scholarly journals Resistance Training Controls Arterial Blood Pressure in Rats with L-NAME- Induced Hypertension

2013 ◽  
Author(s):  
Ayslan Jorge Santos de Araujo ◽  
Anne Carolline Veríssimo dos Santos ◽  
Karine dos Santos Souza ◽  
Marlúcia Bastos Aires ◽  
Valter Joviniano Santana-Filho ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Resistance Training ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Induced Hypertension

Strength training reduces arterial blood pressure but not sympathetic neural activity in young normotensive subjects

2003 ◽  
Vol 94 (6) ◽  
pp. 2212-2216 ◽  
Author(s):  
Jason R. Carter ◽  
Chester A. Ray ◽  
Emily M. Downs ◽  
William H. Cooke
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Resistance Training ◽  
Exercise Training ◽  
Resistance Exercise ◽  
Arterial Blood Pressure ◽  
Whole Body ◽  
Arterial Blood ◽  
Blood Pressures ◽  
Body Resistance

The effects of resistance training on arterial blood pressure and muscle sympathetic nerve activity (MSNA) at rest have not been established. Although endurance training is commonly recommended to lower arterial blood pressure, it is not known whether similar adaptations occur with resistance training. Therefore, we tested the hypothesis that whole body resistance training reduces arterial blood pressure at rest, with concomitant reductions in MSNA. Twelve young [21 ± 0.3 (SE) yr] subjects underwent a program of whole body resistance training 3 days/wk for 8 wk. Resting arterial blood pressure ( n = 12; automated sphygmomanometer) and MSNA ( n = 8; peroneal nerve microneurography) were measured during a 5-min period of supine rest before and after exercise training. Thirteen additional young (21 ± 0.8 yr) subjects served as controls. Resistance training significantly increased one-repetition maximum values in all trained muscle groups ( P < 0.001), and it significantly decreased systolic (130 ± 3 to 121 ± 2 mmHg; P = 0.01), diastolic (69 ± 3 to 61 ± 2 mmHg; P = 0.04), and mean (89 ± 2 to 81 ± 2 mmHg; P = 0.01) arterial blood pressures at rest. Resistance training did not affect MSNA or heart rate. Arterial blood pressures and MSNA were unchanged, but heart rate increased after 8 wk of relative inactivity for subjects in the control group (61 ± 2 to 67 ± 3 beats/min; P = 0.01). These results indicate that whole body resistance exercise training might decrease the risk for development of cardiovascular disease by lowering arterial blood pressure but that reductions of pressure are not coupled to resistance exercise-induced decreases of sympathetic tone.

scholarly journals Erythropoietin-induced hypertension in rat is not mediated by alterations of plasma endothelin, vasopressin, or atrial natriuretic peptide levels.

1997 ◽  
Vol 8 (6) ◽  
pp. 901-905
Author(s):  
X J Zhou ◽  
D Pandian ◽  
X Q Wang ◽  
N D Vaziri
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Clinical Studies ◽  
Controlled Study ◽  
Recombinant Erythropoietin ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Atrial Natriuretic

Regular administration of recombinant erythropoietin (EPO) in patients with chronic renal failure (CRF) is frequently complicated by a rise in arterial blood pressure. Clinical studies intended to discern the possible role of endothelin (ET) in the pathogenesis of EPO-induced hypertension have produced contradictory results. Given the limitations of the clinical studies, this placebo-controlled study was carried out in CRF (5/6 nephrectomized) rats treated with either EPO, 150 U/kg intraperitoneally, or the vehicle alone twice weekly for 6 wk. Plasma ET was measured at baseline, and weeks 2, 4, and 6. In addition, plasma arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) were determined at the conclusion of the study period. As expected, blood pressure rose markedly after 1 wk of EPO therapy as compared with the placebo therapy. However, there was no significant difference in plasma ET levels between the EPO- and placebo-treated groups during the study period. Likewise, EPO therapy had no effect on plasma ANP level but depressed plasma AVP concentration. Thus, this placebo-controlled animal study revealed that EPO therapy markedly raised arterial blood pressure but had no effect on plasma ET in the CRF rats. This observation suggests that EPO-induced hypertension in this model is not mediated by an increased circulating ET level. However, the possible effect, if any, of EPO on local vascular tissue ET level is uncertain and awaits further investigation.

Orchidectomy attenuates impaired endothelial effects of a high-salt diet in Sprague–Dawley rats

2011 ◽  
Vol 89 (4) ◽  
pp. 295-304 ◽  
Author(s):  
A.K. Oloyo ◽  
O.A. Sofola ◽  
C.N. Anigbogu
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
High Salt ◽  
Sprague Dawley ◽  
High Salt Diet ◽  
Salt Diet ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Induced Hypertension

The effect of sex hormones on vascular reactivity is considered one of the underlying factors contributing to gender differences in cardiovascular functions and diseases. Experiments were designed to investigate the role of androgens in salt-induced hypertension by assessing the relaxation response of isolated aortic rings to acetylcholine and sodium nitroprusside in the presence or absence of l-nitroarginine methyl ester in Sprague–Dawley rats. The rats were either orchidectomized or sham-operated, with or without testosterone replacement, and were placed on a normal or high-salt diet for 6 weeks. The results indicate a significant increase (p < 0.001) in the mean arterial blood pressure of rats on the high-salt diet, when compared with control or orchidectomized rats. Orchidectomy elicited a reduction in mean arterial blood pressure (p < 0.01), while testosterone replacement normalized mean arterial blood pressure to values seen in intact rats on the high-salt diet. The high-salt diet reduced the relaxation response to acetylcholine both in the presence and absence of inhibition of endothelial nitric oxide synthase with l-nitroarginine methyl ester. Bilateral orchidectomy attenuated the impaired endothelial function induced by the high-salt diet in rats, but this was reversed by concomitant administration of testosterone, suggesting a role for androgens in enhancing long-term vascular smooth muscle tone and hence maintenance of high blood pressure in salt-induced hypertension.

scholarly journals Effects of Rut-bpy (Cis-[Ru(bpy)2(SO3)(NO)]PF 6), a novel nitric oxide donor, in L-NAME-induced hypertension in rats

2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 57-59 ◽  
Author(s):  
Marcio Wilker Soares Campelo ◽  
Ana Paula Bomfim Soares Campelo ◽  
Luiz Gonzaga de França Lopes ◽  
Armenio Aguiar dos Santos ◽  
Sergio Botelho Guimarães ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Methyl Ester ◽  
Arterial Blood Pressure ◽  
Wistar Rats ◽  
Nitric Oxide Donor ◽  
Hypertensive Rats ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Male Wistar Rats

PURPOSE: To evaluate the effect of Rut-bpy (Cis-[Ru(bpy)2(SO3)(NO)]PF 6), a novel nitric oxide donor in Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats. METHODS: Twenty-four male Wistar rats were randomly assigned to four groups (n=6), named according to the treatment applied (G1-Saline, G2-Rut-bpy, G3-L-NAME and G4-L-NAME+Rut-bpy). L-NAME (30 mg/Kg) was injected intraperitoneally 30 minutes before the administration of Rut-bpy (100 mg/Kg). Mean abdominal aorta arterial blood pressure (MAP) was continuously monitored. RESULTS: Mean arterial blood pressure (MAP) in G3 rats rose progressively, reaching 147±16 mmHg compared with 100±19 mm Hg in G1 rats (p<0.05). In G4 rats, treated with L-NAME+Rut-bpy, MAP reached 149+11 mm Hg while in G2 rats, treated with Rut-bpy, MAP values were 106±11 mm Hg. In G1 rats these values decreased progressively reaching 87+14 mm Hg after 30 minutes. An important finding was the maintenance of the MAP throughout the experiment in G2 rats. CONCLUSION: Rut-bpy does not decrease the MAP in L-Name induced hypertensive rats. However, when it is used in anesthetized hypotensive rats a stable blood pressure is obtained.

Managing high blood pressure in pregnancy

1993 ◽  
Vol 31 (14) ◽  
pp. 53-56
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
High Blood Pressure ◽  
Chronic Hypertension ◽  
Pregnancy Induced Hypertension ◽  
Hypertension In Pregnancy ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
In Pregnancy

Raised arterial blood pressure is common in pregnancy. Usually it is due solely to the pregnancy and resolves within days or weeks of delivery (pregnancy-induced hypertension – PIH). Occasionally it is chronic hypertension which predates or begins during pregnancy; it persists after delivery. In some women it is a mixture of both, with pregnancy-induced hypertension superimposed on existing chronic hypertension. In this article we discuss the risks to mother and fetus of hypertension in pregnancy and review its prevention and management.

Sign in / Sign up

Export Citation Format

Share Document