Neurotransmitter release and vascular reactivity in spontaneously hypertensive rats.

Tsuda, Kazushi; Kuchii, Masato; Kusuyama, Yoshio; Hano, Takuzo; Nishio, Ichiro; Matsuyama, Yoshiaki

doi:10.1253/jcj.48.1263

Cited by 30 publications

(16 citation statements)

References 20 publications

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“…The importance of Ca++ in neurotransmitter release has been demonstrated by many authors.1)-3) The term "stimulus-secretion coupling" suggests that the Ca++-influx across the cell membrane is an inevitable concomitant of the stimulus, and is necessary for transmitter release. Our previous reports also showed that Ca++-antagonists, such as verapamil and diltiazem, affected both pre-and post-synaptic sites of resistance vessels and caused a decrease in electrically-stimulated norepinephrine release from the adrenergic nerve endings distributed in rat mesenteric arteries, in addition to direct effects on vascular smooth muscle.11), 12) It is generally accepted that calmodulin is an intracellular Ca++-binding protein that modulates the effects of Ca++ on several important enzyme systems. The present study with calmodulin antagonists13),14) is an attempt to evaluate the contributions of endogenous calmodulin to both norepinephrine release from adrenergic nerve endings and vascular muscle contractions.…”

Section: Discussionmentioning

confidence: 93%

Effects of calmodulin antagonists on norepinephrine release and vascular responsiveness in rat mesenteric vasculature.

Tsuda¹,

Nishio²,

Masuyama³

1987

Jpn Heart J

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SUMMARYThis study was designed to investigate the role of calmodulin in adrencrgic neurotransmission of resistance vessels. The effects of various calmodulin antagonists (trifluoperazine, W-7, calmidazolium, chlorpromazine, fluphenazine) on the vascular responsiveness and norepinephrine overflow from adrenergic nerve endings were examined in perfused rat mesenteric vasculature preparations. Pressor responses to electrical nerve stimulation or exogenous norepinephrine were inhibited dose-dependently by each calmodulin antagonist.Norepinephrine overflow from the sympathetic nerve endings during electrical nerve stimulation was also suppressed by calmodulin antagonists.These results indicate that calmodulin antagonists affected both pre-and post-synaptic sites of adrenergic neurotransmission, suggesting that calmodulin is involved both in neurosecretion and vascular smooth muscle contractions in peripheral resistance vessels.

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Section: Discussionmentioning

confidence: 93%

Effects of calmodulin antagonists on norepinephrine release and vascular responsiveness in rat mesenteric vasculature.

Tsuda¹,

Nishio²,

Masuyama³

1987

Jpn Heart J

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“…Earlier studies by Tsuda et al [13] demonstrated reduced noradrenaline release from sympathetic nerves in 20-22week-old SHR, but the response to nerve stimulation was still increased. In our study, performed in older SHR, the neurogenic response was reduced to the same extent as the response to exogenous noradrenaline.…”

Section: Reduction Of Baroreflex Blood Pressure Oscillations In 12-momentioning

confidence: 86%

Reduction of baroreflex blood pressure oscillations in 12-month-old SHR: Central and peripheral mechanisms

Тарасова

Лукошкова

et al. 2014

2014 8th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO)

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The aim of this study was to reveal the changes of short-term cardiovascular variability in rats with sustained primary hypertension and correlate them with functional alterations of peripheral arteries. 12-month-old SHR as compared to Wistar rats demonstrated prominent reductions of mean arterial pressure and pulse interval spectral powers in the range 0.25-0.75 Hz. These alterations were associated with prominent reductions of cardiac baroreflex gain and constrictor responses of small arteries to electrical stimulation of sympathetic fibers and exogenous noradrenaline. We suggest that both central and peripheral mechanisms are responsible for the reduction of baroreflex arterial pressure oscillations in mature SHR.

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“…Previously it was shown that the pressor responses and NE overflow during electrical nerve stimulation were completely blocked by guanethidine (Tsuda et al 1984b), which provided evidence that the stimulation was neuronal in nature.…”

Section: Preparation Of Perfused Mesenteric Vasculaturesmentioning

confidence: 97%

Presynaptic α₂‐adrenoceptor‐mediated modulation of norepinephrine release from vascular adrenergic neurons in reduced renal mass salt hypertensive rats

Tsuda¹,

Kimura

Shima

et al. 1992

Clin Exp Pharma Physio

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The present study was designed to investigate the presynaptic alpha 2-adrenoceptor function to inhibit norepinephrine (NE) release in blood vessels of reduced renal mass salt hypertensive rats (Na-loaded HT). Isolated perfused mesenteric vasculatures were prepared from Na-loaded HT and normotensive control rats (NT-control), and the NE release and vascular responsiveness were examined. Periarterial nerve stimulation caused a significantly greater release of NE and pressor responses in Na-loaded HT than in NT-control. Yohimbine, a potent alpha 2-adrenoceptor antagonist, demonstrated the facilitatory effects on NE release during nerve stimulation. The effects were significantly attenuated in Na-loaded HT compared with NT-control. These results demonstrate that vascular sympathetic nervous activity might be enhanced in Na-loaded HT. Furthermore, the increased NE release from vascular adrenergic neurons in Na-loaded HT could partially depend on impaired presynaptic alpha 2-adrenoceptor-mediated modulation, which might contribute to the pathogenesis and maintenance of this form of salt-dependent hypertension.

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Neurotransmitter release and vascular reactivity in spontaneously hypertensive rats.

Cited by 30 publications

References 20 publications

Effects of calmodulin antagonists on norepinephrine release and vascular responsiveness in rat mesenteric vasculature.

Effects of calmodulin antagonists on norepinephrine release and vascular responsiveness in rat mesenteric vasculature.

Reduction of baroreflex blood pressure oscillations in 12-month-old SHR: Central and peripheral mechanisms

Presynaptic α₂‐adrenoceptor‐mediated modulation of norepinephrine release from vascular adrenergic neurons in reduced renal mass salt hypertensive rats

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Neurotransmitter release and vascular reactivity in spontaneously hypertensive rats.

Cited by 30 publications

References 20 publications

Effects of calmodulin antagonists on norepinephrine release and vascular responsiveness in rat mesenteric vasculature.

Effects of calmodulin antagonists on norepinephrine release and vascular responsiveness in rat mesenteric vasculature.

Reduction of baroreflex blood pressure oscillations in 12-month-old SHR: Central and peripheral mechanisms

Presynaptic α2‐adrenoceptor‐mediated modulation of norepinephrine release from vascular adrenergic neurons in reduced renal mass salt hypertensive rats

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Presynaptic α₂‐adrenoceptor‐mediated modulation of norepinephrine release from vascular adrenergic neurons in reduced renal mass salt hypertensive rats