Acute exercise enhances nitric oxide modulation of vascular response to phenylephrine

Patil, Rahul; DiCarlo, Stephen E.; Collins, Heidi L.

doi:10.1152/ajpheart.1993.265.4.h1184

Cited by 67 publications

(95 citation statements)

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“…94 In a separate study using rats, increased iliac blood flow was demonstrated to be mediated by decreased adrenergic receptor sensitivity. 95 Although no PEH was observed in that study and the reduced sensitivity could be related to numerous factors, inhibition of nitric oxide attenuated the decreased sensitivity after exercise, suggesting that nitric oxide may be partly responsible for the decreased sensitivity post exercise. Using ganglionic blocked, intact, Dahl salt-sensitive rats, Van Ness et al 48 found an exercise induced attenuation in blood pressure responsiveness to the ␣-adrenergic agonist phenylephrine that persisted until the cessation of measurement at 30 min post infusion.…”

Section: Reduced Vascular Sensitivity/nitric Oxidementioning

confidence: 59%

Potential causes, mechanisms, and implications of post exercise hypotension

2002

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Post exercise hypotension (PEH) is a phenomenon of a prolonged decrease in resting blood pressure in the minutes and hours following acute exercise. Knowledge of PEH is potentially useful in designing first line strategies against hypertension as well as allowing a further understanding of blood pressure regulation in both Keywords: blood pressure; vascular; cardiac; opioids; exercise Blood pressure responses during exerciseDuring dynamic exercise, cardiac output increases dramatically to ensure adequate perfusion to the working musculature. This increase is achieved by a withdrawal of parasympathetic tone (causing an increased heart rate and contractility), an increase in sympathetic activity (directly and indirectly increasing heart rate and contractility) and pronounced vasoconstriction of the venous vasculature (causing a greater venous return and therefore stroke volume). In parallel, the need for increased blood flow and oxygen delivery to the exercising muscle is achieved through regional vasodilation of those arterioles supplying blood to the exercising tissue in combination with a vasoconstriction of arterioles, which perfuse non-essential tissues. Although the mechanism of vasodilation at the onset of exercise is not fully understood, many compounds (eg, potassium, adenosine, nitric oxide, etc) have been implicated in the exercise induced changes. Contraction of the active muscle mass also assists in returning blood towards the heart. This 'muscle pump' effect further increases venous return and stroke volume.Increased cardiac output and vasoconstriction in non-exercising vascular beds increases systolic blood pressure (SBP), but the significant vasodilation at the exercising muscle beds helps to buffer this increase and results in a minimal rise in diastolic blood pressure (DBP). As exercise continues Correspondence: JR MacDonald, McMaster University Medical Centre, Room 4U18, 1200 Main Street West, Hamilton, Ontario L8N 3Z5, Canada. E-mail: jaymacȰmcmaster.ca health and disease. Following a brief review of blood pressure responses to exercise, this paper will provide a current and comprehensive summary of PEH and integrate the current state of knowledge surrounding it.

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Section: Reduced Vascular Sensitivity/nitric Oxidementioning

confidence: 59%

Potential causes, mechanisms, and implications of post exercise hypotension

2002

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“…␣-Adrenergic vasoconstriction has been reported to be antagonized by NO in isolated blood vessels (5,6), in microvascular preparations of anesthetized rats and dogs (7,8), in the hindlimb of conscious rats (9), and in the contracting hindlimb of anesthetized rats (11). This antagonistic effect of NO is more potent for ␣ 2 -rather than ␣ 1 -adrenergic vasoconstriction in rat skeletalmuscle microcirculation (7) and in the canine coronary vascular bed (10).…”

Section: Discussionmentioning

confidence: 99%

“…Although such metabolic modulation negates an otherwise deleterious effect of adrenergic vasoconstriction on muscle perfusion, little is known about the specific metabolites involved. NO may be one such metabolite, as suggested by increasing evidence demonstrating NO-mediated antagonism of ␣-adrenergic vasoconstriction both in isolated blood vessels and in intact vascular beds (5)(6)(7)(8)(9)(10). Further support for the concept that NO is involved in the local metabolic modulation of adrenergic vasoconstriction is provided by a recent study in rats demonstrating that inhibition of NO synthase (NOS) enhances sympathetic vasoconstriction in the contracting hindlimb (11).…”

mentioning

confidence: 99%

Impaired metabolic modulation of α-adrenergic vasoconstriction in dystrophin-deficient skeletal muscle

Thomas

Sander

Lau

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

331

384

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The neuronal isoform of nitric oxide synthase (nNOS) is highly expressed in mammalian skeletal muscle, but its functional role has not been defined. NO has been implicated in the local metabolic regulation of blood f low in contracting skeletal muscle in part by antagonizing sympathetic vasoconstriction. We therefore hypothesized that nNOS in skeletal muscle is the source of the NO mediating the inhibition of sympathetic vasoconstriction in contracting muscle. In the mdx mouse, a model of Duchenne muscular dystrophy in which dystrophin deficiency results in greatly reduced expression of nNOS in skeletal muscle, we found that the normal ability of skeletal muscle contraction to attenuate ␣-adrenergic vasoconstriction is defective. Similar results were obtained in mutant mice that lack the gene encoding nNOS. Together these data suggest a specific role for nNOS in the local metabolic inhibition of ␣-adrenergic vasoconstriction in active skeletal muscle.To sustain physical activity, increases in skeletal muscle blood flow must closely match oxygen and substrate delivery to the increased metabolic rate of the contracting muscles. Although contracting skeletal muscle produces a number of vasodilator metabolites, the precise contributions of the various metabolites in mediating exercise-induced increases in muscle blood flow have been difficult to define.One of the ways in which metabolites produced in contracting skeletal muscle may contribute to blood flow regulation during exercise is by opposing adrenergic vasoconstriction. An emerging body of evidence indicates that in mammalian skeletal muscle ␣-adrenergic vasoconstriction is very sensitive to inhibition by local metabolic products of skeletal muscle contraction (1-4). Although such metabolic modulation negates an otherwise deleterious effect of adrenergic vasoconstriction on muscle perfusion, little is known about the specific metabolites involved. NO may be one such metabolite, as suggested by increasing evidence demonstrating NO-mediated antagonism of ␣-adrenergic vasoconstriction both in isolated blood vessels and in intact vascular beds (5-10). Further support for the concept that NO is involved in the local metabolic modulation of adrenergic vasoconstriction is provided by a recent study in rats demonstrating that inhibition of NO synthase (NOS) enhances sympathetic vasoconstriction in the contracting hindlimb (11).Until recently, the source of NO involved in muscle blood flow regulation during exercise was assumed to be the vascular endothelium, in which the endothelial isoform of NOS (eNOS) is abundantly expressed (12). In contracting muscle, the increased shear stress caused by elevated blood flow would seem to be an ideal stimulus to activate eNOS and increase endothelial NO production (13). However, the recent identification of the neuronal isoform of NOS (nNOS) in skeletal muscle provides another potential source of NO (14,15). Conceivably, NO produced by nNOS in the skeletal muscle fibers could diffuse to nearby arterioles, resulting in vaso...

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“…Investigations with animal models have suggested that the occurrence of PEH may be mediated by NO (Howard & DiCarlo, 1992;Patil, DiCarlo & Collins, 1993). However, the relationship between these factors and mechanisms in humans remain inconclusive.…”

Section: S80mentioning

confidence: 99%

“…This phenomenon is known as post-exercise hypotension (PEH) and has been suggested to be dependent of NO release, which is a powerful vasodilator (Asano et al, 2012;Santana et al, 2011;Patil, DiCarlo, & Collins, 1993). However the mechanisms and the relationships between NO release and PEH remain inconclusive (Halliwill, Minson, & Joyner, 2000;Pescatello, Fargo, Leach, & Scherzer, 1991), especially for T2D .…”

Section: Introductionmentioning

confidence: 99%

Cycling above rather than below lactate threshold is more effective for nitric oxide release and post-exercise blood pressure reduction in individuals with type-2 diabetes

Asano

Browne

Sotero

et al. 2013

Motriz: rev. educ. fis.

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Abstract-The purposes of this study were to analyze and compare the effects of exercise performed in different intensities, above and below lactate threshold (LT) on post-exercise blood pressure (BP) and nitric oxide (NO) responses in individuals with type 2 diabetes (T2D). For this, 11 T2D underwent the following sessions: 1) control session; 2) 20-min of moderate cycling (80% LT); and 3) 20-min of high intensity cycling (120%LT) on a cycle ergometer. Plasma NO and BP measurements were carried out at rest and at 15 and 45 min of post-sessions. When compared to rest, only the exercise session performed at 120%LT elicited an increase of NO (from 7.2 to 9.5 µM, p<0.05), as well as a decrease in systolic BP (from 126.6±7.9 to 118.7±3.9 mmHg, p<0.05) during the post-exercise period. In conclusion, the results suggest that NO release and post-exercise BP decrease are intensity-dependent for individuals with T2D.Keywords: nitric oxide, type-2 diabetes, high intensity exercise Resumo-"Ciclismo acima do limiar de lactato é mais efetivo que abaixo para liberação de óxido nítrico e redução da pressão arterial pós-exercício em indivíduos com diabetes tipo 2." Os objetivos do presente estudo foram analisar e comparar os efeitos do exercício realizado em diferentes intensidades, acima e abaixo do limiar de lactato (LL), sobre a resposta da pressão arterial (PA) e óxido nítrico (NO) em indivíduos com diabetes tipo 2 (DM2). Para tanto, 11 DM2 foram submetidos às seguintes sessões: 1) sessão controle; 2) 20 min de exercício em cicloergômetro em intensidade moderada (80%LL); e 3) 20 min de exercício em cicloergômetro em alta intensidade (120%LL). O NO plasmático e as medidas de PA foram realizadas no repouso, bem como aos 15 e 45 min do período de recuperação de todas as sessões. Quando comparado ao período de repouso, somente a sessão de exercício realizado a 120%LL promoveu aumento do NO (de 7,2 para 9,5 µM, p<0,05) e, por conseguinte, uma diminuição na pressão arterial sistólica (de 126,6±7,9 para 118,7±3,9 mmHg, p<0,05) durante o período de recuperação pós-exercício. Em conclusão, os resultados sugerem que a liberação de NO e a diminuição da PA parecem ser intensidade-dependente para indivíduos com DM2.Palavras-chaves: óxido nítrico, diabetes tipo 2, exercício de alta intensidadeResumen-"Ciclismo arriba del umbral de lactato es más efectivo que abajo para la liberación de óxido nítrico y reducción de la presión arterial después del ejercicio en individuos con diabetes tipo 2." Los objetivos del presente estudio fueron examinar y comparar los efectos del ejercicio realizado en diferentes intensidades, arriba y abajo del umbral de lactato (UL), sobre la respuesta de la presión arterial (PA) y el óxido nítrico (NO) en individuos con diabetes tipo 2 (DM2). Por lo tanto, 11 DM2 se sometieron las siguientes sesiones: 1) sesión control; 2) 20 min de ejercicio en cicloergómetro a una intensidad moderada (80%UL); y 3) 20 min de ejercicio en cicloergómetro a una intensidad alta (120%UL). El NO plasmático y las mediciones de la PA fuer...

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Acute exercise enhances nitric oxide modulation of vascular response to phenylephrine

Cited by 67 publications

References 0 publications

Potential causes, mechanisms, and implications of post exercise hypotension

Potential causes, mechanisms, and implications of post exercise hypotension

Impaired metabolic modulation of α-adrenergic vasoconstriction in dystrophin-deficient skeletal muscle

Cycling above rather than below lactate threshold is more effective for nitric oxide release and post-exercise blood pressure reduction in individuals with type-2 diabetes

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