Vascular Smooth Muscle Membrane Potential and a Ouabain-Like Humoral Factor in One-Kidney, One-Clip Hypertension in Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 31s-33s ◽  
Author(s):  
Motilal B. Pamnani ◽  
David R. Harder ◽  
Stephen J. Huot ◽  
Howard J. Bryant ◽  
Francis A. Kutyna ◽  
...  
Keyword(s):  
Muscle Cells ◽  
Muscle Membrane ◽  
Hypertensive Rats ◽  
Transmembrane Potentials ◽  
Voltage Dependent ◽  
Smooth Muscle Membrane ◽  
Vascular Muscle Cells ◽  
Dependent Mechanism ◽  
Normotensive Control

1. Transmembrane potentials (Em) of vascular muscle cells in caudal arteries in vitro from one-kidney, one-clip hypertensive and one-kidney, sham-clipped normotensive rats were measured. 2. The Em recorded in hypertensive rats was significantly lower (depolarized) than that recorded in normotensive control rats. 3. Boiled plasma supernatants from hypertensive rats depolarized the muscle cells in normotensive caudal artery but had no effect on muscle cells in arteries from hypertensive rats. 4. Boiled plasma supernatants from normotensive control rats had no effect on the Em of either animal. 5. Ouabain depolarized muscle cells of the normotensive artery only and the magnitude of depolarization induced was nearly the same as that produced by the supernatant from the hypertensive animals. 6. These data suggest that a ouabain-like humoral substance may play a role in the pathophysiology of one-kidney, one-clip hypertension through a voltage-dependent mechanism.

Regulation of membrane potential and diameter by voltage-dependent K+ channels in rabbit myogenic cerebral arteries

1995 ◽  
Vol 269 (1) ◽  
pp. H348-H355 ◽  
Author(s):  
H. J. Knot ◽  
M. T. Nelson
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Transmural Pressure ◽  
Muscle Membrane ◽  
K Channels ◽  
Wide Range ◽  
Voltage Dependent

The hypothesis that voltage-dependent K+ channels are involved in the regulation of arterial smooth muscle membrane potential and blood vessel diameter was tested by examining the effects of inhibitors [4-aminopyridine (4-AP) and 3,4-diaminopyridine (3,4-DAP)] of voltage-dependent K+ channels on the membrane potential and diameter of pressurized small (100- to 300-microns diam) cerebral arteries from rabbit. In response to graded elevations in transmural pressure (20-100 mmHg), the membrane potential of smooth muscle cells in these arteries depolarized and the arteries constricted. 4-AP (1 mM) and 3,4-DAP (1 mM) depolarized cerebral arteries by 19 and 21 mV, respectively, when they were subjected to a transmural pressure of 80 mmHg. 3-Aminopyridine (3-AP, 1 mM), which is a relatively poor inhibitor of voltage-dependent K+ channels, depolarized smooth muscle cells in the arteries by 1 mV. 4-AP and 3,4-DAP constricted pressurized (to 80 mmHg) cerebral arteries. 3-AP had little effect on arterial diameter. 4-AP increased the arterial constriction to transmural pressure over a wide range of pressures (40-90 mmHg). The effects of 4-AP and 3,4-DAP on membrane potential and diameter were not prevented by inhibitors of calcium channels, calcium-activated K+ channels, ATP-sensitive K+ channels, inward rectifier K+ channels, blockers of adrenergic, serotonergic, muscarinic, and histaminergic receptors, or removal of the endothelium. These results suggest that voltage-dependent K+ channels are involved in the regulation of membrane potential and response of small cerebral arteries to changes in intravascular pressure.

In vitro synthesis of 32P-labelled phosphatidylinositol 4,5-bisphosphate and its hydrolysis by smooth muscle membrane-bound phospholipase C

1987 ◽  
Vol 145 (2) ◽  
pp. 673-679 ◽  
Author(s):  
Hans-Jürgen Fülle ◽  
Dieter Höer ◽  
Waltraud Lache ◽  
Walter Rosenthal ◽  
Günter Schultz ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Phospholipase C ◽  
Muscle Membrane ◽  
In Vitro Synthesis ◽  
Smooth Muscle Membrane ◽  
Membrane Bound

Physiological roles and properties of potassium channels in arterial smooth muscle

1995 ◽  
Vol 268 (4) ◽  
pp. C799-C822 ◽  
Author(s):  
M. T. Nelson ◽  
J. M. Quayle
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Katp Channels ◽  
Muscle Cells ◽  
Muscle Membrane ◽  
K Channel ◽  
Arterial Smooth Muscle ◽  
K Channels ◽  
Smooth Muscle Membrane

This review examines the properties and roles of the four types of K+ channels that have been identified in the cell membrane of arterial smooth muscle cells. 1) Voltage-dependent K+ (KV) channels increase their activity with membrane depolarization and are important regulators of smooth muscle membrane potential in response to depolarizing stimuli. 2) Ca(2+)-activated K+ (KCa) channels respond to changes in intracellular Ca2+ to regulate membrane potential and play an important role in the control of myogenic tone in small arteries. 3) Inward rectifier K+ (KIR) channels regulate membrane potential in smooth muscle cells from several types of resistance arteries and may be responsible for external K(+)-induced dilations. 4) ATP-sensitive K+ (KATP) channels respond to changes in cellular metabolism and are targets of a variety of vasodilating stimuli. The main conclusions of this review are: 1) regulation of arterial smooth muscle membrane potential through activation or inhibition of K+ channel activity provides an important mechanism to dilate or constrict arteries; 2) KV, KCa, KIR, and KATP channels serve unique functions in the regulation of arterial smooth muscle membrane potential; and 3) K+ channels integrate a variety of vasoactive signals to dilate or constrict arteries through regulation of the membrane potential in arterial smooth muscle.

Contracture and change in membrane potential produced by sodium removal in the dog trachea and bronchiole

1989 ◽  
Vol 67 (5) ◽  
pp. 2078-2086 ◽  
Author(s):  
Y. Ito ◽  
T. Inoue
Keyword(s):  
Membrane Potential ◽  
Mechanical Response ◽  
Muscle Tone ◽  
Smooth Muscles ◽  
Muscle Membrane ◽  
Tetraacetic Acid ◽  
Mechanical Responses ◽  
Sodium Removal ◽  
Voltage Dependent ◽  
Smooth Muscle Membrane

Mechanical responses and changes in membrane potential induced by Na removal were investigated in dog tracheal and bronchiolar smooth muscles. In both muscles, reduction of the external Na concentration ([Na]o) to less than 70 mM produced a sustained contracture, dose dependently. The relative amplitude of the Na-free contracture was greater than that induced by excess [K]o in the trachealis. Readmission of 1-10 mM Na, after exposure to Na-free solution, relaxed the contracture evoked by Na removal, and the degree of relaxation was dependent on [Na] readmitted. In the absence of both Na and Ca, some tension remained, and readmission of Ca increased the muscle tone. Even after pretreatment with Ca-free ethylene glycol-bis (beta-aminoethylether)-N,N,N,N′-tetraacetic acid- (0.2 mM) containing solution for 30 min, removal of Na caused some mechanical response in both muscles. D 600 (10(-7) to 10(-4) M), a blocker of voltage-dependent Ca2+ influx, suppressed the response to Na removal, but 10(-4) M D 600 did not completely block the contracture. Na removal depolarized the smooth muscle membrane to a greater extent in the bronchiole than in the trachealis. It was concluded that an increase in Ca permeability across the membrane and inhibition of the Na-Ca exchange mechanism in the absence of Na are responsible for the generation of Na-free contracture in both muscles.

A novel mechanism for vasoconstrictor action of 8-isoprostaglandin F2α on retinal vessels

1998 ◽  
Vol 274 (5) ◽  
pp. R1406-R1416 ◽  
Author(s):  
Isabelle Lahaie ◽  
Pierre Hardy ◽  
Xin Hou ◽  
Haroutioun Hasséssian ◽  
Pierre Asselin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Retinal Vessels ◽  
Thromboxane Receptor ◽  
Voltage Dependent ◽  
Thromboxane Receptor Antagonist

Using a video-imaging technique, we characterized the effects of 8-isoprostaglandin F2α(8-iso-PGF2α) on retinal vasculature from piglets. 8-Iso-PGF2α potently contracted (EC50 = 5.9 ± 0.5 nM) retinal vessels. These effects were completely antagonized by the cyclooxygenase inhibitor indomethacin, the thromboxane synthase blocker CGS-12970, the thromboxane receptor antagonist L-670596, and the putative inhibitor of the non-voltage-dependent receptor-operated Ca2+ pathway SKF-96365; constrictor effects of 8-iso-PGF2α were also partly attenuated by the ETA-receptor blocker BQ-123 and an inhibitor of endothelin-converting enzyme, phosphoramidon, but was negligibly affected by the L-type voltage-gated Ca2+ channel blocker nifedipine. Correspondingly, 8-iso-PGF2αelicited endothelin release from retinal preparations, which was markedly reduced by SKF-96365. 8-Iso-PGF2α also increased thromboxane production in the retina and cultured endothelial cells, but not on retinovascular smooth muscle cells; these effects of 8-iso-PGF2α were blocked by indomethacin, CGS-12970, SKF-96365, and EGTA, but not by nifedipine. 8-Iso-PGF2α also increased Ca2+ transients in retinal endothelial cells, which were inhibited by SKF-96365 and EGTA, but not by nifedipine, whereas in smooth muscle cells U-46619, but not 8-iso-PGF2α, stimulated a rise in Ca2+ transients. Finally, H2O2+ FeCl2 (in vitro) and anoxia followed by reoxygenation (in vivo) stimulated formation of 8-iso-PGF2α in the retina. In conclusion, 8-iso-PGF2α-induced retinal vasoconstriction is mediated by cyclooxygenase-generated formation of thromboxane and, to a lesser extent, by endothelin after Ca2+ entry into cells, possibly through receptor-operated channels. Retinal vasoconstriction to 8-isoprostanes might play a role in the genesis of ischemic retinopathies.

scholarly journals Progesterone regulation of vascular thromboxane A2receptors in rhesus monkeys

2001 ◽  
Vol 281 (4) ◽  
pp. H1498-H1507 ◽  
Author(s):  
Richard D. Minshall ◽  
Dusan Pavcnik ◽  
Perry V. Halushka ◽  
Kent Hermsmeyer
Keyword(s):  
Rhesus Monkeys ◽  
Carotid Arteries ◽  
Muscle Cells ◽  
Maximum Density ◽  
Vascular Muscle ◽  
Progesterone Treatment ◽  
Vascular Muscle Cells

We hypothesized that progesterone regulates thromboxane A2 receptor (TxA2R) density in primate vascular muscle and that TxA2R density correlates with coronary reactivity in vivo and in vitro. Reactivity to serotonin + U-46619 was determined by angiography in surgically postmenopausal [ovariectomized (Ovx)] rhesus monkeys without progesterone replacement and after 2-wk progesterone treatment (1–2 ng/ml). In untreated Ovx animals, 100 μmol/l serotonin + 1 μmol/l U-46619 (syringe concentrations) provoked vasospasm-like constrictions in six of six monkeys; zero of six progesterone-treated monkeys developed vasospasms. Sustained Ca2+ responses in vascular muscle cells isolated from Ovx coronaries (208 ± 63% of basal 20 min after stimulation) treated with serotonin + U-46619 contrasted with transient Ca2+ responses (143 ± 18% of basal and decreasing 5 min after stimulation) in progesterone-treated monkeys. The maximum density of [1 S-(1 I,2 J(5 Z),3 I(1 E,3 R*),4 I)]-7-[3-(3-hydroxy-4-(4′-[125I]iodophenoxy)- 1-butenyl)-7-oxabicyclo[2.2.1]heptan-2-yl]-5-heptenoic acid ([125I]-BOP) binding was greater ( P< 0.01) in carotid arteries and aortic membranes from Ovx (109 ± 11 fmol/mg) compared with progesterone-treated (43 ± 15 fmol/mg) monkeys. TxA2R immunolabeling revealed greater coronary TxA2R labeling in Ovx compared with progesterone-treated monkeys. The results suggest that progesterone can decrease arterial TxA2R in Ovx monkeys.

De novo formation of vascular receptors for bradykinin

1978 ◽  
Vol 56 (4) ◽  
pp. 674-677 ◽  
Author(s):  
D. Regoli ◽  
F. Marceau ◽  
J. Barabé
Keyword(s):  
Actinomycin D ◽  
De Novo ◽  
Jugular Vein ◽  
The Other ◽  
Muscle Membrane ◽  
Mesenteric Vein ◽  
Stable Component ◽  
Different Types ◽  
Smooth Muscle Membrane

Two different types of receptors for bradykinin have been found in isolated veins of the rabbit. The first receptor is a stable component of the smooth muscle membrane and it is found in the jugular vein, while the second is generated de novo during incubation in vitro and it is present in the mesenteric vein. Actinomycin D and cycloheximide block the generation of receptors in the mesenteric vein, without exerting any action either on receptors for other agonists (e.g. substance P) in the same tissue, or on the other receptor for bradykinin in the jugular vein.

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