Effect of chronic dietary treatment with L-tryptophan on the maintenance of hypertension in spontaneously hypertensive rats

Chronic dietary administration of L-tryptophan at 2.5 and 5.0% by weight reduced the elevated systolic blood pressure of spontaneously hypertensive (SH) rats. Blood pressure was reduced significantly by 3 weeks after initiation of treatment and continued to fall during the course of the 15 weeks of treatment. Body weights of the treated rats were not affected significantly by treatment, nor were daily food and fluid intakes and urine outputs. SH rats, treated with the higher dose of tryptophan, also significantly reduced their urinary outputs of epinephrine and norepinephrine compared with SH controls, while both doses of tryptophan increased urinary outputs of dopamine significantly above that of SH controls. Treatment with tryptophan increased significantly the specific binding of [125I]angiotensin II (Ang II) to membranes from the diencephalon in a dose-dependent manner. Measurement of catecholamine concentration of the supernatant from homogenates used for the Ang II binding assay revealed a significant correlation between the specific binding of Ang II to brain membranes of the two tryptophan-treated groups and the concentration of norepinephrine in the supernatant. There was also a significant correlation between the specific binding of Ang II and the concentratiion of dopamine in the supernatant of the control group and the group treated with the higher dose of tryptophan. These results show that chronic dietary administration of tryptophan can reduce the elevated blood pressure of SH rats and support the possibility that this neutral amino acid may act via its effect on the concentration of the neurohormones, norepinephrine and dopamine, in the diencephalon to regulate the binding of Ang II to its receptors.Key words: tryptophan, spontaneous hypertension, brain angiotensin binding, urinary catecholamines.

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Interleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice

Mediators of Inflammation ◽

10.1155/2020/5741047 ◽

2020 ◽

Vol 2020 ◽

pp. 1-12 ◽

Cited By ~ 1

Author(s):

Yunzhao Yang ◽

Shaoqun Tang ◽

Chunchun Zhai ◽

Xin Zeng ◽

Qingjian Liu ◽

...

Keyword(s):

Blood Pressure ◽

Smooth Muscle ◽

Angiotensin Ii ◽

Inflammatory Response ◽

Vascular Dysfunction ◽

Control Group ◽

Dependent Manner ◽

Ang Ii ◽

Stat3 Pathway

Background. Multiple interleukin (IL) family members were reported to be closely related to hypertension. We aimed to investigate whether IL-9 affects angiotensin II- (Ang II-) induced hypertension in mice. Methods. Mice were treated with Ang II, and IL-9 expression was determined. In addition, effects of IL-9 knockout (KO) on blood pressure were observed in Ang II-infused mice. To determine whether the effects of IL-9 on blood pressure was mediated by the signal transducer and activator of the transcription 3 (STAT3) pathway, Ang II-treated mice were given S31-201. Furthermore, circulating IL-9 levels in patients with hypertension were measured. Results. Ang II treatment increased serum and aortic IL-9 expression in a dose-dependent manner; IL-9 levels were the highest in the second week and continued to remain high into the fourth week after the treatment. IL-9 KO downregulated proinflammatory cytokine expression, whereas it upregulated anti-inflammatory cytokine levels, relieved vascular dysfunction, and decreased blood pressure in Ang II-infused mice. IL-9 also reduced smooth muscle 22α (SM22α) expression and increased osteopontin (OPN) levels both in mice and in vitro. The effects of IL-9 KO on blood pressure and inflammatory response were significantly reduced by S31-201 treatment. Circulating IL-9 levels were significantly increased in patients with the hypertension group than in the control group, and elevated IL-9 levels positively correlated with both systolic blood pressure and diastolic blood pressure in patients with hypertension. Conclusions. IL-9 KO alleviates inflammatory response, prevents phenotypic transformation of smooth muscle, reduces vascular dysfunction, and lowers blood pressure via the STAT3 pathway in Ang II-infused mice. IL-9 might be a novel target for the treatment and prevention of clinical hypertension.

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Burnout of the Mind – Burnout of the Body?

Journal of Psychophysiology ◽

10.1027/0269-8803/a000182 ◽

2018 ◽

Vol 32 (1) ◽

pp. 30-42 ◽

Cited By ~ 2

Author(s):

Claudia Traunmüller ◽

Kerstin Gaisbachgrabner ◽

Helmut Karl Lackner ◽

Andreas R. Schwerdtfeger

Keyword(s):

Blood Pressure ◽

Allostatic Load ◽

Maslach Burnout Inventory ◽

The Body ◽

Lower Percentage ◽

Control Group ◽

Urinary Catecholamines ◽

Morning Cortisol ◽

The Mind ◽

Cortisol Increase

Abstract. In the present paper we investigate whether patients with a clinical diagnosis of burnout show physiological signs of burden across multiple physiological systems referred to as allostatic load (AL). Measures of the sympathetic-adrenergic-medullary (SAM) axis and the hypothalamic-pituitary-adrenal (HPA) axis were assessed. We examined patients who had been diagnosed with burnout by their physicians (n = 32) and were also identified as burnout patients based on their score in the Maslach Burnout Inventory-General Survey (MBI-GS) and compared them with a nonclinical control group (n = 19) with regard to indicators of allostatic load (i.e., ambulatory ECG, nocturnal urinary catecholamines, salivary morning cortisol secretion, blood pressure, and waist-to-hip ratio [WHR]). Contrary to expectations, a higher AL index suggesting elevated load in several of the parameters of the HPA and SAM axes was found in the control group but not in the burnout group. The control group showed higher norepinephrine values, higher blood pressure, higher WHR, higher sympathovagal balance, and lower percentage of cortisol increase within the first hour after awakening as compared to the patient group. Burnout was not associated with AL. Results seem to indicate a discrepancy between self-reported burnout symptoms and psychobiological load.

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Blood Pressure-Lowering Effect of Wine Lees Phenolic Compounds Is Mediated by Endothelial-Derived Factors: Role of Sirtuin 1

Antioxidants ◽

10.3390/antiox10071073 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1073

Author(s):

Raúl López-Fernández-Sobrino ◽

Jorge R. Soliz-Rueda ◽

Javier Ávila-Román ◽

Anna Arola-Arnal ◽

Manuel Suárez ◽

...

Keyword(s):

Blood Pressure ◽

Antihypertensive Effect ◽

Sirtuin 1 ◽

Dependent Manner ◽

Blood Pressure Lowering Effect ◽

Synthesis Inhibitor ◽

Spontaneously Hypertensive ◽

Lowering Effect ◽

Pressure Lowering ◽

Endothelial Gene Expression

The antihypertensive effect of wine lees powder (WLPW) from a Cabernet grape variety was related to its high content in flavanols and anthocyanins compounds. This study investigates the involvement of endothelial-derived factors and SIRT1 in its bioactivity. Spontaneously hypertensive rats (SHR) were orally administered water or WLPW (125 mg/kg bw). Posteriorly, both groups were intraperitoneally administered saline, Nω-nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthesis inhibitor, indomethacin, a prostacyclin synthesis inhibitor, or sirtinol, an inhibitor of sirtuins. Blood pressure (BP) was recorded before and 6 h after WLPW administration. In an additional experiment, SHR were administered water or WLPW and endothelial expressions of eNos, Sirt1, Nox4, and Et1 were determined. The BP-lowering properties of WLPW were abolished by L-NAME and partially reduced by indomethacin, demonstrating that WLPW antihypertensive effect was mediated by changes in NO availability, although prostacyclin also contributed to this activity. Moreover, BP-lowering effect was reduced by sirtinol, indicating that WLPW decreased BP in a SIRT1-dependent manner. Furthermore, WLPW upregulated eNos and Sirt1 and downregulated Nox4 and Et1 endothelial gene expression. These results evidence the vasoprotective effect of WLPW and show that its antihypertensive effect in SHR is endothelium dependent and mediated by SIRT1.

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System-based DNA microarray analyses of different gene expression profile in spontaneously hypertensive rats treated with Songling Xuemaikang Capsule reveals underlying causal mechanisms.

10.21203/rs.2.14612/v1 ◽

2019 ◽

Author(s):

Li-tao Liu ◽

Cui-qi Yan ◽

Qiao-xin Tang ◽

Man-xi Zhao ◽

Chuan-zhen Teng ◽

...

Keyword(s):

Gene Expression ◽

Vascular Remodeling ◽

Spontaneously Hypertensive Rats ◽

Control Group ◽

Causal Network ◽

Ang Ii ◽

Dosage Group ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Songling Xuemaikang Capsule

Abstract Background: Hypertension is considered the major risk factor for human health in the world. Songling Xuemaikang Capsule (SXC) is clinically used as a medicine for the prevention and treatment of cardiovascular and cerebrovascular diseases such as hypertension and hyperlipidemia. However, the underlying mechanisms have yet to be fully identified. Methods: Valsartan, as a positive control drug, high- and low-dose of SXC were orally administration with for 28 days to investigate the anti-hypertensive effect of SXC in spontaneously hypertensive rats (SHRs). The serum levels of aldosterone and Angiotensin II (Ang II) were detected. The gene expression profiling was performed in the thoracic aorta of SHRs using the Whole Rat Genome Oligo nucleotide Microarray. The integrated causal network analysis was performed to understand the mechanism of antihypertensive effect of SXC. Results: The results shown that the systolic and diastolic blood pressure were significant decreased in SXC low-dosage group and high-dosage group compared with the control group respectively. SXC low and high-dosage treatment decreased serum aldosterone levels significantly but increased serum Ang II compared with the control group respectively. Causal network analysis shown that treatment with SXC reversing the vascular remodeling process, inhibiting vascular inflammation and atherosclerosis, reversing endothelial cells dysfunction and likely reducing peripheral vascular resistance by down-regulated processes related to vascular remodeling, dyslipidemia, the complement system, leukocyte rolling, and endothelial dysfunction. In addition, SXC treatment may also activate fibrinolysis and regulate lipid and glucose metabolism. Conclusions: Those obtained data could help our understanding and potential utilization of SXC in the treatment or prevention of hypertension。

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Abstract P104: Renin Angiotensin System (RAS) Modulation in Hypertension Program by Maternal Intrauterine Malnutrition

Hypertension ◽

10.1161/hyp.66.suppl_1.p104 ◽

2015 ◽

Vol 66 (suppl_1) ◽

Author(s):

Rafael S Banti ◽

Rodrigo Yokota ◽

Danielle S Aragão ◽

Adriana Souza ◽

Amanda Pedroso ◽

...

Keyword(s):

Blood Pressure ◽

Renin Angiotensin System ◽

Control Group ◽

Ang Ii ◽

Alternative Pathways ◽

Angiotensin Peptides ◽

Increased Risk ◽

Ace Activity ◽

Intrauterine Malnutrition ◽

Group D

Intrauterine malnutrition (IM) during the early stages of development can alter the function of organs and tissues and can predict a lifetime of increased risk for adverse health outcomes, such as diabetes and hypertension. The kidney plays a key role in the development of hypertension programmed by IM, with the participation of the RAS. Our objectives were to study ACE activity and angiotensin peptides levels in tissues. Pregnants Wistar rats were separated into two groups: control group (C), fed ad libitum, and malnourished group (D) submitted to food restriction (diet 50% of the amount of feed consumed by the group C). After birth the offspring were kept as experimental groups C and D, respectively. At 4 months of age, the animals were sacrificed, heart and kidney tissues were collected to quantify angiotensin peptides and ACE activity. The offspring born with low birth weight. Kidney ACE activity was higher in group D compared to group C (299 ±86.7 vs. 253.4 ±84.82 mU/mg, p<0.05), differing from Heart (D versus C: 0.15 ± 0.08 vs. 0.24 ±0.09 mU/mg). Group D presented high blood pressure values compared to group C (140.6 ±2.8 vs. 124,3±2.6 mmHg). Kidney and heart Ang II levels were increased in group D being significant when compared to group C (238.26 ±25.1 vs. 161.85 ±45.6 pmol/g and 397.89±74.9 vs. 223.33±48.7 pmol/g, p<0.05, respectively). The same was observed for Ang I. The vasodilator peptide Ang1-7 levels in group D from kidney and heart were lower in comparison with group C, thus emphasizing an enabling environment for hypertension (220.74 ± 48.74 vs. 288.09 ± 47 pmol/g and 152.1±41.2 pmol/g vs. 228.93±41.2 pmol/g, p<0.05, respectively). Our results indicate that perturbed maternal nutritional status alters tissue RAS resulting in higher blood pressure in the offspring, demonstrated by increased renal ACE activity and Ang II levels, with reduced Ang 1-7. The increase of Ang I and II in the heart, despite low ACE activity in this tissue suggests the activation of RAS alternative pathways. This study describes for the first time that low levels of Ang 1-7 contributed to the early development of hypertension.

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Abstract P041: Proximal Tubule-specific Deletion Of Angiotensin Ii Type 1a Receptors In The Kidney Lowers Basal Blood Pressure And Attenuates Angiotensin Ii-induced Hypertension By Increasing Glomerular Filtration And The Pressure-natriuresis Response

Hypertension ◽

10.1161/hyp.76.suppl_1.p041 ◽

2020 ◽

Vol 76 (Suppl_1) ◽

Author(s):

Xiao C Li ◽

Ana P Leite ◽

Liang Zhang ◽

Jia L Zhuo

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Proximal Tubule ◽

Pressor Response ◽

Control Group ◽

Ang Ii ◽

Induced Hypertension ◽

Basal Blood Pressure ◽

Pressure Natriuresis ◽

Specific Deletion

The present study tested the hypothesis that intratubular angiotensin II (Ang II) and AT 1a receptors in the proximal tubules of the kidney plays an important role in basal blood pressure control and in the development of Ang II-induced hypertension. Mutant mice with proximal tubule-specific deletion of AT 1a receptors in the kidney, PT- Agtr1a -/- , were generated to test the hypothesis. Eight groups (n=7-12 per group) of adult male wild-type (WT) and PT- Agtr1a -/- mice were infused with or without Ang II for 2 weeks (1.5 mg/kg, i.p.). Basal systolic, diastolic, and mean arterial pressures were ~13 ± 3 mmHg lower in PT- Agtr1a -/- than WT mice ( P <0.01). Basal glomerular filtration rate (GFR), as measured using transdermal FITC-sinistrin, was significantly higher in PT- Agtr1a -/- mice (WT: 160.4 ± 7.0 μl/min vs. PT- Agtr1a -/- : 186.0 ± 6.0 μl/min, P <0.05). Basal 24 h urinary Na + excretion (U Na V) was significantly higher in PT- Agtr1a -/- than WT mice ( P <0.01). In response to Ang II infusion, both WT and PT- Agtr1a -/- mice developed hypertension, and the magnitude of the pressor response to Ang II was similar in WT (Δ43 ± 3 mmHg, P <0.01) and PT- Agtr1a -/- mice (Δ39 ± 5 mmHg, P <0.01). However, the absolute blood pressure level was still 16 ± 3 mmHg lower in PT- Agtr1a -/- mice ( P <0.01). Ang II significantly decreased GFR to 132.2 ± 7.0 μl/min in WT mice ( P <0.01), and to 129.4 ± 18.6 μl/min in PT- Agtr1a -/- mice ( P <0.01), respectively. In WT mice, U Na V increased from 139.3 ± 22.3 μmol/24 h in the control group to 196.4 ± 29.6 μmol/24 h in the Ang II-infused group ( P <0.01). In PT- Agtr1a -/- mice, U Na V increased from 172.0 ± 10.2 μmol/24 h in the control group to 264.7 ± 35.4 μmol/24 h in the Ang II-infused group ( P <0.01). The pressor response to Ang II was attenuated, while the natriuretic response was augmented by losartan in WT and PT- Agtr1a -/- mice ( P <0.01). Finally, proximal tubule-specific deletion of AT 1a receptors significantly augmented the pressure-natriuresis response and natriuretic responses to acute saline infusion ( P <0.01) or a 2% high salt diet ( P <0.01). We concluded that deletion of AT 1a receptors selectively in the proximal tubules lowers basal blood pressure and attenuates Ang II-induced hypertension by increasing GFR and promoting the natriuretic response in PT- Agtr1a -/- mice.

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VSMC-Specific Deletion of FAM3A Attenuated Ang II-Promoted Hypertension and Cardiovascular Hypertrophy

Circulation Research ◽

10.1161/circresaha.119.315558 ◽

2020 ◽

Vol 126 (12) ◽

pp. 1746-1759 ◽

Cited By ~ 2

Author(s):

Rui Xiang ◽

Ji Chen ◽

Shuangyue Li ◽

Han Yan ◽

Yuhong Meng ◽

...

Keyword(s):

Blood Pressure ◽

Cardiovascular Diseases ◽

Internal Mammary Artery ◽

Ang Ii ◽

Hypertensive Patients ◽

Spontaneously Hypertensive ◽

Internal Mammary ◽

Atp Signaling ◽

Regulation Of Blood Pressure ◽

Specific Deletion

Rationale: Dysregulated purinergic signaling transduction plays important roles in the pathogenesis of cardiovascular diseases. However, the role and mechanism of vascular smooth muscle cell (VSMC)-released ATP in the regulation of blood pressure, and the pathogenesis of hypertension remain unknown. FAM3A (family with sequence similarity 3 member A) is a new mitochondrial protein that enhances ATP production and release. High expression of FAM3A in VSMC suggests it may play a role in regulating vascular constriction and blood pressure. Objective: To determine the role and mechanism of FAM3A-ATP signaling pathway in VSMCs in the regulation of blood pressure and the pathogenesis of hypertension. Methods and Results: In the media layer of hypertensive rat and mouse arteries, and the internal mammary artery of hypertensive patients, FAM3A expression was increased. VSMC-specific deletion of FAM3A reduced vessel contractility and blood pressure levels in mice. Moreover, deletion of FAM3A in VSMC attenuated Ang II (angiotensin II)-induced vascular constriction and remodeling, hypertension, and cardiac hypertrophy in mice. In cultured VSMCs, Ang II activated HSF1 (heat shock factor 1) to stimulate FAM3A expression, activating ATP-P2 receptor pathway to promote the change of VSMCs from contractile phenotype to proliferative phenotype. In the VSMC layer of spontaneously hypertensive rat arteries, Ang II-induced hypertensive mouse arteries and the internal mammary artery of hypertensive patients, HSF1 expression was increased. Treatment with HSF1 inhibitor reduced artery contractility and ameliorated hypertension of spontaneously hypertensive rats. Conclusions: FAM3A is an important regulator of vascular constriction and blood pressure. Overactivation of HSF1-FAM3A-ATP signaling cascade in VSMCs plays important roles in Ang II-induced hypertension and cardiovascular diseases. Inhibitors of HSF1 could be potentially used to treat hypertension.

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Dietary calcium modulates renal BBM angiotensin II binding and Na(+)-H+ antiporter activity in SHR

AJP Renal Physiology ◽

10.1152/ajprenal.1991.260.5.f657 ◽

1991 ◽

Vol 260 (5) ◽

pp. F657-F662

Author(s):

M. Levi ◽

W. L. Henrich

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Brush Border Membrane ◽

Spontaneously Hypertensive Rat ◽

Ang Ii ◽

Blood Pressure Lowering Effect ◽

Spontaneously Hypertensive ◽

Pressure Lowering ◽

Number Of Binding Sites ◽

Dissociation Constant Kd

Dietary Ca is an important modulator of blood pressure in the spontaneously hypertensive rat (SHR). Since the kidney plays a key role in the pathogenesis of hypertension, the purpose of this study was to determine the potential renal mechanisms of the blood pressure-lowering effect of increasing dietary Ca content. In 21-day-old SHR fed 0.1 vs. 3.6% Ca diet for 14 days, increasing dietary Ca had no significant effects on basal [704 +/- 50 in 0.1% Ca vs. 784 +/- 61 ng angiotensin I (ANG I).mg-1.h-1 in 3.6% Ca, P = not significant (NS)], isoproterenol-stimulated (1,057 +/- 52 in 0.1% Ca vs. 1,104 +/- 59 ng ANG I.mg-1.h-1 in 3.6% Ca, P = NS), or angiotensin II (ANG II)-inhibited (370 +/- 50 in 0.1% Ca vs. 411 +/- 39 ng ANG I.mg-1.h-1 in 3.6% Ca, P = NS) renal superficial cortical slice renin release. In contrast, in apical brush-border membrane (BBM) vesicles isolated from the superficial cortex, increasing dietary Ca caused a significant decrease in ANG II binding, which was mediated by a decrease in the number of binding sites (Bmax, 376 +/- 14 in 0.1% Ca vs. 234 +/- 6 fmol ANG II/mg BBM protein in 3.6% Ca, P less than 0.01), and no change in the affinity [dissociation constant (Kd), 17.8 +/- 1.4 in 0.1% Ca vs. 13.4 +/- 2.8 nM ANG II in 3.6% Ca, P = NS].(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of chlorothiazide on serial measurements of exchangeable sodium and blood pressure in spontaneously hypertensive rats

Clinical Science ◽

10.1042/cs0690511 ◽

1985 ◽

Vol 69 (5) ◽

pp. 511-515 ◽

Cited By ~ 2

Author(s):

P. J. O. Manhem ◽

S. A. Clark ◽

W. B. Brown ◽

G. D. Murray ◽

J. I. S. Robertson

Keyword(s):

Blood Pressure ◽

Body Weight ◽

Spontaneously Hypertensive Rats ◽

Tap Water ◽

Treated Group ◽

Temporal Association ◽

Control Group ◽

Exchangeable Sodium ◽

Hypertensive Rats ◽

Spontaneously Hypertensive

1. Chlorothiazide (100 mg/kg body weight) was given by gavage daily to spontaneously hypertensive rats for 4 weeks. Another group of spontaneously hypertensive rats was given only tap water and served as control. 2. Measurements of total exchangeable sodium, blood pressure and weight were performed for 2 weeks before and for 4 weeks during treatment. 3. Before treatment, exchangeable sodium, blood pressure and weight were similar in the two groups of rats. 4. Chlorothiazide significantly attenuated the blood pressure increase in spontaneously hypertensive rats, the effect being most marked during the first 2 1/2 weeks of treatment and less thereafter. 5. Rats in the chlorothiazide-treated group gained weight more slowly than did those of the control group. 6. Exchangeable sodium, expressed as mmol/kg body weight, did not differ significantly between the two groups at any stage. 7. When exchangeable sodium was expressed as mmol/rat, there was a more gradual rise in the chlorothiazide-treated animals, in accordance with their slower gain in weight. 8. There was no temporal association between the antihypertensive effect of chlorothiazide and changes in exchangeable sodium. 9. Thus whereas chlorothiazide treatment of spontaneously hypertensive rats slows the increase of both weight and exchangeable sodium, other mechanisms are apparently responsible for the antihypertensive action of the drug.

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Effects of Qigong on Blood Pressure, Blood Pressure Determinants and Ventilatory Function in Middle-Aged Patients with Essential Hypertension

The American Journal of Chinese Medicine ◽

10.1142/s0192415x03001120 ◽

2003 ◽

Vol 31 (03) ◽

pp. 489-497 ◽

Cited By ~ 44

Author(s):

Myung Suk Lee ◽

Myeong Soo Lee ◽

Euy-Soon Choi ◽

Hun-Taeg Chung

Keyword(s):

Blood Pressure ◽

Essential Hypertension ◽

Vital Capacity ◽

Forced Expiratory Volume ◽

Control Group ◽

Middle Aged ◽

Aged Patients ◽

Urinary Catecholamines ◽

Baseline Values ◽

Sympathetic Nervous

This study was designed to measure changes in blood pressure (BP), urinary catecholamines and ventilatory functions of patients with mild essential hypertension after 10 weeks of Qigong (Shuxinpingxuegong). Fifty-eight patients volunteered to participate in this study and were randomly divided into either a Qigong group (n = 29), or a control group (n = 29). Systolic blood pressure and diastolic blood pressure decreased significantly in the Qigong group such that both became significantly lower after 10 weeks in the Qigong than in the control group. Also, there was a significant reduction of norepinephrine, metanephrine and epinephrine compared to baseline values in the Qigong group. The ventilatory functions, forced vital capacity and forced expiratory volume per sec, were increased in the Qigong group but not the control. These results suggest that Qigong may stabilize the sympathetic nervous system is effective in modulating levels of urinary catecholamines and BP positively, and in improving ventilatory functions in mildly hypertensive middle-aged patients.

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