Vascular smooth muscle calcium waves in isolated arterioles : interactions between intraluminal pressure and intracellular calcium handling

2010 ◽  
Author(s):  
◽  
Srikanth Reddy Ella
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Physiological Role ◽  
Wave Activity ◽  
Calcium Handling ◽  
Intraluminal Pressure ◽  
General Level ◽  
Control Element ◽  
Myogenic Response ◽  
Ip3 Receptors

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Arterioles, an important control element in the circulatory system regulate blood flow in part though a phenomenon known as the 'Myogenic Response'. Myogenic response of small vessels is their ability to constrict in response to increase in intraluminal pressure or conversely dilate in response to a reduction in pressure. Calcium (Ca[superscript 2+]) is an important and essential signaling element for myogenic constriction. Apart from steady elevations in smooth muscle intracellular Ca[superscript 2+] in response to agonists or intraluminal pressure, several local and temporal Ca[superscript 2+] events such as sparks, waves, flashes also exist. These temporal Ca[superscript 2+] events are differentially regulated in several vascular beds and are poorly understood. Therefore, the current project aimed to understand the effects of intraluminal pressure on arteriolar vascular smooth muscle Ca+ waves in rat cremaster muscle arterioles. The project aimed to investigate the mechanisms underlying the generation of Ca[superscript 2+] waves and postulate a possible physiological role for the Ca[superscript 2+] waves. Increases in intraluminal pressure increased the Ca[superscript 2+] wave activity, described by the number of cells exhibiting Ca[superscript 2+] waves and their frequency. Ca[superscript 2+] waves occurred due to the activation of the IP3 receptors present on the sarcoplasmic reticulum in the cells. The presence of Ca[superscript 2+] waves in the smooth muscle cells provided a general level of vascular activation, wherein the wave activity is modulated to change the temporal responses of the myogenic behaviour. Elimination of Ca[superscript 2+] waves delayed the myogenic constriction, while increased Ca[superscript 2+] wave activity fastened the myogenic constriction.--From public.pdf

Modulation of myogenic responsiveness by CO2 in rat diaphragmatic arterioles: role of the endothelium

1997 ◽  
Vol 272 (3) ◽  
pp. H1419-H1425 ◽  
Author(s):  
M. M. Nagi ◽  
M. E. Ward
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Intraluminal Pressure ◽  
Negative Slope ◽  
Myogenic Tone ◽  
Internal Diameter ◽  
Myogenic Response ◽  
Inhibitory Mechanisms ◽  
Flow Through

The effect of hypercapnia on the myogenic response was determined in arterioles (80- to 100-microm internal diameter) isolated from the diaphragms of rats killed by decapitation. All arterioles were exposed to step changes in intraluminal pressure over a range of 10-200 mmHg and had no flow through their lumen. In five separate groups of vessels (n = 7 per group), PCO2 of the superfusing buffer was adjusted to 40, 60, 80, 90, or 100 mmHg. In three further groups of vessels (n = 7 per group), the endothelium was removed by low-pressure air perfusion (2 ml at 20 mmHg) and PCO2 of the superfusing buffer was adjusted to 40, 80, or 100 mmHg. In endothelium-intact vessels, increasing PCO2 to 80 mmHg enhanced the myogenic response, as reflected by a negative slope of the pressure-diameter relationship (slope = -0.164 +/- 0.03 vs. 0.004 +/- 0.02 for vessels at PCO2 = 40 mmHg, P < 0.05). With a PCO2 of 100 mmHg, dilation accompanied increasing intraluminal pressure and the slope of the pressure-diameter curve was positive (0.154 +/- 0.03, P < 0.05 for difference from vessels at PCO2 = 40 mmHg). In deendothelialized vessels, the curve was shifted upward in a parallel manner during exposure to increased PCO2 levels. Moderate hypercapnia (PCO2 < 80 mmHg) elicits endothelium-dependent enhancement of myogenic tone. Severe hypercapnia (PCO2 > 80 mmHg) inhibits myogenic tone through a direct effect on vascular smooth muscle and through endothelium-dependent inhibitory mechanisms.

Length-tension relationship of vascular smooth muscle in single arterioles

1989 ◽  
Vol 256 (3) ◽  
pp. H630-H640 ◽  
Author(s):  
M. J. Davis ◽  
R. W. Gore
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Wall Stress ◽  
Physiological Saline ◽  
Intraluminal Pressure ◽  
Cheek Pouch ◽  
Hamster Cheek Pouch ◽  
Longitudinal Response ◽  
Physiological Saline Solution ◽  
Relationship Of

Longitudinal response gradients in the microcirculation may in part be explained in terms of the length-tension relationship of vascular smooth muscle at different points along the vascular tree. To test this hypothesis, four branching orders of arterial vessels (20-80 microns ID) were dissected from the hamster cheek pouch and cannulated with concentric micropipettes. Intraluminal pressure was monitored with a servo-null micropipette, and arteriolar dimensions were measured using a videomicrometer. All arterioles developed spontaneous tone in physiological saline solution. Pressure-diameter curves were recorded for maximally activated vessels and for passive vessels. Maximal active wall tension varied nearly threefold, but maximal active medial wall stress (approximately 4 x 10(6) dyn/cm2) varied only approximately 20% between the different vessel orders. These data support the concept that smooth muscle cells from vessels of different sizes are mechanically similar but do not completely explain the longitudinal response gradients reported in the cheek pouch microcirculation. An analysis of the effect of arteriolar wall buckling suggests that the luminal folds that develop at short vessel radii may broaden the peak of the active stress-length curve and extend the pressure range over which arterioles are most sensitive to physical and chemical stimuli.

scholarly journals Remanent cell traction force in renal vascular smooth muscle cells induced by integrin-mediated mechanotransduction

2013 ◽  
Vol 304 (4) ◽  
pp. C382-C391 ◽  
Author(s):  
Lavanya Balasubramanian ◽  
Chun-Min Lo ◽  
James S. K. Sham ◽  
Kay-Pong Yip
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Resistance ◽  
Vascular Smooth Muscle Cells ◽  
Traction Force ◽  
Muscle Cells ◽  
Myogenic Response ◽  
Cell Traction ◽  
Renal Vascular

It was previously demonstrated in isolated renal vascular smooth muscle cells (VSMCs) that integrin-mediated mechanotransduction triggers intracellular Ca2+ mobilization, which is the hallmark of myogenic response in VSMCs. To test directly whether integrin-mediated mechanotransduction results in the myogenic response-like behavior in renal VSMCs, cell traction force microscopy was used to monitor cell traction force when the cells were pulled with fibronectin-coated or low density lipoprotein (LDL)-coated paramagnetic beads. LDL-coated beads were used as a control for nonintegrin-mediated mechanotransduction. Pulling with LDL-coated beads increased the cell traction force by 61 ± 12% (9 cells), which returned to the prepull level after the pulling process was terminated. Pulling with noncoated beads had a minimal increase in the cell traction force (12 ± 9%, 8 cells). Pulling with fibronectin-coated beads increased the cell traction force by 56 ± 20% (7 cells). However, the cell traction force was still elevated by 23 ± 14% after the pulling process was terminated. This behavior is analogous to the changes of vascular resistance in pressure-induced myogenic response, in which vascular resistance remains elevated after myogenic constriction. Fibronectin is a native ligand for α5β1-integrins in VSMCs. Similar remanent cell traction force was found when cells were pulled with beads coated with β1-integrin antibody (Ha2/5). Activation of β1-integrin with soluble antibody also triggered variations of cell traction force and Ca2+ mobilization, which were abolished by the Src inhibitor. In conclusion, mechanical force transduced by α5β1-integrins triggered a myogenic response-like behavior in isolated renal VSMCs.

Failure of cdc2 promoter activation and G2/M transition by ANG II and AVP in vascular smooth muscle cells

1999 ◽  
Vol 277 (2) ◽  
pp. H515-H523 ◽  
Author(s):  
Nobuya Fujita ◽  
Yusuke Furukawa ◽  
Naoki Itabashi ◽  
Yasushi Tsuboi ◽  
Michio Matsuda ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Physiological Role ◽  
Muscle Cells ◽  
Nuclear Antigen ◽  
Ang Ii ◽  
Promoter Activation ◽  
Mrna Induction

The physiological role of the vasoconstrictive hormones arginine vasopressin (AVP) and angiotensin II (ANG II) in the development of vascular hyperplasia is still unclear. We examined the effects of these hormones on cell cycle regulation of cultured rat vascular smooth muscle cells (VSMC). AVP and ANG II were able to induce G1/S transition and DNA synthesis in serum-starved quiescent VSMC but failed to promote further progression into G2/M phases. AVP and ANG II enhanced the expression and activity of cdk2, cyclin E, and proliferating cell nuclear antigen but did not induce expression of cdc2/cyclin B complex, a critical regulator of G2/M transition. The failure of cdc2 mRNA induction was found to be caused by a defect in cdc2 promoter activation. Binding of free E2F-1 to the cdc2 promoter did not occur in hormone-treated VSMC, which may account for the defective induction of cdc2. The absence of cdc2 promoter activation and G2/M transition may be important for the prevention of hyperplasia under physiological conditions but underlies the hypertrophy of VSMC.

scholarly journals Altered Calcium Handling Between Healthy And Atherosclerotic Vascular Smooth Muscle

2009 ◽  
Vol 96 (3) ◽  
pp. 117a ◽  
Author(s):  
Marie-Ann Ewart ◽  
Susan Currie ◽  
John G. McCarron ◽  
Simon Kennedy
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Calcium Handling

Dysfunction of calcium handling by smooth muscle in hypertension

1985 ◽  
Vol 63 (4) ◽  
pp. 366-374 ◽  
Author(s):  
C. Y. Kwan
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cardiovascular System ◽  
Control Systems ◽  
Active Transport ◽  
Smooth Muscles ◽  
Peripheral Resistance ◽  
Calcium Handling ◽  
Experimental Hypertension

Dysfunction of ion handling, including binding and fluxes (passive and active transport) of physiologically important ions such as potassium, sodium, calcium, and magnesium, by vascular smooth muscle cell membranes has repeatedly been reported to be associated with the pathophysiology of hypertension. The specific purpose of this review is to summarize and evaluate the evidence for alterations of calcium ion (Ca2+) handling by vascular smooth muscle in various forms of hypertension in the animal model on the basis that regulation of cytoplasmic Ca2+ concentration is a complex and yet vitally important process for a normal function of vascular smooth muscle and that derangement of such a regulation may result in excessive retention of cytoplasmic Ca2+, contribute toward increase of total peripheral resistance, and ultimately lead to elevation of blood pressure. Emphasis is placed upon the consideration of the usefulness of the subcellular membrane fractionation technique in studies of binding and transport of Ca2+ by vascular and nonvascular smooth muscle membranes from genetic as well as experimental hypertensive rats. The limitations of the interpretation of data using such an approach are also considered. Decreased active transport of Ca2+ across isolated plasma membrane vesicles from large and small arteries occurs in several but not all forms of hypertension. This membrane abnormality also occurs in nonvascular smooth muscles and other tissues or cells not confined to the cardiovascular system in genetic hypertension, but not in experimental hypertension. A hypothesis of general membrane defects in spontaneous hypertension is proposed. Since the long-term regulation of blood pressure at the sites of resistant blood vessels is under finely integrated and interacting control systems, namely, the myogenic, neurogenic, and humoral controls, involving many tissues or cells not necessarily confined to cardiovascular system, membrane abnormalities in Ca2+ handling by tissues in each or a combination of these control systems can conceivably lead to hypertension.

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