Modulation of Cardiac Growth by Sympathethic Innervation: Differential Response between Normotensive and Hypertensive Rats

1993 ◽  
pp. 83-91
Author(s):  
Dianne L. Atkins
Keyword(s):  
Differential Response ◽  
Hypertensive Rats ◽  
Cardiac Growth

Ventricular morphology and pumping ability of exercised spontaneously hypertensive rats

1978 ◽  
Vol 235 (2) ◽  
pp. H193-H199 ◽  
Author(s):  
M. A. Pfeffer ◽  
B. A. Ferrell ◽  
J. M. Pfeffer ◽  
A. K. Weiss ◽  
M. C. Fishbein ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Spontaneously Hypertensive Rats ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Ventricular Performance ◽  
Cardiac Growth ◽  
Spontaneously Hypertensive ◽  
Chamber Volume ◽  
Before And After ◽  
The Right

Spontaneously hypertensive rats (SHR) and two strains of normotensive Wistar rats were subjected to a 5 day/wk swimming program to determine whether the heart of the SHR could respond to an additional stimulus to cardiac growth. Swimming was tolerated well by all rats. Although body weight of the exercised groups was not significantly reduced, both the right and left ventricular weights of all exercised groups were increased. Left ventricular circumference and chamber volume were increased without a change in free wall thickness in all exercised groups. Ventricular performance was assessed by peak cardiac output and stroke volume attained during rapid intravenous volume loading, both before and after autonomic inhibition. After combined cholinergic and beta-adrenergic inhibition, all exercised rats had slower heart rates and higher peak stroke volume than respectively sedentary controls. Thus, exercised SHR had the same alterations in cardiac mass and performance as exercised normotensive rats. Despite the initial presence of left ventricular hypertrophy, the SHR responded appropriately to an additional stimulus for adaptive cardiac growth.

scholarly journals Long Withdrawal of Methylphenidate Induces a Differential Response of the Dopaminergic System and Increases Sensitivity to Cocaine in the Prefrontal Cortex of Spontaneously Hypertensive Rats

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0141249 ◽  
Author(s):  
Maurício dos Santos Pereira ◽  
Matheus Figueiredo Sathler ◽  
Thais da Rosa Valli ◽  
Richard Souza Marques ◽  
Ana Lucia Marques Ventura ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Spontaneously Hypertensive Rats ◽  
Dopaminergic System ◽  
Differential Response ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

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