Endothelial regulation of coronary vascular tone in vitro: contribution of endothelin receptor subtypes and nitric oxide

1993 ◽  
Vol 243 (3) ◽  
pp. 281-286 ◽  
Author(s):  
John Pernow ◽  
Agnes Modin
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Receptor Subtypes ◽  
Endothelin Receptor ◽  
Coronary Vascular Tone

scholarly journals Control of coronary vascular tone by nitric oxide.

1990 ◽  
Vol 66 (6) ◽  
pp. 1561-1575 ◽  
Author(s):  
M Kelm ◽  
J Schrader
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Coronary Vascular Tone

CELLULAR LOCALIZATION OF ENDOTHELIN RECEPTOR SUBTYPES IN THE RAT KIDNEY FOLLOWING IN VITRO LABELLING

1996 ◽  
Vol 23 (6-7) ◽  
pp. 524-531 ◽  
Author(s):  
Rachael Dean ◽  
Jialong Zhuo ◽  
Daine Alcorn ◽  
David Casley ◽  
Frederick AO Mendelsohn
Keyword(s):  
Cellular Localization ◽  
Rat Kidney ◽  
Receptor Subtypes ◽  
Endothelin Receptor

scholarly journals L-Arginine/Nitric Oxide Pathway and KCa Channels in Endothelial Cells: A Mini-Review

2020 ◽  
Author(s):  
Marcelo González ◽  
José Carlos Rivas
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Function ◽  
Vascular Tone ◽  
Molecular Mechanisms ◽  
Cardiovascular Health ◽  
Kca Channels ◽  
Subsequent Activation ◽  
Regulation Of Vascular Tone

The endothelium is an organ with a key role in the maintenance of cardiovascular health through the regulation of vascular tone, vascular resistance, blood flow, and arterial pressure. These functions are related with the synthesis and release of vasoactive molecules, mainly vasodilators like nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Both factors are released and diffused from endothelial cells to the smooth muscle cells, where there is a subsequent activation of signaling pathways that finally decrease the intracellular calcium to induce the vascular relaxation. The study of the molecular mechanisms that underlie the endothelial function still is in development, but from the evidence obtained from the endothelial cells in vitro studies are possible to partially describe the pathways to regulate the physiological endothelial function and the disturbances in pathological conditions. In this mini-review, we describe the main mechanisms for NO synthesis and the role of potassium channels related with EDHF. We include schemes and graphical summaries for better understanding of the molecular regulation of vascular tone in the human cardiovascular system.

scholarly journals The Role of Endothelin and Endothelin Receptor Subtypes in Regulation of Fetal Pulmonary Vascular Tone

1994 ◽  
Vol 35 (6) ◽  
pp. 664-670 ◽  
Author(s):  
Jackson Wong ◽  
Jeffrey R Fineman ◽  
Michael A Heymann
Keyword(s):  
Vascular Tone ◽  
Receptor Subtypes ◽  
Endothelin Receptor

Endothelin and nitric oxide mediate adaptation of the cortical collecting duct to metabolic acidosis

2006 ◽  
Vol 291 (4) ◽  
pp. F866-F873 ◽  
Author(s):  
Shuichi Tsuruoka ◽  
Seiji Watanabe ◽  
Jeffrey M. Purkerson ◽  
Akio Fujimura ◽  
George J. Schwartz
Keyword(s):  
Nitric Oxide ◽  
Metabolic Acidosis ◽  
Receptor Antagonist ◽  
Guanylate Cyclase ◽  
Kinase Inhibitor ◽  
Collecting Duct ◽  
Bicarbonate Transport ◽  
Receptor Subtypes ◽  
Cortical Collecting Duct

Endothelin (ET) and nitric oxide (NO) modulate ion transport in the kidney. In this study, we defined the function of ET receptor subtypes and the NO guanylate cyclase signaling pathway in mediating the adaptation of the rabbit cortical collecting duct (CCD) to metabolic acidosis. CCDs were perfused in vitro and incubated for 3 h at pH 6.8, and bicarbonate transport or cell pH was measured before and after acid incubation. Luminal chloride was reversibly removed to isolate H+ and HCO3− secretory fluxes and to raise the pH of β-intercalated cells. Acid incubation caused reversal of polarity of net HCO3− transport from secretion to absorption, comprised of a 40% increase in H+ secretion and a 75% decrease in HCO3− secretion. The ETB receptor antagonist BQ-788, as well as the NO synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), attenuated the adaptive decrease in HCO3− secretion by 40%, but only BQ-788 inhibited the adaptive increase in H+ secretion. There was no effect of inactive d-NAME or the ETA receptor antagonist BQ-123. Both BQ-788 and l-NAME inhibited the acid-induced inactivation (endocytosis) of the apical Cl−/HCO3− exchanger. The guanylate cyclase inhibitor LY-83583 and cGMP-dependent protein kinase inhibitor KT-5823 affected HCO3− transport similarly to l-NAME. These data indicate that signaling via the ETB receptor regulates the adaptation of the CCD to metabolic acidosis and that the NO guanylate cyclase component of ETB receptor signaling mediates downregulation of Cl−/HCO3− exchange and HCO3− secretion.

scholarly journals Endothelium-derived relaxing factor, nitric oxide: effects on and production by mesangial cells and the glomerulus.

1993 ◽  
Vol 3 (8) ◽  
pp. 1435-1441
Author(s):  
L Raij ◽  
P J Shultz
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Glomerular Mesangial Cells ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor

The endothelium-derived relaxing factor nitric oxide (EDRF/NO) is a labile, endogenous vasodilator that is important in the control of systemic vascular tone. This review focuses on the effects of EDRF/NO on glomerular mesangial cells in vitro and on the role of EDRF/NO in mesangial and glomerular physiology and pathophysiology in vivo. It was concluded that EDRF/NO can stimulate increases in cGMP, inhibit mesangial cell contraction, and inhibit growth factor-induced proliferation of mesangial cells in culture. Furthermore, incubation with endotoxin or cytokines stimulates mesangial cells to produce EDRF/NO, via an inducible NO synthase enzyme. Therefore, it is likely that NO could play a role in the inflammatory response within the glomerulus. Finally, recent studies providing evidence that EDRF/NO is functional within the glomerulus in vivo, especially during endotoxemia and inflammation are also reviewed.

Thrombin Does Not Alter Vascular Hyporeactivity in Models of Endotoxin-Induced Septic Shock in Rats

1995 ◽  
Vol 88 (2) ◽  
pp. 149-157 ◽  
Author(s):  
Viviane Martin ◽  
Marie-Louise Wiesel ◽  
Anne Albert ◽  
Alain Beretz
Keyword(s):  
Nitric Oxide ◽  
Disseminated Intravascular Coagulation ◽  
Vascular Tone ◽  
Endotoxic Shock ◽  
Vascular Wall ◽  
Anticoagulant Treatment ◽  
Intravascular Coagulation ◽  
Vascular Hyporeactivity

1. Hypotension and vascular hyporesponsiveness to vasoconstrictors are observed during endotoxic shock, and are associated with increased production of nitric oxide in the vascular wall. Disseminated intravascular coagulation is another feature of septicaemia. We hypothesized that thrombin generated during disseminated intravascular coagulation might modulate the changes in vascular tone induced by endotoxin. 2. Incubation of rat aortic rings for 4 h with α-thrombin (0.003–3.0 NIH units/ml) did not change their reactivity to noradrenaline. Incubation for 4 h with lipopolysaccharide increased the EC50 for noradrenaline, whereas co-incubation of thrombin (0.5 NIH units/ml) with lipopolysaccharide did not alter this hyporeactivity to noradrenaline. 3. In vivo in rats, lipopolysaccharide caused early (1 h) and late (4–6 h) hyporeactivity to noradrenaline. In rats infused with lipopolysaccharide and heparin (1 U min−1 kg−1, 0.4 ml/h) or hirudin (2.2 mg ml−1 kg−1, 0.8 ml/h), vasopressor responses to noradrenaline were not different from those after infusion of lipopolysaccharide alone. Aortic rings taken from rats receiving both anticoagulant treatment and lipopolysaccharide had the same sensitivity to noradrenaline as those obtained from rats receiving lipopolysaccharide alone. 4. Our results suggest that, in vivo, disseminated intravascular coagulation does not modify the early and late effects of lipopolysaccharide on arterial pressure and that, in vitro, thrombin neither induces hyporeactivity to noradrenaline nor modifies lipopolysaccharide-induced hyporeactivity. We propose that thrombin generated during disseminated intravascular coagulation in rats does not play a major role in the alterations of vascular tone observed during endotoxic shock.

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