K+ Secretion in Strial Marginal Cells is Stimulated via β1-Adrenergic Receptors but not via β2-Adrenergic or Vasopressin Receptors

2000 ◽  
Vol 175 (3) ◽  
pp. 191-202 ◽  
Author(s):  
P. Wangemann ◽  
J. Liu ◽  
M. Shimozono ◽  
S. Schimanski ◽  
M.A. Scofield
1997 ◽  
Vol 114 (1-2) ◽  
pp. 107-116 ◽  
Author(s):  
Hiroshi Sunose ◽  
Jianzhong Liu ◽  
Daniel C. Marcus
Keyword(s):  

2006 ◽  
Vol 219 (1-2) ◽  
pp. 66-73 ◽  
Author(s):  
Jun Ho Lee ◽  
Jeong-Hwa Heo ◽  
Sun O. Chang ◽  
Chong-Sun Kim ◽  
Seung-Ha Oh

1987 ◽  
Vol 252 (5) ◽  
pp. E699-E702 ◽  
Author(s):  
B. L. Roth ◽  
J. A. Spitzer

Sepsis and septic shock are complicated by a number of hemodynamic and metabolic aberrations. These include catecholamine refractoriness and altered glucose metabolism. Recently, a nonshock rat model of continuous endotoxin infusion via an implanted osmotic pump was developed that reproduces some of the metabolic and cardiovascular findings of human sepsis. By using this model, we have found a decreased number of hepatic plasma membrane alpha 1-adrenergic and [Arg8]vasopressin receptors in rats continuously infused with endotoxin. There was a significant decrease in [3H]prazosin (35 +/- 7%) and [3H] [Arg8]vasopressin (43 +/- 8%) receptors after 30 h of continuous endotoxin infusion with no change in affinity. The ability of norepinephrine to form the high-affinity complex with alpha 1-adrenergic receptors was not altered after chronic endotoxin infusion. The results are consistent with the concept that alterations in receptor number might underlie certain of the metabolic consequences of chronic sepsis.


2001 ◽  
Vol 182 (3) ◽  
pp. 171-181 ◽  
Author(s):  
P. Wangemann ◽  
J. Liu ◽  
E.Q. Scherer ◽  
M. Herzog ◽  
M. Shimozono ◽  
...  

VASA ◽  
2017 ◽  
Vol 46 (6) ◽  
pp. 431-439 ◽  
Author(s):  
Ana Gabriela Conceição-Vertamatti ◽  
Filipy Borghi ◽  
Fernando Canova ◽  
Dora Maria Grassi-Kassisse

Abstract. Hypertension is a silent and multifactorial disease. Over two centuries ago, the first device to record blood pressure was developed, making it possible to determine normotension and to establish criteria for hypertension. Since then, several studies have contributed to advance knowledge in this area, promoting significant advances in pharmacological treatments and, as a result, increasing survival of hypertensive people. The main models developed for the study of hypertension and the main findings in the vascular area are included in this review. We considered aspects related to vascular reactivity, changes in the population, and action of beta adrenergic receptors in the pathogenesis of hypertension.


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