Myogenic tone in isolated perfused resistance vessels from rats

Uchida, Eiichi; Df, Bohr

doi:10.1152/ajplegacy.1969.216.6.1343

Cited by 47 publications

(19 citation statements)

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“…It is currently believed that myogenic constriction in response to increased intralumenal pressure is initiated by vascular smooth muscle membrane depolarization, which then permits extracellular Ca 2ϩ entry through voltage-gated Ca 2ϩ channels (12,32). The dependence on extracellular Ca 2ϩ for contraction and myogenic tone in isolated skeletal muscle (19,49) and mesenteric (33) resistance arteries has been established. There is some evidence that the myogenic response may also involve release of Ca 2ϩ from intracellular stores (11,37).…”

Section: Fig 5 Representative Profiles Of the Vasoconstrictor Dynammentioning

confidence: 99%

Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca²⁺release mechanism

Colleran

Behnke

Wilkerson

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Colleran PN, Behnke BJ, Wilkerson MK, Donato AJ, Delp MD. Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca 2ϩ release mechanism. Am J Physiol Regul Integr Comp Physiol 294: R1577-R1585, 2008. First published March 19, 2008 doi:10.1152/ajpregu.00084.2008.-Previous work has shown that orthostatic hypotension associated with cardiovascular deconditioning results from inadequate peripheral vasoconstriction. We used the hindlimb-unloaded (HU) rat in this study as a model to induce cardiovascular deconditioning. The purpose of this study was to test the hypothesis that 14 days of HU diminishes vasoconstrictor responsiveness of mesenteric resistance arteries. Mesenteric resistance arteries from control (n ϭ 43) and HU (n ϭ 44) rats were isolated, cannulated, and pressurized to 108 cm H2O for in vitro experimentation. Myogenic (intralumenal pressure ranging from 30 to 180 cm H2O), KCl (2-100 mM), norepinephrine (NE, 10 Ϫ9 -10 Ϫ4 M) and caffeine (1-20 mM) induced vasoconstriction, as well as the temporal dynamics of vasoconstriction to NE, were determined. The active myogenic and passive pressure responses were unaltered by HU when pressures remained within physiological range. However, vasoconstrictor responses to KCl, NE, and caffeine were diminished by HU, as well as the rate of constriction to NE (C, 14.8 Ϯ 3.6 m/s vs. HU 7.6 Ϯ 1.8 m/s). Expression of sarcoplasmic reticulum Ca 2ϩ ATPase 2 and ryanodine 3 receptor mRNA was unaffected by HU, while ryanodine 2 receptor mRNA and protein expression were diminished in mesenteric arteries from HU rats. These data suggest that HU-induced and microgravity-associated orthostatic intolerance may be due, in part, to an attenuated vasoconstrictor responsiveness of mesenteric resistance arteries resulting from a diminished ryanodine 2 receptor Ca 2ϩ release mechanism.hindlimb unloading; vasoconstrictor responsiveness FOLLOWING EXPOSURE TO WEIGHTLESSNESs, many astronauts experience postflight orthostatic hypotension (6, 52) due, in part, to a diminished ability of the cardiovascular system to rapidly elevate peripheral vascular resistance (PVR) (1,2,8,36,52,53). It has been proposed that the diminished ability to elevate PVR following spaceflight may result from altered function of the afferent limb of the baroreceptors, central integration, sympathetic efferents, or end-organ responsiveness to sympathetic stimulation (8). Evidence for end-organ (vascular) hyporesponsiveness has been provided by Whitson et al. (54) and Levine et al. (27), who reported no difference in preflight vs. postflight PVR during orthostasis despite higher postflight levels of plasma catecholamine concentration and muscle sympathetic nerve activity. Similar reductions in vasoconstrictor responsiveness have been reported by investigators using prolonged bedrest (44, 46). Therefore, evidence suggests endorgan responsiveness to vasoconstrictor stimuli is diminished in humans following microgravity and bedrest deconditioning.In addition, orthostatic intol...

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Section: Fig 5 Representative Profiles Of the Vasoconstrictor Dynammentioning

confidence: 99%

Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca²⁺release mechanism

Colleran

Behnke

Wilkerson

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Besides controlling most of the mechanisms implicated in muscle development and regeneration, calcium is required in the proper functioning of smooth muscles cells, maintaining arteriolar tone [75], and myogenic constriction [76]. In skeletal muscle, contraction requires transient increases in intracellular calcium concentration [77].…”

Section: Introductionmentioning

confidence: 99%

Calcium's Role in Mechanotransduction during Muscle Development

Damm

Egli

2014

Cell Physiol Biochem

11,388

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Mechanotransduction is a process where cells sense their surroundings and convert the physical forces in their environment into an appropriate response. Calcium plays a crucial role in the translation of such forces to biochemical signals that control various biological processes fundamental in muscle development. The mechanical stimulation of muscle cells may for example result from stretch, electric and magnetic stimulation, shear stress, and altered gravity exposure. The response, mainly involving changes in intracellular calcium concentration then leads to a cascade of events by the activation of downstream signaling pathways. The key calcium-dependent pathways described here include the nuclear factor of activated T cells (NFAT) and mitogen-activated protein kinase (MAPK) activation. The subsequent effects in cellular homeostasis consist of cytoskeletal remodeling, cell cycle progression, growth, differentiation, and apoptosis, all necessary for healthy muscle development, repair, and regeneration. A deregulation from the normal process due to disuse, trauma, or disease can result in a clinical condition such as muscle atrophy, which entails a significant loss of muscle mass. In order to develop therapies against such diseased states, we need to better understand the relevance of calcium signaling and the downstream responses to mechanical forces in skeletal muscle. The purpose of this review is to discuss in detail how diverse mechanical stimuli cause changes in calcium homeostasis by affecting membrane channels and the intracellular stores, which in turn regulate multiple pathways that impart these effects and control the fate of muscle tissue.

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“…Ca 2+ plays an essential role in regulating blood vessel caliber or resistance, even in the absence of neurohumeral substances. 21 Increased Ca 2+ concentration has been shown to induce vasospasm in isolated cerebral arteries; vasospasm is amplified by lowering Mg 2+ concentration and alleviated by increasing it. 22 Hypomagnesemia causes increased cerebral vascular tension, whereas hypermagnesemia reverses vasospasm induced by hallucinogens, alcohol, serotonin, and potassium chloride.…”

Section: Camentioning

confidence: 99%

Action of magnesium sulfate in the treatment of preeclampsia-eclampsia.

Sadeh

1989

Stroke

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Recent evidence supports the concept that cerebral vasospasm is involved in the pathogenesis of eclampsia. Magnesium, which has a beneficial effect in eclampsia, may act by opposing calcium-dependent arterial constriction, thereby relieving vasospasm. Magnesium may also antagonize the increase in intracellular calcium concentration caused by ischemia and thus prevent cell damage and death. Magnesium might have a role in the treatment of cerebral vasospasm and ischemia, such as occurs in subarachnoid hemorrhage, ischemic stroke, and brain trauma. M agnesium sulfate has been advocated for treating toxemia of pregnancy since 1925,!-2 and despite controversy surrounding its mode of action, is still considered, especially in the US, to be the drug of choice for the control and prevention of eclamptic convulsions. A suggestion that magnesium sulfate controls convulsions by blocking peripheral neuromuscular transmission was based on animal studies by Hilmy and Somjen, 3 in which raised serum magnesium levels caused skeletal muscle paralysis but failed to cause anesthesia in humans. 4 The authors concluded that the brain is protected from hypermagnesemia by a barrier mechanism. However, many clinical studies and widely accumulated experiences have since shown that the antieclamptic effect is attained at serum levels of magnesium below those depressing neuromuscular transmission.5 Borges and Gucer 6 found magnesium sulfate to be effective in suppressing topical penicillin-induced epileptic activity in animals at serum levels similar to those reported to control seizures in eclamptic patients. However, the relevance of the experimental technique of these authors to eclampsia is uncertain. Donaldson 7 suggested that eclampsia is a hypertensive encephalopathy and argued against the use of magnesium in eclampsia because it is not an antihypertensive agent. However, eclampsia may be seen with blood pressure below the range that produces encephalopathy. Sibai et al 8 found no correlation between blood pressure and electroencephalographic (EEG) abnormality in preeclamptic-eclamptic patients or between Received February 6, 1989; accepted March 15, 1989. the percentage rise in mean arterial blood pressure from the last prenatal visit to the time of EEG recording and EEG changes. These findings do not suggest any direct relation between the degree of hypertension and eclamptic convulsions.

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Myogenic tone in isolated perfused resistance vessels from rats

Cited by 47 publications

References 1 publication

Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca²⁺release mechanism

Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca²⁺release mechanism

Calcium's Role in Mechanotransduction during Muscle Development

Action of magnesium sulfate in the treatment of preeclampsia-eclampsia.

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Myogenic tone in isolated perfused resistance vessels from rats

Cited by 47 publications

References 1 publication

Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca2+release mechanism

Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca2+release mechanism

Calcium's Role in Mechanotransduction during Muscle Development

Action of magnesium sulfate in the treatment of preeclampsia-eclampsia.

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Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca²⁺release mechanism

Simulated microgravity alters rat mesenteric artery vasoconstrictor dynamics through an intracellular Ca²⁺release mechanism