Showing papers by "Roland E. Schmieder published in 1997"
TL;DR: The close and partially independent correlation between salt intake and hypertensive target organ disease suggests dietary sodium to be a direct perpetrator of cardiovascular disease.
Abstract: Experimental and clinical data suggest salt intake to be an important factor in the pathogenesis of essential hypertension. However, the relationship between dietary sodium and blood pressure has been found to be relatively weak, perhaps because casual blood pressure levels fluctuate considerably. We hypothesized that a closer correlation could be expected between salt intake and the degree of hypertensive target organ disease. We reviewed the literature for studies dealing with 24-hour urinary sodium excretion (as a measure of salt intake) and hypertensive target organ disease as assessed by left ventricular structure and function, microproteinuria, cerebrovascular disease, and arterial compliance. Salt intake as assessed by 24-hour urinary sodium excretion was found to be a close independent determinant of left ventricular mass in 9 different studies worldwide. A reduction in dietary sodium has been shown to reduce left ventricular hypertrophy. There is clinical and experimental evidence, particularly in salt-sensitive patients, that salt intake directly affects hypertensive renal disease, cerebrovascular disease, and compliance of the large arteries. The close and partially independent correlation between salt intake and hypertensive target organ disease suggests dietary sodium to be a direct perpetrator of cardiovascular disease. Arch Intern Med. 1997;157:2449-2452
123 citations
TL;DR: Even in early essential hypertension, glomerular hyperfiltration is evident during sympathetic nervous system activation, which is mediated by postglomerular vasoconstriction, which may contribute to, or trigger, the development of essential hypertension.
Abstract: Glomerular hyperfiltration may be important for the development of essential hypertension. Both the renin-angiotensin system and the sympathetic nervous system influence renal hemodynamic regulation. To test the hypothesis that glomerular hyperfiltration can be unmasked by sympathetic nervous system activation, renal hemodynamics and humoral components of the renin-angiotensin system were examined at rest and during mental stress in 45 young normotensive healthy subjects and 37 young people with mild essential hypertension. GFR and renal plasma flow (RPF) were determined with inulin and para-aminohippuric acid clearance at rest and during stress. At rest, RPF, GFR, filtration fraction, plasma renin activity, angiotensin (Ang) II concentrations, and serum aldosterone values were similar in normotensive and hypertensive subjects. After stress, blood pressure increased (P < 0.01), but this was nearly identical in normotensive and hypertensive subjects (7.05 +/- 6.9 versus 7.03 +/- 4.6 mmHg, NS). The decrease in RPF (-27 +/- 54 versus -22 +/- 25 ml/min per 1.73 m2, NS) was also similar in the two groups. In contrast, the increase in GFR (+ 10.5 +/- 7.2 versus 6.08 +/- 5.7 ml/min per 1.73 m2, P < 0.001) and filtration fraction (+2.48 +/- 1.38 versus 1.82 +/- 1.49%, P < 0.05) was more marked in hypertensive than in normotensive subjects. The concomitant increase in Ang II concentrations was greater in hypertensive than in normotensive subjects (+4.6 +/- 1.0 versus -1.0 +/- 0.45 pg/ml, P < 0.001). The increase in GFR during mental stress was correlated with the increment in Ang II concentrations (r = 0.39, P < 0.001). Compared with the placebo control phase, blockade of the renin-angiotensin system with an angiotensin-converting enzyme inhibitor attenuated the increase in GFR during stress in hypertensive (8.04 +/- 5.01 versus 10.1 +/- 5.7 ml/min per 1.73 m2, P < 0.05), but not in normotensive, subjects. Even in early essential hypertension, glomerular hyperfiltration is evident during sympathetic nervous system activation, which is mediated by postglomerular vasoconstriction. This early stress-induced glomerular hyperfiltration may contribute to, or trigger, the development of essential hypertension.
82 citations
TL;DR: Pharmacologic stimulation disclosed a blunted response of endothelium-dependent action in the arterial compliance of the conduit arteries in hypertensive subjects, which suggests an impaired endothelial function reserve in persons with essential hypertension.
27 citations
TL;DR: The correlation between erythropoietin and renal vascular changes which is already present in borderline hypertension and is confirmed in established hypertension indicates an involvement of erythrooietIn in the development of essential hypertension.
Abstract: The presence of normal concentrations of endogenous erythropoietin in all groups suggests a dysregulation dynamics at dierent stages of essential hypertension. haemodynamics Methods. We examined 47 patients with borderline essential hypertension (age 26±3 years) and 49 patients with established essential hypertension WHO stage I-II (age 52±10 years), and compared them to 42 Introduction normotensive individuals (age 26±3 years). The con- centration of erythropoietin (radioimmunoassay), 24-h Progressively increased total peripheral resistance is a ambulatory blood pressure (Spacelab 90207), systemic characteristic haemodynamic feature in the develop- haemodynamics ( Doppler sonography) and renal ment of essential hypertension even in the early stage haemodynamics (para-aminohippuric acid and inulin of essential hypertension (1 ). Human recombinant clearance) were determined. erythropoietin ( Epo), administered for the correction Results. Erythropoietin was within normal range and of anaemia in patients with end-stage renal disease, similar among the three groups. In patients with estab- elevates arterial blood pressure in 25-30% of patients lished essential hypertension, a close correlation was on maintenance haemodialysis (2,3) which seems to be found between erythropoietin and systolic (r=0.45, due to a parallel increase of total peripheral resistance P<0.002) and diastolic (r=0.51, P<0.001) ambulat- (4,5). The elevation of the haematocrit, however, with ory blood pressure. In contrast, ambulatory blood the subsequent reduction of luxury perfusion in the pressure was not correlated with erythropoietin in periphery, does not or, if at all, only in part, account subjects with borderline hypertension. Total peripheral for the increase of total peripheral resistance after resistance (r=0.41, P<0.02) was linked to erythropo- treatment with Epo (6,7). ietin in established but not in borderline hypertension. A possible explanation for the blood pressure However, erythropoietin was inversely correlated with increase by Epo may be the fact that erythropoietin renal plasma flow in both established and borderline has been described to have vasoconstricting properties hypertension (r='0.33, P<0.05, and r='0.34, on isolated renal resistance vessels (8). Moreover, P<0.05 respectively). In normotensive subjects, in endothelial cells have erythropoietin receptors and contrast, erythropoietin was not correlated with any respond with proliferation to Epo stimulation (9 ). of the determined variables. In neither group erythro- These non-haemodynamic eects may lead to elevated poietin was linked to the haematocrit or hemoglobin vascular resistance and increased blood pressure. concentration. Of note, patients on maintenance haemodialysis with Conclusion. The correlation between erythropoietin a positive family history of arterial hypertension are and renal vascular changes which is already present in at higher risk to respond with an increase of blood borderline hypertension and is confirmed in established pressure to Epo treatment (10 ). Therefore, genetic hypertension indicates an involvement of erythro- predisposition to hypertension is an important factor poietin in the development of essential hypertension. not only for essential hypertension, but also for the development of arterial hypertension secondary to Epo
21 citations
TL;DR: It is suggested that endogenous erythropoietin might be an aggravating or even a promoting factor in the pathogenesis of essential hypertension.
20 citations
TL;DR: In this article, the authors measured postganglionic sympathetic-nerve activity in the blood vessels of skeletal muscle by means of intraneural microelectrodes in nine women with preeclampsia, eight norm-ensive pregnant women, six norm-otensive non-pregnant women, and seven non-m pregnant women with hypertension, both at rest and during noninvasive cardiovascular-reflex testing (with the Valsalva maneuver and the cold pressor test).
Abstract: Background Preeclampsia is characterized by a marked increase in peripheral vascular resistance leading to an increase in blood pressure, but the triggering mechanisms are unclear. Methods To determine whether augmented sympathetic vasoconstrictor activity may be an important mechanism in mediating the increase in vasomotor tone, we measured postganglionic sympathetic-nerve activity in the blood vessels of skeletal muscle by means of intraneural microelectrodes in nine women with preeclampsia, eight normotensive pregnant women, six normotensive nonpregnant women, and seven nonpregnant women with hypertension, both at rest and during noninvasive cardiovascular-reflex testing (with the Valsalva maneuver and the cold pressor test). Results The mean (±SE) rate of sympathetic-nerve activity in the normotensive pregnant women (10±1 bursts per minute) was not significantly different from that in normotensive nonpregnant women (12±2 bursts per minute) or hypertensive nonpregnant women (15±3 bursts per minute). In...
16 citations
TL;DR: Both the α- and the β-blocker lowered blood pressure to a similar extent measured by 24-h blood pressure monitoring, and the left ventricular mass was comparably reduced in both cohorts.
13 citations
TL;DR: The calcium channel blocker nitrendipine exerted beneficial effects on cardiac structure in patients after renal transplantation independent of blood pressure, and endocrine parameters, lipids and blood glucose were not different between the two groups.
Abstract: stable phase. Normotensive patients received nitrendipplantation; calcium channel blocker; blood pressure ine 2◊5 mg daily or placebo, hypertensive patients received 2◊10 mg up to 2◊20 mg nitrendipine daily or placebo. To achieve adequate blood pressure control, all patients with still elevated blood pressure on Introduction study medication received antihypertensive drugs other than calcium channels blockers. Ambulatory blood Left ventricular hypertrophy (LVH ) has been identified pressure recording and 2D-guided M-mode echocardi- as a poor prognostic indicator in patients with essential ography were performed at baseline and upon comple- hypertension as well as in patients with secondary tion of the study. In addition, laboratory workup hypertension [1,2,3 ]. Since LVH increases the risk for (including serum creatinine and lipids) was done, and cardiac complications in hypertensive patients, studies serum aldosterone, plasma renin activity, plasma have been undertaken to investigate whether LVH angiotensin II and blood glucose levels were measured regression during treatment with antihypertensive in all patients at baseline and after at least 12 months drugs reduces the risk of cardiac complications in of therapy. Ambulatory blood pressure was almost patients with LVH. Indeed, regression of LVH below identical between both groups at study baseline and 200 g was shown to improve overall prognosis in follow-up. In renal transplant patients on nitrendipine, essential hypertensives [4,5]. Similarly, a preliminary posterior wall thickness (’0.10±1.77 mm) and septal report of an ongoing prospective study [6 ] revealed wall thickness (’0.83±2.23 mm) did not change sig- that regression of LVH improved cardiovascular nificantly from baseline. In contrast, posterior wall prognosis. thickness (0.71±0.92 mm, P<0.01) and septal Calcium channel blockers have been shown to wall thickness (0.97±2.20 mm, P<0.05) increased in reverse LVH in patients with essential hypertension, patients on placebo, which diered from the observed although they have been considered to be somewhat changes on nitrendipine (ANOVA: P=0.093 and P= less eective than ACE-inhibitors [6,7]. Recently, a 0.048, respectively). Relative wall thickness, a para- randomized study comparing eects of nitrendipine meter for concentric left ventricular hypertrophy, and captopril on left ventricular mass and circadian became numerically smaller on nitrendipine therapy blood pressure in patients with essential hypertensives, from 0.46±0.07 to 0.44±0.09 (’0.02±0.09, NS) but demonstrated a comparable degree of circadian blood increased from 0.42±0.08 to 0.48±0.08 in the placebo pressure reduction and regression of LVH for both drugs [8 ]. In a recent meta-analysis that included only
12 citations
TL;DR: In this article, regression of left ventricular hypertrophy by drug treatment has emerged as a desirable goal in patients with echocardiographically determined left ventricyclic thrombocytopenias.
Abstract: In numerous studies left ventricular hypertrophy has been clearly established to be a strong, blood-pressure independent risk factor for cardiovascular morbidity and mortality. In fact, increased echocardiographic left ventricular mass has been shown to predict cardiovascular complications not only in patients with hypertension, but also in the general population. Preliminary data revealed that regression of left ventricular hypertrophy indeed reduces cardiovascular complications. As a consequence, regression of left ventricular hypertrophy by drug treatment has emerged as a desirable goal in patients with echocardiographically determined left ventricular hypertrophy. These findings raised the question, whether certain antihypertensive drugs differ in their ability to reduce left ventricular mass. To resolve this issue several comparative studies and some meta-analyses have been carried out.
10 citations
TL;DR: No significant differences in cardiac output, total peripheral resistance, renal blood flow, and renal vascular resistance were found between the two racial populations, and indices of myocardial structure were comparable between black and white hypertensive patients.
8 citations
TL;DR: In conclusion, intermittent rather than life-long antihypertensive treatment may be possible in hypertensive patients with low resting blood pressure, high cardiac output, low total peripheral resistance and low left ventricular mass.
Abstract: Antihypertensive therapy has been thought to be a life-long treatment. Nevertheless, antihypertensive medication may be discontinued in a substantial proportion of hypertensive patients at least for s
TL;DR: It is demonstrated that an alpha1-blocker such as bunazosin develops the same blood pressure–lowering effect as beta-blockers, but with a significantly better profile with regard to glucose metabolism, and can be recommended for obese hypertensives without any special care for glucose metabolism.
Abstract: Antihypertensive drugs, recommended by the World Health Organization for use in monotherapy, exert different effects on glucose and lipid metabolism. In our study we compared the effects of the beta-blocker atenolol (AT) and the alpha1-blocker bunazosin (BU) on glucose metabolism. The doses administered were chosen to produce similar antihypertensive effects with both drugs. The study was conducted as a bicenter, parallel, controlled, and double-blind study. All patients suffered from mild to moderate primary hypertension, were obese (body mass index >26 kg/m2), but were nondiabetic. After a drug-free period of 4 weeks, patients were treated either with 6 and 12 mg of bunazosin (n = 15) or with 50 and 100 mg of atenolol (n = 17) once daily for 12 weeks. Glucose metabolism was measured by the iv glucose tolerance test (GTT) and the euglycemic hyperinsulinemic clamp test. The results show a similar blood pressure reduction with both drugs. However, their effects on glucose metabolism were significantly (p < 0.05) different: The area under the curve (AUC) of glucose in the iv GTT increased 26.8% during atenolol treatment but decreased 30% during bunazosin treatment. The same influence on the AUC of insulin was observed [AT +478.5 ± 441.8 (+22%) vs. BU, −588.5 ± 411.1 (−22%)]. Similar changes were found in the glucose clamp test. The metabolic clearance rate increased 11.4% during bunazosin use and decreased 8.4% during atenolol use to the same degree that the insulin sensitivity index changed (BU +13.2% vs. AT −21.9%). The differences between the two treatment regimes were statistically significant (p < 0.05). These results in obese hypertensives confirm the well-known negative effects of beta-blockers on glucose metabolism. Additionally, they demonstrate that an alpha1-blocker such as bunazosin develops the same blood pressure–lowering effect as beta-blockers, but with a significantly better profile with regard to glucose metabolism. Therefore, the use of alpha1-blockers can be recommended for obese hypertensives without any special care for glucose metabolism.
01 Jan 1997
TL;DR: Eine Langzeitbehandlung mit Antihypertensiva noch viel mehr gegen kardiovaskulare Morbiditat and Mortalitat schutzt, als es fruhere Ergebnisse aus klinischen Untersuchungen haben vermuten lassen (34).
Abstract: Unkontrollierte persistierende Blutdruckerhohungen stellen einen der wichtigsten unabhangigen Hauptrisikofaktoren fur zerebrovaskulare Schadigungen , kardiale Komplikationen und fortgeschrittene Nierenerkrankung dar. Eine adaquate medikamentose Behandlung des Bluthochdrucks fuhrte zu einer deutlichen Reduktion der kardiovaskularen Mortalitat und Morbiditat (14, 30). Neue Ergebnisse der Framingham-Studien von mittlerweile uber 20 Jahre „follow-up“ weisen darauf hin, das eine Langzeitbehandlung mit Antihypertensiva noch viel mehr gegen kardiovaskulare Morbiditat und Mortalitat schutzt, als es fruhere Ergebnisse aus klinischen Untersuchungen haben vermuten lassen (34). Die hochste Gesamtuberlebenszeit war bei Mannern mit einem systolischen Blutdruck von weniger als 134 mmHg unter antihypertensiver Behandlung assoziiert, bei Frauen weniger als 149 mmHg systolisch und fur beide Geschlechter mit einem diastolischen Blutdruck von weniger als 95 mmHg (6). Eine Metaanalyse von 14 randomisierten klinischen Studien konnte eine 42 % ige Reduktion der Inzidenz fur Schlaganfalle bei einer Abnahme des diastolischen Blutdrucks von 5 – 6 mmHg feststellen (14). Die Abnahme der Schlaganfallrate war in einem vergleichbaren Umfang ubereinstimmend in Langzeitbeobachtungsstudien festgestellt worden, in denen bei einer entsprechenden Blutdruckabnahme eine 35 – 40 %ige Abnahme der Schlaganfallereignisse zu verzeichnen war. Zusammenfassend unterstreichen die dargestellten Ergebnisse die Notwendigkeit, eine antihypertensive Therapie konsequent durchzufuhren.
TL;DR: The haemodynamic characteristics in the different developmental stages of essential hypertension may vary considerably and are also influenced by ageing, therefore, the proper use of anti-hypertensive drug treatment should be directed individually according to the underlying haemodynamics disturbances.
Abstract: The haemodynamic changes that occur during the development of established essential hypertension can be detected only by longitudinal studies Several long-term studies thus indicate that the circulation in essential hypertension shifts from a ‘high-output, normal resistance' state in young age toward a ‘low-output, high-resistance' state in old age However, this pattern is not a uniform one, and essential hypertension may also start by an increase in peripheral resistance without a prior phase of an elevated cardiac output The reasons for these different haemodynamic patterns are not yet understood Sympathetic overactivity may, at least in part, be responsible for the haemodynamic changes seen in the starting phase of essential hypertension The haemodynamic characteristics in the different developmental stages of essential hypertension may vary considerably and are also influenced by ageing Therefore, the proper use of anti-hypertensive drug treatment should be directed individually according to the underlying haemodynamic disturbances