Angiotensin II Upregulates the Expression of L‐type Calcium Channels, Inositol Trisphosphate Receptors and Ryanodine Receptors in Rat Mesenteric Vascular Bed

Calcium plays an important role in the regulation of meiotic maturation in mammalian oocytes. In the present study, mycotoxin cyclopiazonic acid (CPA), an inhibitor of calcium-dependent ATPases, was used to mobilize intracellular calcium deposits in growing pig oocytes, which had not attained full meiotic competence and in which maturation is thus spontaneously blocked at the metaphase I stage. CPA treatment significantly increased the ratio of growing oocytes that are able to overcome the spontaneously occurring metaphase I block to complete their maturation at the metaphase II stage. CPA treatment of a least 2 hours’ duration is necessary to overcome the metaphase I block in growing oocytes. A similar effect upon release from the spontaneous meiotic block at the metaphase I stage was observed after treatment of growing pig oocytes with thapsigargin, another inhibitor of endogenous calcium-dependent ATPases. Numerous calcium deposits in vacuoles, the mitochondria and on the surface of yolk granules in growing pig oocytes were observed. CPA treatment is able to mobilize calcium from the mitochondria, but deposits in vacuoles and deposits on the surface of yolk granules seem to remain intact after CPA treatment. A microinjection of heparin, which is known to bind with the inositol trisphosphate receptors, significantly decreased the ratio of CPA-treated growing oocytes overcoming the block at the metaphase I stage. This indicates that CPA might mobilize calcium in growing pig oocytes through inositol trisphosphate receptors. On the other hand, a microinjection of procaine or a microinjection of ruthenium red, both inhibitors of ryanodine receptors, did not prevent the overcoming of the metaphase I block, induced by CPA treatment. The calcium channel blocker, verapamil, significantly reduces the proportion of CPA-treated growing oocytes that overcome the metaphase I block. This indicates that the influx of calcium from extracellular sources is necessary to over-come the metaphase I block. The calmodulin inhibitors ophiobolin A and W7 also reduce the proportion of CPA-treated growing oocytes overcoming the metaphase I block.

Download Full-text

Faculty Opinions recommendation of Bile acids induce Ca2+ release from both the endoplasmic reticulum and acidic intracellular calcium stores through activation of inositol trisphosphate receptors and ryanodine receptors.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1048146.500061 ◽

2006 ◽

Author(s):

Antony Galione

Keyword(s):

Endoplasmic Reticulum ◽

Intracellular Calcium ◽

Bile Acids ◽

Inositol Trisphosphate ◽

Ryanodine Receptors ◽

Calcium Stores ◽

Inositol Trisphosphate Receptors ◽

Intracellular Calcium Stores

Download Full-text

Potentiation of Pressor Effects of Noradrenaline and Potassium Ions in the Rat Mesenteric Arteries by Physiological Concentrations of Angiotensin II: Effects of Prostaglandin E2 and Cortisol

Clinical Science ◽

10.1042/cs0530233 ◽

1977 ◽

Vol 53 (3) ◽

pp. 233-239 ◽

Cited By ~ 2

Author(s):

K. Kondo ◽

M. S. Manku ◽

D. F. Horrobin ◽

R. Boucher ◽

J. Genest

Keyword(s):

Angiotensin Ii ◽

Prostaglandin E2 ◽

Potassium Chloride ◽

Prostaglandin Synthesis ◽

Mesenteric Arteries ◽

Potassium Ions ◽

Vascular Bed ◽

Vasoconstrictor Response ◽

Mesenteric Vascular Bed

1. In the perfused rat mesenteric vascular bed, the effects of angiotensin II, cortisol and prostaglandin E2 on the vascular responses to noradrenaline or potassium chloride were studied. 2. Angiotensin II in subpressor concentrations potentiated the vasoconstrictor response to noradrenaline and potassium chloride. This effect of angiotensin II was inhibited in the presence of indomethacin and prostaglandin E2. 3. Cortisol in physiological concentrations inhibited the potentiating effect of angiotensin II. 4. Prostaglandin E2 enhanced the vasoconstrictor response to noradrenaline. This effect was not abolished by cortisol. 5. These results suggest that some actions of angiotensin II and cortisol in vivo are mediated by the regulation of prostaglandin synthesis or release.

Download Full-text

The role of bradykinin, AT2 and angiotensin 1-7 receptors in the EDRF-dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat

British Journal of Pharmacology ◽

10.1038/sj.bjp.0705669 ◽

2004 ◽

Vol 141 (5) ◽

pp. 860-866 ◽

Cited By ~ 33

Author(s):

R Soares De Moura ◽

A C Resende ◽

A F Emiliano ◽

T Tano ◽

A C Mendes-Ribeiro ◽

...

Keyword(s):

Angiotensin Ii ◽

Vasodilator Effect ◽

Vascular Bed ◽

Mesenteric Vascular Bed

Download Full-text

Calcium Transients in 1B5 Myotubes Lacking Ryanodine Receptors Are Related to Inositol Trisphosphate Receptors

Journal of Biological Chemistry ◽

10.1074/jbc.m100118200 ◽

2001 ◽

Vol 276 (25) ◽

pp. 22868-22874 ◽

Cited By ~ 37

Author(s):

Manuel Estrada ◽

Cesar Cárdenas ◽

José L. Liberona ◽

M. Angélica Carrasco ◽

Gregory A. Mignery ◽

...

Keyword(s):

Inositol Trisphosphate ◽

Ryanodine Receptors ◽

Calcium Transients ◽

Inositol Trisphosphate Receptors

Download Full-text

Ca2+ waves require sequential activation of inositol trisphosphate receptors and ryanodine receptors in pancreatic acini

Gastroenterology ◽

10.1053/gast.2002.30982 ◽

2002 ◽

Vol 122 (2) ◽

pp. 415-427 ◽

Cited By ~ 74

Author(s):

M.Fatima Leite ◽

Angela D. Burgstahler ◽

Michael H. Nathanson

Keyword(s):

Inositol Trisphosphate ◽

Ryanodine Receptors ◽

Pancreatic Acini ◽

Inositol Trisphosphate Receptors ◽

Sequential Activation

Download Full-text

Vasoplegia in sepsis depends on the vascular system, vasopressor, and time-point: a comparative evaluation in vessels from rats subjected to the cecal ligation puncture model

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2015-0514 ◽

2016 ◽

Vol 94 (11) ◽

pp. 1227-1236 ◽

Cited By ~ 1

Author(s):

Angélica K. Bernardelli ◽

Rita de C.V. de A.F. Da Silva ◽

Thiago Corrêa ◽

José Eduardo Da Silva-Santos

Keyword(s):

Angiotensin Ii ◽

Carotid Arteries ◽

Vascular System ◽

Cecal Ligation ◽

Mesenteric Arteries ◽

Vasoactive Agent ◽

Vascular Bed ◽

Time Period ◽

Cecal Ligation Puncture ◽

Mesenteric Vascular Bed

We evaluated the effects of phenylephrine, norepinephrine, angiotensin II, and vasopressin in mesenteric, renal, carotid, and tail arteries, and in perfused mesenteric vascular bed from rats subjected to the cecal ligation and puncture (CLP) model of sepsis. Phenylephrine and angiotensin II were less efficacious in mesenteric arteries from the CLP 6 h and CLP 18 h groups than in preparations from non-septic animals, but no differences were found for norepinephrine and vasopressin between the preparations. In renal arteries, none of the vasoconstrictors had impaired activity in the CLP groups. Nonetheless, carotid arteries from the CLP 18 h group presented reduced reactivity to all vasoconstrictors tested, but only phenylephrine and norepinephrine had their effects reduced in carotid arteries from the CLP 6 h group. Despite the reduced responsiveness to phenylephrine, tail arteries from septic rats were hyperreactive to vasopressin and norepinephrine at 6 h and 18 h after the CLP surgery, respectively. The mesenteric vascular bed from CLP groups was hyporeactive to phenylephrine, norepinephrine, and angiotensin II, but not to vasopressin. The vascular contractility in sepsis varies from the well-described refractoriness, to unaltered or even hyperresponsiveness to vasoconstrictors, depending on the vessel, the vasoactive agent, and the time period evaluated.

Download Full-text