scholarly journals Angiotensin II receptors and renin release in rat glomerular afferent arterioles

1994 ◽  
Vol 46 (6) ◽  
pp. 1570-1573 ◽  
Author(s):  
Christos Chatziantoniou ◽  
Jean-Claude Dussaule ◽  
William J. Arendshorst ◽  
Raymond Ardaillou
1996 ◽  
Vol 270 (5) ◽  
pp. F718-F727 ◽  
Author(s):  
B. L. Jensen ◽  
O. Skott

Calcium-activated chloride channels have been proposed to control renin release from juxtaglomerular cells and to be involved in the excitation-contraction coupling of the renal afferent arteriole. The hypothesis was tested on renin release from rat glomeruli and in microperfused rabbit afferent arterioles with the chloride channel blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Renin secretion was equally enhanced by omission of extracellular calcium and by addition of 0.5 mM DIDS. The inhibitory effect of calcium was blocked by DIDS. The stimulatory effects of low calcium [with or without ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] and DIDS were not additive. In the absence of chloride, basal renin release was suppressed and the stimulatory effect of DIDS was abolished. The DIDS-induced enhancement of renin release was not dependent on bicarbonate. Norepinephrine (5 x 10(-7)-1 x 10(-6) M) and angiotensin II (1 x 10(-8)-10(-6) M) evoked reversible and dose-dependent contractions of microperfused rabbit afferent arterioles. DIDS (0.5 mM) did not affect the basal diameter of the arterioles but strongly inhibited the response to angiotensin II and attenuated the duration of the contractile response to norepinephrine. The results support the hypothesis that DIDS-sensitive calcium-activated chloride channels are involved in regulation of renin release and in the afferent arteriolar contraction after angiotensin II but do not play a pivotal role in the response to norepinephrine.


1974 ◽  
Vol 249 (3) ◽  
pp. 825-834 ◽  
Author(s):  
Hartmut Glossmann ◽  
Albert J. Baukal ◽  
Kevin J. Catt

1984 ◽  
Vol 247 (2) ◽  
pp. F246-F251 ◽  
Author(s):  
W. S. Spielman

The action of theophylline on the adenosine-induced decrease in renin release was studied in anesthetized dogs. Adenosine inhibited renin release, decreased GFR and fractional sodium excretion, and decreased the concentration of angiotensin II in the renal lymph. Theophylline (5 mumol/min intrarenally) had no significant effect on GFR or RBF yet produced a significant increase in the release of renin and the fractional excretion of sodium. The intrarenal infusion of adenosine (3 X 10(-7) mol/min) during theophylline infusion produced no effect on GFR or RBF, but fractional sodium excretion and renin release were significantly decreased. Adenosine was infused at a lower dose (3 X 10(-8) mol/min) during theophylline (5 X 10(-6) mol/min) infusion in a second group of dogs. With the exception of fractional sodium excretion, all effects of adenosine were effectively antagonized by theophylline. Theophylline at 5 X 10(-6) mol/min, which stimulates renin release and effectively antagonizes the renal effects of adenosine, had no detectable effect on cAMP measured in renal cortex. Furthermore, no change in cortical cAMP was observed until theophylline was increased 50-fold over the dose effective in antagonizing adenosine. These findings demonstrate that theophylline, at concentrations having no effect on cortical cAMP, antagonizes the effect of adenosine on renin release. The results are also consistent with the view that theophylline stimulates renin release by a mechanism other than its action on cAMP.


GPCRs ◽  
2020 ◽  
pp. 415-427
Author(s):  
Khuraijam Dhanachandra Singh ◽  
Sadashiva S. Karnik

1993 ◽  
Vol 13 (3) ◽  
pp. 233-245 ◽  
Author(s):  
Takaya Sato ◽  
Masami Niwa ◽  
Akihiko Himeno ◽  
Keisuke Tsutsumi ◽  
Tsugio Amemiya

1989 ◽  
Vol 7 (9) ◽  
pp. 757???762 ◽  
Author(s):  
Bao M. Twu ◽  
Michael E. Cannon ◽  
Chen H. Hsu

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