Activity In Essential Hypertension Research Articles

Correlations of attended and unattended blood pressure with sympathetic nervous system activity in essential hypertension

Abstract Background/Introduction Measurement of unattended blood pressure (BP) may provide additional information over conventionally attended BP. Moreover, hypertension is related to sympathetic drive while there are scarce data on the diverse links of attended and unattended BP with muscle sympathetic nerve activity (MSNA) in hypertensive patients. Purpose The aim of this study was to appraise the relation of BP levels in the attended and unattended setting with MSNA in patients with essential hypertension. Methods We studied 117 patients with essential hypertension (age: 58±11 years, 60 males, office BP: 142/85±17/10 mmHg, 24-hour BP: 133/80±11/9 mmHg). In all participants sympathetic drive was assessed by MSNA estimations based on established methodology (microneurography). Both unattended BP (patient alone in the room, an oscillometric device programmed to perform 3 BP measurements, at 1-minute intervals, after 5 minutes) and attended BP were measured with the same device, on the same day of MSNA recording, in random order. Patients were divided into the combined attended and unattended hypertensive group when BP≥140/90 mmHg in both attended and unattended BP estimations and to the attended hypertensive group when only attended BP≥140/90 mmHg. Results Patients with combined attended and unattended hypertension (n=70) compared to those with attended hypertension (n=47) did not differ regarding 24-h ambulatory BP levels, glucose levels, renal function and left ventricular mass index (p=NS for all). Moreover, patients with combined attended and unattended hypertension compared to those with attended hypertension were characterized by greater levels of MSNA (43.7±9.9 vs 37.7±9.7 bursts per minute, p=0.032). In all participants, sympathetic nerve traffic as assessed by resting MSNA was related to attended systolic BP (r=0.270, p=0.003), attended diastolic BP (r=0.344, p=0.001), unattended systolic BP (r=0.263, p=0.004) and unattended diastolic BP (r=0.274, p=0.003). Conclusions The phenotype of combined attended and unattended hypertension compared to attended hypertension is accompanied by higher sympathetic nervous system activation. Moreover, the close association of MSNA with attended and unattended BP levels in essential hypertension, further supports the key role of sympathetic drive in modulating BP. Funding Acknowledgement Type of funding source: None

Effects of acute and chronic exercise in patients with essential hypertension: benefits and risks.

The importance of regular physical activity in essential hypertension has been extensively investigated over the last decades and has emerged as a major modifiable factor contributing to optimal blood pressure control. Aerobic exercise exerts its beneficial effects on the cardiovascular system by promoting traditional cardiovascular risk factor regulation, as well as by favorably regulating sympathetic nervous system (SNS) activity, molecular effects, cardiac, and vascular function. Benefits of resistance exercise need further validation. On the other hand, acute exercise is now an established trigger of acute cardiac events. A number of possible pathophysiological links have been proposed, including SNS, vascular function, coagulation, fibrinolysis, and platelet function. In order to fully interpret this knowledge into clinical practice, we need to better understand the role of exercise intensity and duration in this pathophysiological cascade and in special populations. Further studies in hypertensive patients are also warranted in order to clarify the possibly favorable effect of antihypertensive treatment on exercise-induced effects.

Role of 11βHSD Type 2 Enzyme Activity in Essential Hypertension and Children with Chronic Kidney Disease (CKD)

The mineralocorticoid receptor is protected from excess of glucocorticoids by conversion of active cortisol to inactive cortisone by enzyme 11β-hydroxysteroid dehydrogenase type 2 present in the kidney. The metabolites of cortisol and cortisone are excreted in the urine as tetrahydrocortisol (5αTHF+5βTHF) and tetrahydrocortisone (THE), respectively. Patients with chronic kidney disease (CKD) and essential hypertension have a functional defect in their ability to convert cortisol to cortisone, thus leading to the activation of mineralocorticoid receptor. The objective of the investigation was to study the ratio of urinary steroids (5αTHF+5βTHF) to THE in patients with CKD, postrenal transplant, and essential hypertension and to compare the ratio with controls. We enrolled 44 patients (17 with CKD, eight postrenal transplant, 19 with essential hypertension) and 12 controls. We measured spot urinary 5α-THF, 5β-THF, THE, free active cortisol and inactive cortisone by gas chromatography/mass spectrometry. We collected data on age, sex, cause of kidney disease, height, weight, body mass index, blood pressure, serum electrolytes, aldosterone, and plasma renin activity. Blood pressure percentiles and z-scores were calculated. The glomerular filtration rate was calculated using the modified Schwartz formula. The ratios of 5αTHF+5βTHF to THE were significantly higher in patients with CKD [mean±sd score (SDS)=1.31±1.07] as compared with essential hypertension (mean±SDS=0.59±0.23; P=0.02) and controls (mean±SDS=0.52±0.25; P=0.01). In the postrenal transplant group, the ratio was not significantly different (mean±SDS=0.71±0.55). The urinary free cortisol to free cortisone ratios were significantly higher in the hypertension and CKD groups as compared with the controls. The 5αTHF+5βTHF to THE ratio negatively correlated with the glomerular filtration rate and positively correlated with systolic and diastolic blood pressure z-scores. The correlation of the blood pressure z-scores with ratios was stronger in the CKD group than the essential hypertension and posttransplant groups. We have elucidated a functional deficiency of 11β-hydroxysteroid dehydrogenase type 2 in children with CKD and a subset of essential hypertension. Urinary 5α-THF, 5β-THF, and THE analysis by gas chromatography/mass spectrometry should be a part of routine work-up of CKD and hypertensive patients.

Effect of acute administration of vitamin C on muscle sympathetic activity, cardiac sympathovagal balance, and baroreflex sensitivity in hypertensive patients

Essential hypertension is characterized by both increased oxidative stress and sympathetic traffic. Experimental studies have shown that reactive oxygen species can modulate autonomic activity. The aim of this study was to determine whether acute administration of the antioxidant vitamin C modifies sympathetic nerve activity in essential hypertension. Thirty-two untreated patients with essential hypertension and 20 normotensive subjects received vitamin C (3 g intravenously in 5 min) or vehicle. Heart rate, noninvasive beat-to-beat blood pressure, and muscle sympathetic nerve activity (microneurography) were monitored at baseline and up to 20 min after the infusion. Spectral analysis of RR interval variability and spontaneous baroreflex sensitivity were also computed. Vitamin C infusion significantly lowered blood pressure in hypertensive patients but not in normotensive subjects (maximal changes in systolic blood pressure: -4.9 ± 10.1 compared with -0.7 ± 4.0 mm Hg, respectively; P < 0.05). Moreover, muscle sympathetic nerve activity was significantly reduced after vitamin C infusion in hypertensive patients (from 53.3 ± 12.2 to 47.4 ± 11.5 bursts/100 heart beats; P < 0.01) but not in healthy subjects (from 42.0 ± 10.1 to 42.7 ± 11.8 bursts/100 heart beats; NS). On the contrary, in 16 hypertensive patients, sodium nitroprusside in equidepressor doses induced a significant increase in muscle sympathetic nerve activity compared with vitamin C (+10.0 ± 6.9 bursts/100 heart beats). Sympathovagal balance and spontaneous baroreflex sensitivity were restored during vitamin C infusion in hypertensive subjects. These results indicate that acute administration of vitamin C is able to reduce cardiovascular adrenergic drive in hypertensive patients, which suggests that oxidative stress is involved in the regulation of sympathetic activity in essential hypertension.

Clinical Study with Azelnidipine in Patients with Essential Hypertension

A dihydropyridine calcium (Ca) antagonist, azelnidipine (CAS 123524-52-7, Calblock), exhibits hypotensive effects for a prolonged duration, and has been reported to have a strong antiarteriosclerotic action due to its high affinity for vascular tissues and antioxidative action. It has also been reported that azelnidipine does not cause tachycardia associated with the baroreceptor reflex due to vasodilatation. In this study, the antiarteriosclerotic and cardiac hypertrophy-inhibitory effects, and the autonomic nervous activity in essential hypertension of azelnidipine were investigated. The study was performed using the following 2 protocols: 1) Pulse wave velocity (PWV), carotid arterial intima media thickness (IMT), echocardiography, high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), adiponectin, brain natriuretic peptide (BNP), and 8-isoprostane were measured after an initial treatment with azelnidipine. 2) The treatment was switched to azelnidipine in patients who had previously been under treatment with amlodipine for essential hypertension, and 123I-metaiodobenzylguanidine myocardial scintigraphy (123I-MIBG), measurements of plasma norepinephrine, atrial natriuretic peptide (ANP), and BNP, Holter electrocardiography, and heart rate variability analysis were performed. PWV, IMT, hs-CRP, IL-6, and TNF-alpha significantly decreased. The levels of 8-isoprostane, an antioxidative marker, were also significantly decreased, while adioponectin levels were significantly increased after the initial treatment with azelnidipine. After switching from amlodipine, azelnidipine exhibited a hypotensive effects comparable to amlodipine, and significantly decreased heart rate and the total number of extrasystoles. Noradrenaline levels and the LF/HF ratio were significantly decreased, and the washout rate was significantly reduced on 123I-MIBG myocardial scintigraphy. These findings suggest that azelnidipine inhibits the enhancement of sympathetic nervous activity and the progression of arteriosclerosis through its antioxidative effects.

Stress and catecholamines.

Stress and catecholamines.

Correlation of glycyrrhetinic acid–like factors (kidney 11β-HSD2-GALFs) with urinary free cortisol and plasma renin activity in essential hypertension

Previously we reported that urinary levels of glycyrrhetinic acid–like factors (11β-HSD2-GALFs) were increased in a subset of patients with essential hypertension when maintained on a low-Na + diet. The present studies were undertaken to correlate changes in urinary GALF levels with urinary free cortisol (UFC) and plasma renin activity (PRA). The amounts of GALFs markedly increased from 7.38 ± 0.80 to 14.58 ± 1.94 ( P < .0003) in the high/normal renin and from 5.60 ± 0.77 to 8.39 ± 1.08 ( P < .045) in the low renin patients on a low-Na + diet compared with high-Na + diet with no effect in the normotensive controls ( P < .668). The elevated GALF levels in high/normal renin hypertensives maintained on the low-Na + diet strongly correlated with the increased UFC levels and also with PRA; no such correlations were observed with either the normotensive controls or low renin hypertensives. In high/normal renin hypertensives, the elevated 11β-HSD2-GALFs may have two major functions: increased Na + retention by the kidney by allowing cortisol to access the renal mineralocorticoid receptor and increased vascular reactivity by allowing cortisol to access the vascular mineralocorticoid receptor.

The Effect of Chronic Anti-Hypertensive Therapy with Bendroflumethiazide on Sympathetic Drive

Essential hypertension (EHT) and sympathetic activation are recognized as independent cardiovascular risk factors. The effects of several chronic anti-hypertensive therapies on efferent sympathetic nerve activity have been studied previously. Thiazide diuretics are often recommended therapy, either first line, or in combination, although we know little of their effects in this regard. Therefore, this study was designed in patients with untreated EHT to quantify any effect of bendroflumethiazide (BFZ) therapy on muscle sympathetic nerve activity (MSNA).We examined 11 EHT patients before and after 3 ± 0.5 months of oral BFZ therapy (EHT + BFZ) in comparison to 11 age, gender and body weight matched group of patients with mild EHT who were followed up over a similar period of time with no anti-hypertensive therapy (EHT-N). MSNA was quantified as the mean frequency of single units (s-MSNA) and as multiunit bursts (MSNA bursts) using the technique of microneurography. BFZ significantly (at least P < 0.03) increased MSNA by 6.0 ± 2.3 bursts/100 cardiac beats and s-MSNA by 9.0 ± 3.2 impulses/100 cardiac beats from 57 ± 2.3 bursts/100 cardiac beats and 70 ± 3.6 impulses/100 cardiac beats respectively. The increase of indices of sympathetic nerve activity in EHT + BFZ group amounted to at least 9.4 ± 4.6% of baseline values; in contrast, no significant changes occurred over the same time in EHT-N group.These findings of a significant increase in central sympathetic neural drive to the periphery with bendroflumethiazide therapy have implications for the planning of anti-hypertensive therapy if the aim is to reduce the cardiovascular risk associated with sympathetic hyperactivity.

Impact of the components of metabolic syndrome on oxidative stress and enzymatic antioxidant activity in essential hypertension

The objective of the present study was to analyze the impact of metabolic syndrome (MS) and its individual components on oxidative stress (OX) and on the activity of antioxidant enzymes of patients with essential hypertension. One hundred and eighty-seven hypertensives, 127 (61.9%) of them having criteria for MS according to the International Diabetes Federation criteria and 30 healthy normotensive subjects were included. OX status was assessed by measuring glutathione oxidized/glutathione reduced and reactive oxygen species-induced byproducts of lipid peroxidation, malondialdehyde, and DNA damage, 8-oxo-dG genomic and mitochondrial. Antioxidant enzymatic activity of Cu/Zn extracellular-superoxide dismutase (SOD) and catalase (CAT) was measured in plasma and glutathione peroxidase 1 in hemolysed erythrocytes. In mononuclear cells, total-SOD activity, CAT and glutathione peroxidase 1, were assessed as well. The OX state in both blood and peripheral mononuclear cells observed in hypertensives were not enhanced by the addition of components of the so-called MS. Likewise, the reduction in the activity of antioxidant enzymes, both extracellular and cytoplasmic, was not affected by the presence of additional components of the MS. Neither the number of components nor the individual addition of each of them, low high-density lipoprotein, triglycerides, abdominal obesity or fasting glucose, further impact in the OX abnormalities observed in those with only hypertension in absence of other components. In conclusion, the present data indicates that contribution of MS components to the OX burden generated by high blood pressure is minimal.

Essential hypertension seems to result from melatonin-induced epigenetic modifications in area postrema

Essential hypertension is a complex multifactorial disorder with epigenetic and environmental factors contributing to its prevalence. Epigenetic system is a genetic regulatory mechanism that allows humans to maintain extraordinarily stable patterns of gene expression over many generations. Sympathetic nervous system plays a major role in the maintenance of hypertension and the rostral ventrolateral medulla is the main source of this sympathetic activation. A possible mechanism to explain the sympathetic hyperactivity in the rostral ventrolateral medulla is an action of the area postrema. Area postrema seems to be the region where a shift of the set-point to a higher operating pressure occurs resulting in hypertension. But, how can a shift occur in the area postrema. We propose that melatonin-induced epigenetic modifications in the neurons of area postrema plays a role in this shift. Area postrema is reported to contain high levels of melatonin receptors that play a role in the epigenetic modifications in certain cells. Environmental stressors cause epigenetic modifications in the neurons of area postrema via the pineal hormone melatonin and these changes lead to a shift in the set-point to a higher operating pressure. This signal is then sent via efferent projections to key medullary sympathetic nuclei in rostral ventrolateral medulla resulting in increases in sympathetic nerve activity. This model may explain the long-term alterations in sympathetic activity in essential hypertension.

Abnormal heart rate variability in essential hypertension

Abnormal autonomic regulation may contribute to blood pressure elevation in arterial hypertension. This may be reflected in altered heart rate variability (HRV). During rest variations around 0.10 Hz predominantly reflect sympathetic nervous activity and to some extent parasympathetic activity. Variations around 0.30 Hz almost exclusively reflect parasympathetic activity. The aim of the present study was to compare HRV in patients with essential hypertension and healthy control subjects during postural change (PC) and hyperventilation (HV). Patients with essential hypertension (N=16) and normotensive subjects (N=23) participated in this study. HRV was measured during a rest period of 30 minutes in the supine position followed by a 10 minute period of standing, then 10 minutes of supine rest followed by 2 minutes of controlled forced respiration (>20 breaths/min). HRV was measured using ElektroCard 2000 (B&O Medicom). Continous R-R intervals were sampled and power spectral density calculated using Fourier transformation. The 0.04 - 0.15 Hz spectrum was defined as low frequency (LF) and 0.15 - 0.40 Hz as high frequency (HF). The hypertensive group comprised 6 men and 10 women with a mean age of 55 years. The normotensive group comprised 9 men and 14 women with a mean age of 51 years. Mean 24-hour ambulatory BP in the two groups was 151/90 mm Hg and 129/78 mm Hg respectively (p<.001). Spectral analysis showed no difference in LF between the two groups during PC from supine to standing position, but revealed a significantly smaller decrease in LF in the hypertensive group compared to the normotensives during HV (H: -80.57 ms2, N: -165.73 ms2, p=.016) In contrast the fall in HF tended to be lower after PC in the normotensive group than in the hypertensive (H: -15.22 ms2, N: -82.40 ms2, p= .074), whereas no difference was observed in HF during HV. The changes in LF/HF ratio differed significantly between groups. The ratio increased during PC in normal subjects and decreased in hypertensives (H: -25.97 ms2, N: 4.04 ms2, p< .000). HV caused a decrease in LF/HF in both groups, but it was significantly smaller in the hypertensive group (H: -1.02, N: -2.18, p= .043). Patients with essential hypertension have an impaired response to autonomic challenges. Our results suggest increased sympathetic activity in essential hypertension and a disturbed sympathetic vagal balance.

Association of Dopamine .BETA.-Hydroxylase Polymorphism with Hypertension through Interaction with Fasting Plasma Glucose in Japanese

Dopamine-beta-hydroxylase (DBH) catalyzes the conversion of dopamine to norepinephrine and is released from sympathetic neurons into the circulation. Several lines of evidence, including the finding of elevated plasma DBH activity in essential hypertension, suggest an important role of DBH in hypertension. Recently, a novel polymorphism (-1021C/T) in the 5' flanking region of the DBH gene has been shown to account for 35-52% of the variation in plasma DBH activity. We therefore investigated the possible association between the DBH -1021C/T polymorphism and hypertension in a large Japanese population. Moreover, because the development of hypertension is considered to be due at least partly to gene-environmental interactions, we also investigated the possible interactions between the DBH -1021C/T polymorphism and environmental factors. Consequently, we found a significant interaction between the DBH -1021C/T polymorphism and fasting plasma glucose (FPG) in the association with hypertension. CC homozygotes showed a steeper increase in probability of hypertension with FPG than T allele carriers. We also found a marginally significant trend suggesting the presence of an interaction between the DBH -1021C/T polymorphism and FPG in the association with blood pressure. Consistent with the presence of the interaction, we found that a 19 bp sequence containing the DBH -1021C/T polymorphism includes two palindromic non-canonical E boxes separated by 5 bps, and closely resembles the glucose response element of the L-type pyruvate kinase gene. These findings could be helpful in conducting further molecular and biological studies on the relationship among glucose metabolism, the sympathetic nervous system, and hypertension.

Response: Neural Sympathetic Activity in Essential Hypertension

HomeHypertensionVol. 0, No. 1Response: Neural Sympathetic Activity in Essential Hypertension Free AccessOtherPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessOtherPDF/EPUBResponse: Neural Sympathetic Activity in Essential Hypertension Markus P. Schlaich and Murray D. Esler Markus P. SchlaichMarkus P. Schlaich Search for more papers by this author and Murray D. EslerMurray D. Esler Search for more papers by this author Originally published7 Jun 2004https://doi.org/10.1161/01.HYP.0000133818.84998.96Hypertension. 2004;0Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 1, 2018: Ahead of Print "Response: Neural Sympathetic Activity in Essential Hypertension." Hypertension, , pp. – Previous Back to top Next FiguresReferencesRelatedDetails January 2019Vol 0, Issue 1 Advertisement Article InformationMetrics https://doi.org/10.1161/01.HYP.0000133818.84998.96 Originally publishedJune 7, 2004 PDF download Advertisement

Sympathetic nerve activity in essential hypertension. New pathophysiologic aspects

Drug Prescribing for Patients with Chronic Kidney Disease in General Practice: a Cross-Sectional Study

The change and significance of the Na+-K+-ATPase alpha-subunit in ouabain-hypertensive rats.

Ouabain has recently been identified as an endogenous Na+-K+ pump inhibitor having a close association with hypertension. However, some patients with hypertention do not show high levels of endogenous ouabain (EO), and patients with high EO levels do not necessarily suffer from hypertention. It is believed that the Na+-K+-ATPase activity in essential hypertension does not undergo homogenous change. The present study was designed, therefore, to investigate the expression and the significance of the Na+-K+-ATPase alpha-subunit isoforms in kidney tissue in ouabain-hypertensive rats. Ouabain was administered chronically to establish a model of ouabain-hypertensive rats. Biochemical analysis, cytobiology and sABC immunohistochemistry were they used to assay for expression of Na+-K+-ATPase alpha-subunit isoforms in kidney tissue. After the first week of receiving ouabain, 65% (n=13) of rats had hypertension. After the second week, the blood pressure of these 13 hypertensive rats was increased significantly compared to the baseline and control levels (p<0.05). The plasma renin activity was normal, and angiotensin II and aldosterone levels were increased significantly in these rats (p<0.05). But in the other 35% (n=7) of rats of the experimental group, there was no apparent increase in blood pressure after receiving ouabain. The plasma ouabain level in the non-hypertensive subgroup was significantly higher than that in the hypertensive subgroup, but the 86Rb intake and the number of 3H-ouabain binding sites did not decrease. The Na+-K+-ATPase activity showed non-homogeneous changes. In hypertensive rats, the expression levels of ouabain paralleled the degree of hypertension (r=0.88, p<0.05). The positive granules were mainly scattered in the cytoblastoma of the reticular zone of adrenal cortex. There were thus different levels of expression of Na+-K+-ATPase alpha-subunit isoforms in this model. In the hypertension subgroup the alpha1 was most strongly expressed, followed by the alpha2 and alpha3 isforms. But in the non-hypertensive subgroup the order was alpha3 > alpha2 > alpha1. The positive granular was mainly scattered in the convoluted tubules of the kidney. These results suggest that the high level of ouabain and the change of the Na+-K+-ATPase alpha-subunit isoforms may play a critical role in hypertension.

Cortisol inhibits cholinergic vasodilatation in the human forearm

Exogenous cortisol raises blood pressure (BP) in humans and there is accumulating evidence of abnormalities of glucocorticoid activity in essential hypertension. In this study we tested the hypothesis that exogenous cortisol attenuates the cholinergic dilator response in the forearm circulation. Fourteen healthy normotensive men were studied. Using bilateral forearm venous plethysmography, we examined forearm blood flow responses to intra-arterial acetylcholine (ACh) and sodium nitroprusside (SNP) pre- and post- N G -monomethyl- l-arginine (LNMMA) after 2 or 5 days of oral cortisol or placebo in a randomized, double-blind crossover study. Exogenous cortisol increased supine systolic ( P < .05) and standing systolic ( P < .05) BP and produced expected metabolic changes and suppressed serum cortisol concentration ( P < .001). Baseline forearm blood flow did not differ between placebo and cortisol treatments at 2 or 5 days. Cholinergic vasodilatation was impaired after cortisol administration, reaching statistical significance at 5 days ( P < .05). Cortisol did not affect responses to SNP. N G -monomethyl- l-arginine inhibited cholinergic vasodilatation in placebo-treated groups but had no additional effect in the presence of cortisol. These results support our hypothesis and suggest that the mechanism of impaired cholinergic dilatation in glucocorticoid-treated subjects involves abnormalities of the endothelial nitric oxide system.

Evaluation of endothelial function and platelet activity in essential hypertension

Evaluation of endothelial function and platelet activity in essential hypertension

Sympathetic activation in the pathogenesis of hypertension and progression of organ damage.

Although animal models of hypertension have clearly shown that high blood pressure is associated with and is probably caused by an increase in sympathetic cardiovascular influences, a similar demonstration in humans has been more difficult to obtain for methodological reasons. There is now evidence, however, of increased sympathetic activity in essential hypertension. This article will review this evidence by examining data showing that plasma norepinephrine is increased in essential hypertension and that this is also the case for systemic and regional norepinephrine spillover, as well as for the sympathetic nerve firing rate in the skeletal muscle nerve district. Evidence will also be provided that sympathetic activation is a peculiar feature of essential hypertension, particularly in its early stages, with secondary forms of high blood pressure not usually characterized by an increased central sympathetic outflow. Humoral, metabolic, reflex, and central mechanisms are likely to be the factors responsible for the adrenergic activation characterizing hypertension, which may also promote the development and progression of the cardiac and vascular alterations that lead to hypertension-related morbidity and mortality, independent of blood pressure values. This represents the rationale for considering sympathetic deactivation one of the major goals of antihypertensive treatment.

Erythrocyte Na+/Li+ countertransport and Na+/K+‒2Cl− co-transport in essential hypertension

Correspondence| August 24 1999 Erythrocyte Na+/Li+ countertransport and Na+/K+ -2Cl- co-transport in essential hypertension T Hardman; T Hardman Search for other works by this author on: This Site PubMed Google Scholar R H Clifford; R H Clifford Search for other works by this author on: This Site PubMed Google Scholar A S Wierzbicki A S Wierzbicki Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1999) 97 (3): 339–340. https://doi.org/10.1042/cs0970339 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation T Hardman, R H Clifford, A S Wierzbicki; Erythrocyte Na+/Li+ countertransport and Na+/K+ -2Cl- co-transport in essential hypertension. Clin Sci (Lond) 1 September 1999; 97 (3): 339–340. doi: https://doi.org/10.1042/cs0970339 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. The Biochemical Society and the Medical Research Society © 19991999 Article PDF first page preview Close Modal You do not currently have access to this content.

Effect of chronic moxonidine therapy on peripheral sympathetic activity in essential hypertension

Effect of chronic moxonidine therapy on peripheral sympathetic activity in essential hypertension