measurements were performed in all patients. Data obtained before and after 12 months of HRT were compared. No significant differences in blood pressure were observed between the two groups after 12 months of HRT. In the HRT group, the LV mass index (p<0.01), serum ACE activity (p<0.01), and plasma aldosterone (p<0.01) levels were reduced after 12 months of treatment. The changes in serum ACE activity and plasma aldosterone were not correlated with the change in LV mass index in the HRT group. No significant changes in blood pressure, LV mass index, serum ACE activity, plasma aldosterone, or insulin resistance were observed in the control group. HRT contributed to the reduction of LV mass in hypertensive PMW. However, the effect of HRT on LVH did not appear to be associated with changes in growth-promoting factors, such as blood pressure, serum ACE activity, plasma aldosterone, and insulin resistance.     

Plasma concentration of urotensin II is raised in hypertension

OBJECTIVES: Urotensin II is the most potent vasoconstrictor known. Its role in hypertension has not been investigated. Here, we studied the plasma levels in hypertensive and normotensive human subjects. DESIGN: A cross-sectional case-control study. SETTING: Hypertension clinic and research clinic of a university teaching hospital. PARTICIPANTS: Sixty-two hypertensive outpatient subjects (52% male, aged 57 +/- 13 years) and 62 normotensive controls (45% male, aged 54 +/- 13 years) recruited from the general population. MAIN OUTCOME MEASURES: Plasma urotensin II levels measured by radioimmunoassay, systolic and diastolic blood pressure. RESULTS: Plasma urotensin II was 8.8 +/- 0.9 pmol/l in normotensive controls and 13.6 +/- 1.4 pmol/l in hypertensive subjects (P = 0.005). In multiple regression analysis, systolic blood pressure was related to plasma urotensin II (beta = 0.31, P < 0.001) and age (beta = 0.28, P = 0.001), accounting for 10 and 8%, respectively, of the variance in systolic blood pressure. There was no significant correlation with gender, renal function or diabetes. CONCLUSIONS: Plasma urotensin II was raised in hypertensive patients compared to normotensive controls, and was directly related to systolic blood pressure. Our findings raise the possibility that urotensin II may have an aetiological role in hypertension and its complications.     

原发性高血压患者血清肝细胞生长因子的测定

目的:肝细胞生长因子(HGF)是一种特异性内皮生长因子,参与血管内皮损伤修复过程.高血压引起的血管内皮细胞损伤也可能导致HGF异常,为研究这一可能性,本项目测定无肝肾功能损伤及其他并发症的原发性高血压患者及正常对照者的血清HGF浓度.方法:18例男性高血压患者及13例男性正常对照者入选.所有受试者停药二周.血清HGF浓度用酶联免疫分析法(ELISA)测定.结果:正常对照组血清HGF浓度为0.321±0.125 ng/ml; 原发性高血压组为0.368±0.269 ng/ml,二组之间无显著性差异(P>0.05).收缩压,舒张压及平均动脉压与血清HGF水平无相关性.结论:血清HGF在轻,中度原发性高血压患者中并不增高.高血压引起血管内皮细胞损伤时,虽然局部HGF迅速产生,但循环HGF并不受影响.     

Hormone replacement therapy in postmenopausal women with essential hypertension increases circulating plasma levels of bradykinin

Hormone replacement therapy (HRT) reduces the incidence of cardiovascular disease (CVD) in postmenopausal women (PMW). Recently, it has been reported that HRT declines angiotensin converting enzyme (ACE) activity, which may be one of the factors protecting against CVD. We measured the plasma levels of bradykinin, which would be expected to increase because the bradykinin-degrading enzyme (kinase II) is the same as ACE. Treatment with conjugated estrogens (0.625 mg/day) and medroxyprogesterone (2.5 mg/day) was given for 3 months as HRT to 19 hypertensive and 19 normotensive PMW. Plasma bradykinin and ACE activity levels were measured at baseline and after 3 months of HRT. The plasma levels of ACE activity in both the hypertensive and normotensive PMW were significantly reduced by HRT. The plasma levels of bradykinin in the hypertensive PMW were significantly increased by HRT, whereas the administration of HRT tended to increase plasma levels of bradykinin in the normotensive PMW. The increased bradykinin levels with a concomitant decrease of plasma ACE activity by HRT in hypertensive PMW seem to be beneficial for reducing the risk of CVD.     

Serum level of vascular endothelial growth factor is decreased by hormone replacement therapy in postmenopausal women without hypercholesterolemia

The administration of hormone replacement therapy (HRT) to postmenopausal women (PMW) reportedly has beneficial effects on their levels of lipid and lipoproteins. Estrogen retards the development of atherosclerosis induced by a high-fat diet in animals. Although vascular endothelial growth factor (VEGF) may be involved in the development of atherosclerosis in humans, there is no information on effect of estrogen administration on VEGF level and lipid metabolism. We evaluated 64 healthy normotensive or hypertensive PMW before and during the administration of HRT (0.625 mg conjugated equine estrogen combined with 2.5 mg medroxyprogesterone acetate orally) daily for 6 months. All hypertensive PMW were well-controlled on antihypertensive drug therapy. According to their total cholesterol level at baseline, we divided the PMW with HRT (n=54) into a normocholesterolemic group (NC, total cholesterol <220 mg/dl, n=35) and a hypercholesterolemic group (HC, total cholesterol >/=220 mg/dl, n=19). We evaluated the serum levels of VEGF at baseline, and again at 3 and 6 months after starting HRT. HRT significantly (P<0.01) reduced the mean VEGF level from 31.5+/-4.3 pg/ml at baseline to 18.2+/-2.3 pg/ml after 6 months in the NC group. However, the VEGF levels in the HC group and the control group exhibited no significant change at either 3 or 6 months after starting HRT. In summary, HRT, using a combination of conjugated equine estrogen and medroxyprogesterone acetate, reduced the level of VEGF in normocholesterolemic PMW more effectively than in those with hypercholesterolemia.     

Different effects of transdermal and oral hormone replacement therapy on the renin-angiotensin system, plasma bradykinin level, and blood pressure of normotensive postmenopausal women

BACKGROUND: This study compared the efficacy of transdermally administered estradiol with that of orally administered conjugated equine estrogens (CEE) on the renin-angiotensin system, plasma bradykinin level, and blood pressure (BP) in normotensive postmenopausal women (PMW). METHODS: A total of 38 normotensive PMW were randomly assigned to two groups. The transdermal hormone replacement therapy (HRT) group consisted of 19 women treated with a continuous transdermal estradiol patch (36 microg/day) plus cyclic oral medroxyprogesterone acetate (MPA; 2.5 mg/day for 12 days) for 12 months. The oral HRT group consisted of 19 women who received continuous oral CEE (0.625 mg/day) plus cyclic oral MPA (2.5 mg/day for 12 days) for 12 months. Plasma renin activity (PRA), serum angiotensin-converting enzyme (ACE) activity, plasma angiotensin (Ang) I, Ang II, and bradykinin concentrations, and BP were measured before and 12 months after the start of HRT. RESULTS: Transdermal HRT significantly decreased both diastolic and mean BP and concomitantly reduced bradykinin levels (all P < .05). However, no significant changes in PRA, ACE activity, Ang I, or Ang II levels were observed. The BP remained unchanged in the oral HRT group, but the PRA, Ang I, Ang II, and bradykinin levels had significantly increased and ACE activity had significantly decreased (all P < .05) at 12 months after the start of HRT. CONCLUSIONS: Transdermal HRT decreased BP in normotensive PMW without influencing Ang II, whereas oral HRT increased Ang II without altering BP. Transdermal HRT may be more beneficial than oral HRT with regard to BP and Ang II levels.     

Elevated levels of leptin and insulin but not of TNF alpha are associated with hypertension in type 2 diabetic males.

Leptin and TNF alpha are thought to influence blood pressure. Therefore, the aim of our study was to investigate leptin and TNF alpha levels and their association with blood pressure, sex steroids, insulin, creatinine and lipids in type 2 diabetic patients. In 424 type 2 diabetic patients (79 hypertensive females [+Hf], 79 normotensive females [-Hf]; 133 hypertensive males [+Hm], 133 normotensive males [-Hm]) matched for sex, age and BMI serum leptin levels were measured by RIA and TNF alpha, insulin, estradiol, progesterone by ELISA as well as free testosterone by RIA. Leptin levels were comparable in +Hf and -Hf (16.5 +/- 1.0 microg/l vs 16.3 +/- 1.0 microg/l) but higher in +Hm as compared to -Hm (8.3 +/- 0.47 microg/l vs 6.5 +/- 0.34 microg/l; p<0.05). In addition, in comparison to -Hm serum levels of insulin (190 +/- 10 pmol/l vs 161 +/- 11 pmol/l; p< 0.005) and also of creatinine (118.6 +/- 3.6 micromol/l vs 101.7 +/- 2.3; p< 0.0001) were higher in +Hm. Pearson's Correlation coefficient revealed a positive correlation between levels of leptin and diastolic blood pressure (p<0.05) and also between leptin and insulin (p<0.001) in males, however, only before correction for BMI. No correlation between leptin and creatinine was found in males and females. Levels of TNF alpha were comparable in all subgroups. No correlation between levels of TNF alpha and serum leptin levels, blood pressure and insulin was found. In females TNF alpha was positively correlated with creatinine (p<0.001) and in males positively with progesterone (p<0.001). Taken together, higher serum leptin levels were found in hypertensive type 2 diabetic males as compared to normotensives, which may be related to the BMI and higher levels of insulin. These findings are accompanied by a trend to lower levels of free testosterone in hypertensive type 2 diabetic males. TNF alpha levels were comparable in female and male hypertensive and normotensive type 2 diabetic subjects.     

Effects of long‐term transdermal hormone replacement therapy on the renin–angiotensin– aldosterone system,plasma bradykinin levels and blood pressure in normotensive postmenopausal women

Aim: This study was designed to investigate the effects of 24‐month long‐term transdermal hormone replacement therapy (HRT) on the circulating levels of components of the renin–angiotensin–aldosterone system (RAAS) and bradykinin, blood pressure (BP) and lipid profile in normotensive postmenopausal women (PMW). Methods: Twenty‐two normotensive PMW were randomized to receive transdermal HRT (continuous 17‐β estradiol patch at 36 µg/day plus cyclic oral medroxyprogesterone acetate 2.5 mg/day for 12 days/month) (n = 12) or control (n = 10). The plasma renin activity (PRA), serum angiotensin‐converting enzyme (ACE) activity, plasma angiotensin (Ang) I, Ang II, aldosterone, bradykinin, and BP were measured before, and 12 and 24 months after, the start of the HRT. Results: In the HRT group, the diastolic BP and mean BP were significantly decreased at 12 and 24 months (both P < 0.05) after the start of therapy, however, no significant change of the systolic BP was noted during the study period. No changes in the RAAS components or lipid profile were noted in either group. The plasma bradykinin levels were significantly reduced at 12 (P < 0.05) and 24 months (P < 0.01), while no changes were observed in the control group. Conclusion: More than 12 months of long‐term transdermal HRT kept diastolic BP, mean BP and plasma bradykinin levels decreased in normotensive PMW, without influencing any of the components of the RAAS. This therapy may allow optimal blood pressure control and prevent elevation of the cardiovascular risk.     

Hepatocyte growth factor (HGF) as a potential index of severity of hypertension.

Hepatocyte Growth Factor (HGF) is a mesenchyme-derived pleiotropic factor that regulates cell growth, cell motility, and morphogenesis of various cells, and is thus considered a humoral mediator of epithelial-mesenchymal interactions. We previously identified HGF as a novel member of the family of endothelium-specific growth factors. Moreover, the presence of a local HGF system (HGF and its specific receptor, c-met) has been demonstrated in vascular cells both in vitro and in vivo. HGF might contribute to the protection and/or repair of vascular endothelial cells injured by high blood pressure. If so, serum HGF level might be elevated in response to endothelial cell damage. To test this hypothesis, we measured serum levels of HGF in hypertensive and normotensive patients. Serum HGF concentration in hypertensive patients without any complications was significantly higher than that in normal subjects. Interestingly, serum HGF concentration in hypertensive patients with complications was significantly higher than that in either hypertensive patients without complications or normotensive subjects. Of importance, hypertensive patients treated with antihypertensive drugs showed the same level of serum HGF concentration as normotensive subjects. In contrast, serum HGF concentration in diabetic patients without hypertension was significantly lower than that in normal subjects, whereas serum HGF concentration in diabetic patients with hypertension was significantly higher than that in normal subjects. Moreover, serum HGF concentration in diabetic patients with hypertensive complications was even higher than that in diabetics without complications. This review discusses the possibility that HGF may be considered as a new index of the severity of hypertension.     

Serum cortisol in the white-coat phenomenon

BACKGROUND: The rise in blood pressure associated with a clinic visit (the white-coat phenomenon) may result from anxiety or an alerting reaction. There is evidence to suggest that glucocorticoids may be involved in the mechanism of stress-related blood pressure elevation, but the relationship between the white-coat phenomenon and glucocorticoids has not been assessed. DESIGN: Forty-eight young subjects with essential hypertension were compared with 12 control normotensive subjects. METHODS: Home blood pressure monitoring for 7 days and serum cortisol at 0900 h and 2 h rest at 1100 h were measured. The white-coat phenomenon was calculated for systolic and diastolic blood pressure and average home blood pressure. RESULTS: The serum cortisol level was significantly greater at 0900 h than that at 1100 h in the hypertensive subjects and was higher in the hypertensive subjects than in the normotensive subjects (21.5 +/- 0.5 versus 14.3 +/- 0.9 μg/dl), but there was no difference between serum cortisol levels at 1100 h in the two groups. The magnitude of the white-coat phenomenon, which was greater in the hypertensive subjects than in the normotensive group (22 +/- 2/12 +/- 1 versus 4 +/- 3/1 +/- 3 mmHg), correlated with serum cortisol at 0900 h, but not at 1100 h. The higher level of serum cortisol at 0900 h was confirmed by another measurement conducted 4 months later in a subsample of the hypertensive subjects ( n = 18). CONCLUSIONS: These results suggest that the white-coat phenomenon is related to the transient increase in serum cortisol or psychological stress, or both, which can trigger arousal of the hypothalamic pituitary adrenocortical axis.     

B cell secretion and insulin sensitivity in hypertensive and normotensive obese subjects

To test the hypothesis that in obesity hypertension is associated with more pronounced hyperinsulinaemia and insulin resistance we compared plasma insulin levels and insulin sensitivity in a group of 6 obese subjects with untreated hypertension and in a group of 6 obese subjects with normal blood pressure. The two groups were similar for sex, age, body mass index and glucose tolerance. Six nonobese subjects served as controls. The study consisted of a 2-h hyperglycaemic clamp (steady-state plasma glucose = 11 mmol/l) and a 15-min insulin tolerance test (0.1 U/kg body wt). During hyperglycaemic clamp, insulin and C-peptide plasma levels were similar in normotensive and hypertensive obese subjects: the area under the plasma insulin curve was 36,000 +/- 3000 pmol/l X 120 min in the former and 34,000 +/- 1000 pmol/l X 120 min in the latter; the area under the plasma C-peptide curve was 298,000 +/- 26,000 pmol/l X 120 min in the former and 246,000 +/- 26,000 pmol/l X 120 min in the latter (P = n.s.). The ratio M/I between the amount of glucose metabolized (M) and the mean plasma insulin levels (I) during hyperglycaemic clamp was similar in the two groups: 0.59 +/- 0.09 in normotensive and 0.58 +/- 0.08 mg/min X m2 per pmol/l in hypertensive obese subjects (P = n.s.). Also the rate coefficient of glucose disappearance from plasma (K(itt)) after i.v. insulin injection was similar in the two groups (4.08 +/- 0.51 vs. 3.87 +/- 0.53 per cent/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Reduced levels of calcitonin gene-related peptide (CGRP) but not substance P during and after treatment of severe hypertension in man

Little is known of the significance of perivascular peptides in hypertension. In this study we have investigated the circulating levels of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) and substance P- like immunoreactivity (SP-LI) during and after treatment of severe hypertension. Seventeen patients with a mean blood pressure of 204/127 mmHg were included. Circulating levels of CGRP-LI and SP-LI in normotensive controls were 35 +/- 4 and 1.2 +/- 0.1 pmol/l, respectively. In the hypertensives CGRP-LI was significantly lower (22 +/- 3 pmol/l: P less than 0.05) while SP-LI did not differ (1.6 +/- 0.3 pmol/l) from the normotensives. After treatment the circulating level of CGRP-LI was still significantly lower (16 +/- 2 pmol/l: P less than 0.001) while SP-LI remained unchanged when compared with the controls. These observations suggest an involvement of vascular afferent nerves in the aetiology of hypertension in man.     

Increased plasma 8-isoprostane levels in hypertensive subjects: the Tsurugaya Project.

To examine the relationship between 8-isoprostane and blood pressure, we measured plasma 8-isoprostane concentration and home blood pressure levels in an elderly Japanese population. Our study population comprised 569 subjects aged 70 years and over who were not receiving antihypertensive medication. On the basis of their blood pressure values, the participants were classified into three groups: normotensive (home blood pressure <135/85 mmHg), hypertensive (home blood pressure 135/85-160/90 mmHg), and severely hypertensive (home blood pressure > or =160/90 mmHg). The mean plasma 8-isoprostane level in the severely hypertensive group (21.1+/-5.2 pg/ml) was significantly higher than that in the normotensive (20.2+/-4.9 pg/ml) or hypertensive (19.7+/-5.1 pg/ml) group, and this result was unchanged when we adjusted for possible confounding factors such as age, sex, use of vitamin A, C or E supplements, smoking status, drinking status, body mass index, use of non-steroidal anti-inflammatory drugs, history of diabetes, hypercholesterolemia, home heart rate and serum creatinine level. Thus, the level of plasma 8-isoprostane appears to be elevated in older subjects with severe hypertension.     

Insulin, renin-aldosterone system and blood pressure in obese people.

OBJECTIVE: To evaluate the relationship between insulin, the renin-aldosterone system and blood pressure in obese subjects. DESIGN AND METHODS: A cross sectional study of a group of severely obese normotensive subjects who were surgical candidates (n=39; mean BMI: 47.8+/-1.4) and a group of hypertensive patients (n=57; mean BMI: 28.0+/-0.7) twenty-nine of whom had BMI>27. All subjects were studied after 15 days on a balanced diet. Insulin, plasma renin activity and aldosterone were measured. RESULTS: Fasting insulin, plasma renin activity and aldosterone were higher in severely obese normotensive subjects than in hypertensive subjects (respectively 32.3+/-3.0 vs 13.1+/-1.0 mU/l, P=0.0001; 1.34+/-0.22 vs 0.88+/-0.12 ng/ml/h, P=0.04; 137.2+/-16.2 vs 87.9+/-12.1 pg/ml, P=0.015). Insulin was related to BMI and to aldosterone both in normotensive and in hypertensive patients. CONCLUSION: Hyperinsulinemia itself does not determine hypertension; in some people it could play a vasodilator role in opposition to the renin-aldosterone system.     

Nocturnal continuous measurement of blood pressure in sleep apnea syndromes. Comparison between normotensive and hypertensive patients

Sleep apnea syndrome and systemic hypertension are frequently associated but their causal relationship is unclear. We compared the oscillations of systemic blood pressure and heart rate during polysomnography in 8 normotensive subjects (2 females) and 5 hypertensive (supine awake blood pressure: 165 +/- 7/96 +/- 5 mmHg) without treatment. Their ages (normotensive: 52.1 +/- 11.0 yrs, hypertensive: 51.2 +/- 6.4 yrs) and body mass indices (32.6 +/- 9.6 kg/m2 vs 33.2 +/- 5.2 kg/m2 respectively) were not statistically different. Systemic blood pressure was continuously monitored by a non invasive digital plethysmography (Finapres). Both groups had similar respiratory events indices (normotensive: 45.2 +/- 18.1/hr, hypertensive: 48.4 +/- 20.5/hr) and minimal oxygen saturations (79.4 +/- 9.1% vs 82.4 +/- 7.0% respectively). During apneas in slow-wave sleep were observed the minimal values for systolic and diastolic pressures which were significantly higher in hypertensive than in normotensive (138.2 +/- 9.6/83.2 +/- 16.1 mmHg vs 105.9 +/- 11.1/60.5 +/- 10.9 mmHg respectively). During resumption of ventilation maximal blood values were recorded which were also higher in hypertensive than in normotensive (185.0 +/- 13.8/113.2 +/- 21.5 mmHg vs 155.9 +/- 19.8/88.7 +/- 17.1 mmHg respectively) (p less than 0.05). Although absolute variations of blood pressure were similar, relative changes in systolic pressure were significantly higher in normotensive (p less than 0.05). Maximal heart rate was 76.8 +/- 6.2 bpm in normotensive and 76.6 +/- 3.9 bpm in hypertensive during resumption of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Peripheral dopamine synthesis and metabolism in spontaneously hypertensive rats

We have studied several parameters of peripheral dopamine synthesis and metabolism in spontaneously hypertensive rats during the development of hypertension. Compared to Wistar-Kyoto rats, there was an increased dopamine content in 8-week-old spontaneously hypertensive rats in the adrenals (1.6 +/- 0.1 vs. 1.2 +/- 0.1 nmol/pair in Wistar-Kyoto rats) and kidneys (97 +/- 12 vs. 63 +/- 7 pmol/g tissue in Wistar-Kyoto rats), but the dopamine content in peripheral organs from normotensive 4-week-old spontaneously hypertensive rats did not differ from Wistar-Kyoto rats. In the heart, the dopamine increase was observed in 14-week-old spontaneously hypertensive rats (systolic blood pressure: spontaneously hypertensive rats, 189 +/- 9; Wistar-Kyoto rats, 106 +/- 2 mm Hg;) in both atrium (spontaneously hypertensive rats, 133 +/- 14; Wistar-Kyoto rats, 86 +/- 20 pmol/g tissue) and ventricle (spontaneously hypertensive rats, 41 +/- 6; Wistar-Kyoto rats, 23 +/- 5 pmol/g tissue). Urinary free dopamine and dihydroxyphenylacetic acid, but not norepinephrine or normetanephrine, in spontaneously hypertensive rats significantly increased between the ages of 7 and 11 weeks, reflecting the dopamine changes in tissue and suggesting a selective increase of the rate of dopamine synthesis and release.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of ambulatory blood pressure monitoring in kidney disease

High blood pressure is both a cause and a manifestation of renal disease. It has an increasing prevalence among renal patients renal function is declining. Blood pressure is not a constant value, but it shows a high intrinsic and extrinsic variability. It is common to find striking discordances between blood pressure values and target organ damage. The average values obtained through ambulatory blood pressure monitoring (ABPM) are better related with cardiovascular morbility and mortality than office measurement, even in renal disease patients. We report the experience with ABPM on 51 renal patients. None of them was on renal replacement therapy. In 7 out of 14 non treated patients ABPM showed clinic hypertension only. Mean age of truly hypertensive patients was higher, but this difference was not significant (normotensive 31.7 +/- 17.1; hypertensive 49.4 +/- 17.9 years, p < 0.1). There were no sex differences (normotensive, 5 males and 2 females; hypertensive, 4 males and 3 females). Three normotensive patients had chronic renal failure, and as did 6 hypertensive patients (p < 0.1). There were no differences in night-time drop either for systolic (normotensive 3.7 +/- 3.5 hypertensive 6.1 +/- 8.9%) or for diastolic blood pressure (normotensive 10.4 +/- 4.7 hypertensive 6.2 +/- 8.9%). Thirty-seven patients who were on antihypertensive drug treatment: 23 (68.2%) showed hypertension after the ABPM and 14 (37.8%) have normal blood pressure values, more over, 4 of these 14 patients showed hypotension. There were neither age differences between the groups (normotensive 49.0 +/- 12.5, hypertensive 51.9 +/- 15.4 years), nor sex differences (normotensive 9 males and 5 females, hypertensive 11 males and 12 females). The prevalence of renal failure was similar (normotensive, 85.7%; hypertensive, 82.6%). Mean night-time drop was not different (SBP, normotensive 6.1 +/- 7.6 hypertensive 7.2 +/- 7.6%; DBP, normotensive 9.0 +/- 8.3 hypertensive 13.5 +/- 7.6%). ABPM is a helpful diagnostic tool in renal disease as in the non complicated essential hypertension patient, both for experimental and for clinical purposes.     

Mild essential hypertension in nonobese premenopausal women is characterized by low renin.

The pathophysiological mechanisms in hypertension may differ in men and women. Plasma renin activity was measured in 27 premenopausal, never-treated hypertensive women (blood pressure 141 +/- 2/93 +/- 1 mm Hg) and in 18 age-matched normotensive women (blood pressure 113 +/- 2/71 +/- 2 mm Hg). All subjects were unaware of their blood pressure status. The hypertensive women had on average lower plasma renin activity (0.21 +/- 0.03 nmol/L/h) than their normotensive controls (0.42 +/- 0.07 nmol/L/h, P less than .01). Serum estradiol was also lower in the hypertensive women (0.57 +/- 0.06 v 0.81 +/- 0.09 nmol/L, P less than .05). No difference in epinephrine, norepinephrine, atrial natriuretic peptide, or vasopressin was found between the groups. Plasma renin activity was positively correlated to plasma norepinephrine in the hypertensive women only (r = 0.41, P less than .05). Since low renin hypertension is associated with less cardiovascular complications, this may offer an explanation for the better prognosis of hypertension in women.