scholarly journals BDNF contributes to angiotensin II-mediated reductions in peak voltage-gated K+current in cultured CATH.a cells

2015 ◽  
Vol 3 (11) ◽  
pp. e12598 ◽  
Author(s):  
Bryan K. Becker ◽  
Han-jun Wang ◽  
Changhai Tian ◽  
Irving H. Zucker
Keyword(s):  
Angiotensin Ii ◽  
Peak Voltage ◽  
Voltage Gated ◽  
K Current ◽  
Cath.A Cells

scholarly journals Suppression of the delayed rectifier type of voltage gated K+ outward current in megakaryocytes from patients with myelogenous leukemias

Blood ◽  
1995 ◽  
Vol 86 (3) ◽  
pp. 1043-1055 ◽  
Author(s):  
L Kapural ◽  
MB Feinstein ◽  
F O'Rourke ◽  
A Fein
Keyword(s):  
Outward Current ◽  
Myelogenous Leukemia ◽  
Delayed Rectifier ◽  
Contributory Factor ◽  
Voltage Gated ◽  
Acute Myelogenous ◽  
K Current ◽  
Malignant State ◽  
Erythroleukemia Cell ◽  
Normal Human

Abstract In normal human megakaryocytes, we identified a delayed rectifier type of voltage-gated outward K+ current (DRK). In two human megakaryoblastic tumor cell lines (DAMI, CHRF-288–11) and the human erythroleukemia cell line (HEL) the DRK current was not detected. To determine if the absence of the DRK current in the tumor cells is the result of the underlying malignant state, we examined megakaryocytes from myelogenous leukemia patients. In 24 of 29 megakaryocytes from the myelogenous leukemia patients, the DRK current was greatly suppressed, whereas in the remaining 5 megakaryocytes a normal large amplitude DRK current was present. We had the opportunity to reexamine megakaryocytes from a patient with acute promyelocytic leukemia (M3), after chemotherapy. Whereas the DRK current was suppressed before treatment, the current reappeared after chemotherapy. Exposure to the adenylate cyclase activator, forskolin, caused the appearance of a voltage-gated outward current in the megakaryocytes of patients with acute myelogenous leukemia. This finding suggests either that the channels underlying the DRK current are present but somehow suppressed in megakaryocytes from these patients or that forskolin induces a different voltage-gated outward current. We suggest that the megakaryocytes from the myelogenous leukemia patients with suppressed DRK current are abnormal, whereas the others may be normal megakaryocytes. The suppression of the DRK current may be a contributory factor to the dysregulation of thrombopoiesis (Zittoun et al: Semin Hop Paris 44:183, 1968 and Rabellino et al: Blood 63:615, 1984) in myelogenous leukemias.

Angiotensin II type 1 receptor modulation of neuronal K+ and Ca2+ currents: intracellular mechanisms

1996 ◽  
Vol 271 (1) ◽  
pp. C154-C163 ◽  
Author(s):  
C. Sumners ◽  
M. Zhu ◽  
C. H. Gelband ◽  
P. Posner
Keyword(s):  
Angiotensin Ii ◽  
At1 Receptor ◽  
Ang Ii ◽  
Receptor Modulation ◽  
Kinase C ◽  
Intracellular Messengers ◽  
Voltage Dependent ◽  
K Current ◽  
Stimulation Of

Angiotensin II (ANG II) elicits an ANG II type 1 (AT1) receptor-mediated decrease in voltage-dependent K+ current (Ik) and an incrase in voltage-dependent Ca2+ current (ICa) in neurons cocultured from newborn rat hypothalamus and brain stem. Modulation of these currents by ANG II involves intracellular messengers that result from an AT1 receptor-mediated stimulation of phosphoinositide hydrolysis. For example, the effects of ANG II on IK and ICa were abolished by phospholipase C antagonists. The reduction in IK produced by ANG II was attenuated by either protein kinase C (PKC) antagonists or by chelation of intracellular Ca2+. By contrast, PKC antagonism abolished the stimulatory effect of ANG II on ICa. Superfusion of the PKC activator phorbol 12-myristate 13-acetate produced effects on IK and ICa similar to those observed after ANG II. Furthermore, intracellular application of inositol 1,4,5-trisphosphate (IP3) elicited a significant reduction in IK. This suggests that the AT1 receptor-mediated changes in neuronal K+ and Ca2+ currents involve PKC (both IK and ICa) and IP3 and/or intracellular Ca2+ (IK).

Effect of a 14-day hindlimb suspension on cytosolic Ca2+ concentration in rat portal vein myocytes

1997 ◽  
Vol 273 (6) ◽  
pp. H2867-H2875 ◽  
Author(s):  
Jean-Luc Morel ◽  
François-Xavier Boittin ◽  
Guillaume Halet ◽  
Serge Arnaudeau ◽  
Chantal Mironneau ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sarcoplasmic Reticulum ◽  
Portal Vein ◽  
Complete Recovery ◽  
Hindlimb Suspension ◽  
Patch Clamp Technique ◽  
Voltage Gated ◽  
Rat Portal Vein ◽  
Inositol 1,4,5 Trisphosphate

Effects of a 14-day hindlimb suspension were examined on increases in cytosolic Ca2+ concentration ([Ca2+]i) evoked by vasoactive compounds and on Ca2+ channels in rat portal vein myocytes. The maximal increases in [Ca2+]ielicited by caffeine, norepinephrine, and angiotensin II were reduced by 30–50% in suspended rats, and complete recovery was obtained 4 days after suspension removal. In contrast, voltage-gated Ca2+ channels were unaffected by hindlimb suspension. Using both confocal microscopy and the patch-clamp technique, we measured local increases in [Ca2+]iwhich corresponded to activation of a small number of ryanodine-sensitive Ca2+-release channels (Ca2+ sparks) andd- myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]-gated Ca2+ channels. After hindlimb suspension, these local Ca2+events, as well as the Ca2+sensitivity of ryanodine-sensitive Ca2+ release channels, remained unchanged. In contrast, the propagated Ca2+ responses (Ca2+ waves) were significantly reduced in parallel with a noticeable inhibition of [3H]ryanodine binding to vascular membranes. Taken together, these results suggest that inhibition of the vasoconstrictor-induced increases in [Ca2+]iduring long-term suspension may be related to a reduction of the number of functional ryanodine-sensitive and Ins(1,4,5)P3-gated channels in the sarcoplasmic reticulum of rat portal vein myocytes.

Sign in / Sign up

Export Citation Format

Share Document