Effects of Exercise Training on Baroreflex Control of the Cardiovascular System

Krieger, Eduardo Moacyr; Silva, Gustavo José Justo da; Negräo, Carlos Eduardo

doi:10.1111/j.1749-6632.2001.tb03689.x

Cited by 60 publications

(54 citation statements)

References 33 publications

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“…Herein, we have observed that baroreflex sensitivity in normotensive rats is much higher than in SHRs, which supports the previous study. 26 Interventionist attitudes that seek improvement in arterial baroreflex sensitivity are considered to be new strategies for the management of cardiovascular diseases, especially hypertension. 26,33 Recently, we published a study showing that Bj-PRO-10c mediated CNS actions to decrease arterial pressure and HR in SHRs.…”

Section: Discussionmentioning

confidence: 99%

“…26 Interventionist attitudes that seek improvement in arterial baroreflex sensitivity are considered to be new strategies for the management of cardiovascular diseases, especially hypertension. 26,33 Recently, we published a study showing that Bj-PRO-10c mediated CNS actions to decrease arterial pressure and HR in SHRs. Bj-PRO10c-induced intracellular calcium signaling involved the activation of G-protein-coupled receptors and the release of neurotransmitters such as GABA and glutamate.…”

Section: Discussionmentioning

confidence: 99%

“…These data are in agreement with a previous study by Krieger and co-workers demonstrating that SHRs have impaired sensitivity with regard to baroreflex control of HR. 26 After Bj-PRO-10c injection, the baroreflex sensitivity of normotensive rats for the control of HR was unchanged ( Figure 4a); however, baroreflex sensitivity increased among SHRs. The improvement of baroreflex sensitivity occurred only during periods of decreasing MAP (Table 1).…”

Section: Bj-pro-10c Improves Baroreflex Sensitivity Of Shrsmentioning

confidence: 97%

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Brain nitric oxide production by a proline-rich decapeptide from Bothrops jararaca venom improves baroreflex sensitivity of spontaneously hypertensive rats

Lameu

Pontieri

Guerreiro³

et al. 2010

Hypertens Res

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Baroreflex sensitivity is disturbed in many people with cardiovascular diseases such as hypertension. Brain deficiency of nitric oxide (NO), which is synthesized by NO synthase (NOS) in the citrulline-NO cycle (with argininosuccinate synthase (ASS) activity being the rate-limiting step), contributes to impaired baroreflex. We recently showed that a decapeptide isolated from Bothrops jararaca snake venom, denoted Bj-PRO-10c, exerts powerful and sustained antihypertensive activity. Bj-PRO-10c promoted vasodilatation dependent on the positive modulation of ASS activity and NO production in the endothelium, and also acted on the central nervous system, inducing the release of GABA and glutamate, two important neurotransmitters in the regulation of autonomic systems. We evaluated baroreflex function using the regression line obtained by the best-fit points of measured heart rate (HR) and mean arterial pressure (MAP) data from spontaneously hypertensive rats (SHRs) treated with Bj-PRO-10c. We also investigated molecular mechanisms involved in this effect, both in vitro and in vivo. Bj-PRO-10c mediated an increase in baroreflex sensitivity and a decrease in MAP and HR. The effects exerted by the peptide include an increase in the gene expression of endothelial NOS and ASS. Bj-PRO-10c-induced NO production depended on intracellular calcium fluxes and the activation of a G i/o -protein-coupled metabotropic receptor. Bj-PRO-10c induced NO production and the gene expression of ASS and endothelial NOS in the brains of SHRs, thereby improving baroreflex sensitivity. Bj-PRO-10c may reveal novel approaches for treating diseases with impaired baroreflex function. Hypertension Research (2010Research ( ) 33, 1283Research ( -1288 doi:10.1038/hr.2010 Keywords: argininosuccinate synthase; baroreflex sensitivity; Bothrops jararaca venom; nitric oxide; proline-rich oligopeptide INTRODUCTIONThe gaseous messenger NO is involved mainly in the regulation of local and systemic vascular resistance, sodium balance and, consequently, blood pressure control, 1 but it is also a signaling molecule and modulator of brain function. 2 Recent studies relate NO with central cardiovascular control through the regulation of the cardiac and vascular autonomic system via the modulation of the central sites of cardiovascular autonomic neural integration. 3,4 NO is generated in the citrulline-NO cycle by NO synthase (NOS) using L-arginine as a substrate. Three isoforms of NOS have been described: calcium-dependent endothelial (eNOS) and neuronal (nNOS) isoforms and inducible NOS. The expression and activity

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Bj-pro-10c Improves Baroreflex Sensitivity Of Shrsmentioning

confidence: 97%

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Brain nitric oxide production by a proline-rich decapeptide from Bothrops jararaca venom improves baroreflex sensitivity of spontaneously hypertensive rats

Lameu

Pontieri

Guerreiro³

et al. 2010

Hypertens Res

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“…Evidence suggests that moderate exercise reduces the diastolic and systolic pressure in hypertensive humans and animals (2,28,39). The heart rate seems to be reduced by low-intensity exercise training in SHR, likely due to a decrease in the sympathetic tone to the heart (17).…”

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confidence: 99%

Exercise changes regional vascular control by commissural NTS in spontaneously hypertensive rats

Ogihara

Schoorlemmer

Levada

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Ogihara CA, Schoorlemmer GHM, Levada AC, Pithon-Curi TC, Curi R, Lopes OU, Colombari E, Sato MA. Exercise changes regional vascular control by commissural NTS in spontaneously hypertensive rats. Am J Physiol Regul Integr Comp Physiol 299: R291-R297, 2010. First published April 21, 2010 doi:10.1152/ajpregu.00055.2009.-Inhibition of the commissural nucleus of the solitary tract (commNTS) induces a fall in sympathetic nerve activity and blood pressure in spontaneously hypertensive rats (SHR), which suggests that this subnucleus of the NTS is a source of sympathoexcitation. Exercise training reduces sympathetic activity and arterial pressure. The purpose of the present study was to investigate whether the swimming exercise can modify the regional vascular responses evoked by inhibition of the commNTS neurons in SHR and normotensive Wistar-Kyoto (WKY) rats. Exercise consisted of swimming, 1 h/day, 5 days/wk for 6 wks, with a load of 2% of the body weight. The day after the last exercise session, the rats were anesthetized with intravenous ␣-chloralose, tracheostomized, and artificially ventilated. The femoral artery was cannulated for mean arterial pressure (MAP) and heart rate recordings, and Doppler flow probes were placed around the lower abdominal aorta and superior mesenteric artery. Microinjection of 50 mM GABA into the commNTS caused similar reductions in MAP in swimming and sedentary SHR (Ϫ25 Ϯ 6 and Ϫ30 Ϯ 5 mmHg, respectively), but hindlimb vascular conductance increased twofold in exercised vs. sedentary SHR (54 Ϯ 8 vs. 24 Ϯ 5%). GABA into the commNTS caused smaller reductions in MAP in swimming and sedentary WKY rats (Ϫ20 Ϯ 4 and Ϫ16 Ϯ 2 mmHg). Hindlimb conductance increased fourfold in exercised vs. sedentary WKY rats (75 Ϯ 2% vs. 19 Ϯ 3%). Therefore, our data suggest that the swimming exercise induced changes in commNTS neurons, as shown by a greater enhancement of hindlimb vasodilatation in WKY vs. SHR rats in response to GABAergic inhibition of these neurons.GABA; cardiovascular; citrate synthase THE NUCLEUS OF THE SOLITARY tract (NTS) is the primary site in the central nervous system that receives the afferents arising from arterial baro-and chemoreceptors (10, 15). The intermediate NTS receives inputs particularly from arterial baroreceptors, but some of these afferents achieve the commNTS (10, 16). The commNTS also receives inputs from arterial chemoreceptors, and seems to be highly sensitive to carotid chemoreceptor stimulation (8, 9, 11).The possible role of the commNTS as a source of sympathoexcitation was first shown by Nelson et al. (33), which demonstrated that nanoliter injections of L-glutamate into the commNTS evoke elevations in heart rate and arterial pressure mediated by the sympathetic nervous system. Electrolytic lesions or chemical inhibition of the commNTS have been shown to markedly decrease the splanchnic sympathetic nerve activity and arterial pressure in spontaneously hypertensive rats (SHR), which suggested that this subnucleus of the NTS contains neurons tonically active in S...

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“…These findings suggest that the running training reduced both the stress-induced activation of the sympathetic nervous system and the sensitivity of resistance vessels to the secreted NE, leading to the observed decrease in the stress-induced BP response. It has been reported that the operation of the baroreceptor reflex is improved after chronic exercise in SHR 20,21) , which could lead to a decrease in BP. This seems a likely scenario since in our hands, the BP response to stress was decreased in the trained SHR, while the stress-induced HR response underwent no training-related alteration.…”

Section: Discussionmentioning

confidence: 98%

Running training attenuates blood pressure and norepinephrine responses to immobilization stress in spontaneously hypertensive rats

Miyoshi

Watanabe

2013

JPFSM

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We investigated the effects of 4 weeks of running training on the progressive changes in resting blood pressure (BP) and heart rate (HR) that occurred during that period, as well as on the increases in cardiovascular variables and catecholamine levels induced by a novel stress (immobilization stress) in spontaneously hypertensive rats (SHR) and control normotensive Wistar-Kyoto rats (WKY). In addition, rat sensitivity to exogenously infused norepinephrine (NE) was investigated by measuring the induced pressor response. BP was measured by a tail-cuff method (without heating), which is reportedly both sensitive and accurate for noninvasive measurement of BP in conscious rats. Increases in resting systolic BP over the 4-week period were significantly smaller in the trained SHR than in the untrained SHR, but the training had no effect on the changes in resting BP seen in WKY. After the 4-week running training, BP and NE responses to immobilization stress were reduced in the SHR, as was the increase in BP induced by intravenous (IV) infusion of NE. In the WKY, however, neither the BP response to the stress nor that to the IV infusion of NE was changed by running training. These results suggest 1) that such training was beneficial in the SHR, and 2) that the immobilization stressinduced activation of the sympathetic nervous system (as evidenced by the increase in plasma NE) and the sensitivity to NE (as evidenced by the increase in BP induced by exogenous NE) were each attenuated after the 4-week running training in the SHR, with a consequent reduction in the BP response to a novel stress.

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Effects of Exercise Training on Baroreflex Control of the Cardiovascular System

Cited by 60 publications

References 33 publications

Brain nitric oxide production by a proline-rich decapeptide from Bothrops jararaca venom improves baroreflex sensitivity of spontaneously hypertensive rats

Brain nitric oxide production by a proline-rich decapeptide from Bothrops jararaca venom improves baroreflex sensitivity of spontaneously hypertensive rats

Exercise changes regional vascular control by commissural NTS in spontaneously hypertensive rats

Running training attenuates blood pressure and norepinephrine responses to immobilization stress in spontaneously hypertensive rats

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