Regulation of Na-K-Cl cotransport in endothelial cells by atrial natriuretic factor

1989 ◽  
Vol 257 (1) ◽  
pp. C36-C44 ◽  
Author(s):  
M. E. O'Donnell
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Response ◽  
Atrial Natriuretic Factor ◽  
Second Messengers ◽  
Vasoactive Agents ◽  
Cyclic Monophosphate ◽  
Natriuretic Factor ◽  
Endothelial Cell Response ◽  
Atrial Natriuretic

Many vasoactive agents have been shown to bind to specific receptors on endothelial cells. Among these is atrial natriuretic factor (ANF). Binding of ANF to endothelial cells has been demonstrated to induce elevation of intracellular guanosine 3',5'-cyclic monophosphate (cGMP). Other vasoactive agents have been shown to cause elevation of intracellular adenosine 3',5'-cyclic monophosphate (cAMP), Ca, and diacylglycerol. However, the endothelial cell response that occurs subsequent to elevation of cGMP or other second messengers is not well understood. Recently, endothelial cells have been shown to possess a Na-K-Cl cotransport system that is stimulated by vasopressin and bradykinin and inhibited by isoproterenol. Thus it is possible that modulation of Na-K-Cl cotransport may play a role in the endothelial cell response to second messengers that are elevated by ANF and other vasoactive agents. This possibility was examined in the present study by evaluating the effects of a variety of vasoactive agents and their second messengers on endothelial cell Na-K-Cl cotransport. Cotransport was assessed as bumetanide-sensitive K influx in cultured bovine aortic endothelial cells. A number of agents were found to reduce Na-K-Cl cotransport, including ANF, acetylcholine, histamine, and norepinephrine. Cotransport was found to be stimulated by angiotensin II, as well as vasopressin and bradykinin. Na-K-Cl cotransport was also inhibited by elevation of intracellular cGMP or cAMP or by treatment of the cells with phorbol ester to activate protein kinase C. However, A23187-induced elevation of intracellular Ca caused stimulation of Na-K-Cl cotransport.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals CHARACTERIZATION OF ATRIAL NATRIURETIC FACTOR RECEPTORS IN ADRENAL CORTEX, VASCULAR SMOOTH MUSCLE AND ENDOTHELIAL CELLS BY AFFINITY LABELING

1986 ◽  
Vol 7 (1) ◽  
pp. 35-38 ◽  
Author(s):  
MASASHI SHINJO ◽  
YUKIO HIRATA ◽  
HIROMI HAGIWARA ◽  
FUMIAKI AKIYAMA ◽  
KAZUO MURAKAMI ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Adrenal Cortex ◽  
Atrial Natriuretic Factor ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Carbidopa Does Not Affect the Renal Response to Atrial Natriuretic Factor in Man

1989 ◽  
Vol 77 (3) ◽  
pp. 281-285 ◽  
Author(s):  
Helen M. Lewis ◽  
M. R. Wilkins ◽  
M. J. Kendall ◽  
M. R. Lee
Keyword(s):  
Atrial Natriuretic Factor ◽  
Similar Increase ◽  
Double Blind ◽  
Renal Response ◽  
Cyclic Monophosphate ◽  
Natriuretic Factor ◽  
Urinary Dopamine ◽  
Renal Dopamine ◽  
Factor Concentration ◽  
Atrial Natriuretic

1. The dependence of atrial natriuretic factor on renal dopamine for its renal effects in man was examined in 10 healthy volunteers using the dopa decarboxylase inhibitor carbidopa. 2. Each volunteer attended on two occasions, and received an infusion of atrial natriuretic factor (4 pmol min−1 kg−1) for 60 min after pretreatment with either placebo or carbidopa orally. These were administered in random, double-blind fashion. 3. A similar increase in plasma atrial natriuretic factor concentration was seen after atrial natriuretic factor infusion on both visits. 4. Infusion of atrial natriuretic factor produced a small unsustained rise in urinary dopamine excretion. This increase in urinary dopamine excretion was blocked by carbidopa with no effect on the natriuresis. 5. Urinary guanosine 3′:5′-cyclic monophosphate excretion increased in response to the atrial natriuretic factor infusion whether placebo or carbidopa was given. Guanosine 3′:5′-cyclic monophosphate, but not dopamine, may be a mediator of the renal response to atrial natriuretic factor in man.

scholarly journals Mechanisms of the Proinflammatory Response of Endothelial Cells to Candida albicans Infection

2000 ◽  
Vol 68 (3) ◽  
pp. 1134-1141 ◽  
Author(s):  
Alison S. Orozco ◽  
Xiang Zhou ◽  
Scott G. Filler
Keyword(s):  
Endothelial Cells ◽  
Candida Albicans ◽  
Endothelial Cell ◽  
Adhesion Molecule ◽  
Cell Response ◽  
Microbial Pathogens ◽  
Intercellular Adhesion Molecule ◽  
Clear Understanding ◽  
Tnf Α ◽  
Endothelial Cell Response

ABSTRACT Endothelial cells can influence significantly the host inflammatory response against blood-borne microbial pathogens. Previously, we found that endothelial cells respond to in vitro infection with Candida albicans by secreting interleukin 8 (IL-8) and expressing E-selectin, intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1). We have now examined the mechanisms mediating this endothelial cell response. We determined that C. albicans stimulated endothelial cells to synthesize tumor necrosis factor alpha (TNF-α), which in turn induced these infected cells to secrete IL-8 and express E-selectin by an autocrine mechanism. Expression of VCAM-1 was mediated not only by TNF-α but also by IL-1α and IL-1β, all of which were synthesized by endothelial cells in response to C. albicans. These three cytokines remained primarily cell associated rather than being secreted. Candidal induction of ICAM-1 expression was independent of TNF-α, IL-1α, and IL-1β. These observations demonstrate that different proinflammatory endothelial cell responses to C. albicans are induced by distinct mechanisms. A clear understanding of these mechanisms is important for therapeutically modulating the endothelial cell response to C. albicans and perhaps other opportunistic pathogens that disseminate hematogenously.

Mechanism of atrial natriuretic factor-induced inhibition of rat mesangial cell mitogenesis.

1990 ◽  
Vol 259 (3) ◽  
pp. E312 ◽  
Author(s):  
R G Appel
Keyword(s):  
Atrial Natriuretic Factor ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Maximal Response ◽  
Thymidine Uptake ◽  
Dependent Manner ◽  
Cyclic Monophosphate ◽  
3T3 Fibroblasts ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Recent observations suggest that atrial natriuretic factor (ANF) may have growth-inhibitory activity. The present studies were performed to further define this action in rat mesangial cells (which have both biological and clearance ANF receptors) and in 3T3 fibroblasts (which have only clearance ANF receptors). Both cell types were made quiescent by removal of serum and then reactivated by exposure to a serum-free defined medium. ANF inhibited [3H]thymidine uptake in a dose-dependent manner in mesangial cells (half-maximal response 10(-11) M; 47% maximal inhibitory effect) but had no effect in 3T3 fibroblasts. Exogenous 8-bromoguanosine 3',5'-cyclic monophosphate (0.1 mM) inhibited [3H]thymidine uptake by 33% in mesangial cells but had no effect in 3T3 fibroblasts. Counts in mesangial cells exposed to 0.1 mM sodium nitroprusside, which stimulates guanosine 3',5'-cyclic monophosphate (cGMP), were inhibited by 76%. However, this represented a toxic effect, because excessive trypan blue uptake was noted in this condition. Mesangial cell number after 3 days of logarithmic proliferation was reduced by 33% in cells incubated with 1.0 nM ANF compared with vehicle. Incubation of mesangial cell monolayers with ANF caused a concentration-dependent increase in intracellular cGMP accumulation. Threshold responses occurred at concentrations one order of magnitude greater than that resulting in the antimitogenic action. In 3T3 fibroblast monolayers exposed to ANF, cGMP accumulation occurred but was markedly attenuated compared with mesangial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Sustained fetal pulmonary vasodilation with prolonged atrial natriuretic factor and GMP infusions

1991 ◽  
Vol 260 (1) ◽  
pp. H183-H192 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso
Keyword(s):  
Blood Flow ◽  
Pulmonary Circulation ◽  
Atrial Natriuretic Factor ◽  
Pulmonary Blood Flow ◽  
Prostaglandin D2 ◽  
Pressure Flow ◽  
Cyclic Monophosphate ◽  
Natriuretic Factor ◽  
Direct Acting ◽  
Atrial Natriuretic

To study mechanisms of vasodilation and factors that maintain high pulmonary vascular resistance in utero, we measured changes in blood flow and the pressure-flow relationship of the pulmonary circulation during prolonged exposures to direct-acting guanosine 3',5'-cyclic monophosphate (cGMP) vasodilators, atrial natriuretic factor (ANF), and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) and compared hemodynamic responses with other vasodilator stimuli in chronically prepared fetal lambs. The fetus was treated with 2 h of intrapulmonary infusions of ANF (0.15 micrograms/min), 8-BrcGMP (50 micrograms/min), prostaglandin D2 (PGD2, 0.4 micrograms/min), or acetylcholine (ACh, 1.5 micrograms/min) or increases in fetal Po2. Despite continued exposure to increased Po2, PGD2, and ACh, elevations of pulmonary blood flow and slopes of the pressure-flow relationship were not sustained, with both significantly decreased at 2 h from peak values. In contrast, pulmonary blood flow and pressure-flow slopes remained increased throughout 2 h of exposures to ANF and 8-BrcGMP. Adenosine 3',5'-cyclic monophosphate caused less change in blood flow than 8-BrcGMP within the dose range studied. We conclude that unlike other stimuli, direct-acting cGMP vasodilators are able to sustain vascular relaxation of the fetal pulmonary circulation.

Dual modulation of Na/H antiport by atrial natriuretic factor in rat aortic smooth muscle cells

1997 ◽  
Vol 273 (2) ◽  
pp. C643-C652 ◽  
Author(s):  
R. Ricci ◽  
P. Baldini ◽  
L. Bogetto ◽  
P. De Vito ◽  
P. Luly ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Atrial Natriuretic Factor ◽  
Muscle Cells ◽  
Set Point ◽  
Cyclic Monophosphate ◽  
Natriuretic Factor ◽  
Acid Load ◽  
Rate Of Recovery ◽  
Atrial Natriuretic

The aim of the present work was to study the effect of the atrial natriuretic factor (ANF) on the Na/H antiport in rat aorta smooth muscle cells, evaluated as intracellular pH (pHi) recovery after an acid load with ammonium chloride. The Na/H antiport was studied using a fluorescent probe, sensitive to pHi, 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. Our data indicate that ANF modulates the activity of the Na/H antiport in both a dose- and time-dependent manner. Hormone concentrations of 10(-10) M activate the antiport, increasing both the rate of recovery and the set point by approximately 0.2 pH units. This effect is mediated by diacylglycerol as a result of phospholipid hydrolysis by a phospholipase C, even if an involvement of adenosine 3',5'-cyclic monophosphate (cAMP) cannot be ruled out. ANF (10(-7) M) inhibits the antiport, decreasing both the rate of recovery and the set point by approximately 0.3 pH units, because of guanosine 3',5'-cyclic monophosphate production. Both inhibition and stimulation of pHi by ANF were more pronounced when the hormone was given before the acid load, perhaps because of the longer time exposure. We present new hypotheses on the mechanism of action of this paracrine/autocrine factor.

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