Spontaneously hypertensive rats exhibit altered cardiovascular and neuronal responses to muscle contraction

Kramer, Jeffery M.; Waldrop, Tony G.

doi:10.1111/j.1469-445x.2001.tb00036.x

Cited by 4 publications

(2 citation statements)

References 40 publications

(43 reference statements)

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“…Previous studies using rats reported that the blood pressure response to static contraction or to muscle stretch elicited no change (34), an increase (2,19,32), or a decrease (15,22,32). These different responses were attributed to the different anesthetics, which include pentobarbital (2,19,32), chloral hydrate (2,19), halothane (27), and ␣-chloralose (16,22,34). Only two studies used a decerebrate preparation, and both showed consistent pressor reflex response to muscle contraction (23,27).…”

mentioning

confidence: 98%

Exercise pressor reflex in decerebrate and anesthetized rats

Hayashi

2003

American Journal of Physiology-Heart and Circulatory Physiology

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I investigated whether muscular contraction evokes cardiorespiratory increases (exercise pressor reflex) in alpha-chloralose- and chloral hydrate-anesthetized and precollicular, midcollicular, and postcollicular decerebrated rats. Mean arterial pressure (MAP), heart rate (HR), and minute ventilation (Ve) were recorded before and during 1-min sciatic nerve stimulation, which induced static contraction of the triceps surae muscles, and during 1-min stretch of the calcaneal tendon, which selectively stimulated mechanosensitive receptors in the muscles. Anesthetized rats showed various patterns of MAP response to both stimuli, i.e., biphasic, depressor, pressor, and no response. Sciatic nerve stimulation to muscle in precollicular decerebrated rats always evoked spontaneous running, so the exercise pressor reflex was not determined from these preparations. None of the postcollicular decerebrated rats showed a MAP response or spontaneous running. Midcollicular decerebrated rats consistently showed biphasic blood pressure response to both stimulations. The increases in MAP, HR, and Ve were related to the tension developed. The static contractions in midcollicular decerebrated rats (381 +/- 65 g developed tension) significantly increased MAP, HR, and Ve from 103 +/- 12 to 119 +/- 24 mmHg, from 386 +/- 30 to 406 +/- 83 beats/min, and from 122 +/- 7 to 133 +/- 25 ml/min, respectively. After paralysis, sciatic nerve stimulation had no effect on MAP, HR, or Ve. These results indicate that the midcollicular decerebrated rat can be a model for the study of the exercise pressor reflex.

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confidence: 98%

Exercise pressor reflex in decerebrate and anesthetized rats

Hayashi

2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…Em relação ao músculo estriado, Kramer e Waldrop 36 realizaram um estudo da resposta neuronal em SHR, durante contração muscular isométrica, e obtiveram o seguinte resultado: tanto os SHR quanto os WKY, apresentaram significante redução da pressão arterial, evocada pela contração muscular, via nervo tibial; porém, esta redução ocorreu muito rapidamente e não se manteve por toda a contração. Em WKY a média foi de -21.1 ± 1.8 mmHg, enquanto que nos SHR foi de -33.2 ± 1.9 mmHg.…”

Section: -Estudos Morfológicos E Funcio-nais Em Shrunclassified

Ratos Espontaneamente Hipertensos E Neuropatias Periféricas

Fazan¹,

Kalil²,

Alcântara³

et al. 2006

Medicina (Ribeirão Preto)

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Fazan VPS, Kalil ALR, Alcântara ACL, Genari AB, Tavares MR, Rodrigues AR, Salgado HC. Ratos espontaneamente hipertensos e neuropatias periféricas. Medicina (Ribeirão Preto) 2006; 39 (1): 39-50.Resumo: Modelo do Estudo: O presente estudo é uma revisão de literatura sobre o modelo de hipertensão espontânea e as conseqüências da hipertensão para o sistema nervoso periférico, somático e autonômico.Importância do problema: Hipertensão é o principal fator de risco para acidente vascular cerebral e demência vascular, por causar importantes mudanças cerebrovasculares, tornando o cérebro propenso a infartos, microaneurismas e isquemias. As principais mudanças causadas no sistema nervoso central (SNC) pela hipertensão, incluem: diminuição do volume cerebral, aumento no volume dos ventrículos e perda neuronal. Além das alterações no cérebro, a hipertensão causa outros danos que culminam em uma série de alterações patológicas renais e outras doenças, as quais sustentam a elevação da pressão arterial, aumento da freqüência cardíaca, e aumento da resistência vascular periférica. O rato espontaneamente hipertenso (SHR) é reconhecido como um excelente modelo de hipertensão experimental e pode servir como modelo de estudos clínicos da hipertensão essencial humana. Embora esse modelo tenha sido bastante explorado em termos fisiológicos, estudos morfológicos, quando presentes, se limitam aos vasos. Mesmo quando nervos periféricos foram estudados morfologicamente nesses animais, os vasos epineurais, perineurais e endoneurais foram o alvo do estudo. Raros são os estudos que envolvem as fibras nervosas nesse modelo de hipertensão.Comentários: Recentemente, estudamos as alterações do nervo depressor aórtico (NDA) em SHR. Nossos resultados mostraram redução do tamanho das fibras mielínicas e redução do tamanho e número das fibras amielínicas, comparados aos controles normotensos da linhagem Wistar-Kyoto. Outro estudo recente do nosso laboratório mostrou que, embora os níveis pressóricos dos SHR machos, bem como a freqüência cardíaca, sejam muito superiores aos das fêmeas, não há diferença morfológica nos nervos vagos cervicais entre SHR machos e fêmeas. Ainda, fazemos uma descrição morfológica e morfométrica do nervo sural de SHR, fornecendo parâmetros morfológicos para posteriores estudos funcionais.

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In vivo electrophysiological responses of pedunculopontine neurons to static muscle contraction

Plowey

Kramer

Beatty

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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The pedunculopontine nucleus (PPN) has previously been implicated in central command regulation of the cardiorespiratory adjustments that accompany exercise. The current study was executed to begin to address the potential role of the PPN in the regulation of cardiorespiratory adjustments evoked by muscle contraction. Extracellular single-unit recording was employed to document the responses of PPN neurons during static muscle contraction. Sixty-four percent (20/31) of neurons sampled from the PPN responded to static muscle contraction with increases in firing rate. Furthermore, muscle contraction-responsive neurons in the PPN were unresponsive to brief periods of hypotension but were markedly activated during chemical disinhibition of the caudal hypothalamus. A separate sample of PPN neurons was found to be moderately activated during systemic hypoxia. Chemical disinhibition of the PPN was found to markedly increase respiratory drive. These findings suggest that the PPN may be involved in modulating respiratory adjustments that accompany muscle contraction and that PPN neurons may have the capacity to synthesize muscle reflex and central command influences.

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Spontaneously hypertensive rats exhibit altered cardiovascular and neuronal responses to muscle contraction

Cited by 4 publications

References 40 publications

Exercise pressor reflex in decerebrate and anesthetized rats

Exercise pressor reflex in decerebrate and anesthetized rats

Ratos Espontaneamente Hipertensos E Neuropatias Periféricas

In vivo electrophysiological responses of pedunculopontine neurons to static muscle contraction

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