Effect of Stimulation of the Medulla Oblongata on Renin Secretion in Dogs

1971 ◽  
Vol 7 (1) ◽  
pp. 1-10 ◽  
Author(s):  
S.S. Passo ◽  
T.A. Assaykeen ◽  
K. Otsuka ◽  
B.L. Wise ◽  
A. Goldfien ◽  
...  
1982 ◽  
Vol 242 (1) ◽  
pp. R136-R140 ◽  
Author(s):  
E. L. Schiffrin ◽  
J. Genest

Captopril (SQ 14,225), an orally active angiotensin I-converting enzyme (ACE) inhibitor, increased drinking and produced water diuresis in rats when given orally at a dose of 100 mg.kg-1.day-1. Chronic intraperitoneal infusion of angiotensin (ANG) II or the ANG II antagonist [Sar1, Ile8]ANG II abolished this response. Intracerebroventricular (icv) captopril infused chronically reduced the dipsogenic response to oral captopril. [Sar1, Ile8]ANG II (icv) was without effect on captopril-induced drinking. These results suggest that drinking produced by chronic oral treatment of rats with captopril may be caused by the effects of the elevated ANG I concentrations achieved after blockade of ACE and stimulation of renin secretion by captopril. Systemic ANG II may reduce this response by decreasing renin secretion. Systemic [Sar1, Ile8]ANG II presumably blocks brain ANG receptors for blood-borne ANG. Since icv [Sar1, Ile8]ANG II is ineffective, the receptors for systemic and icv ANG appear to be distinct. Orally administered captopril does not diffuse into the brain.


1994 ◽  
Vol 60 (2) ◽  
pp. 205-214 ◽  
Author(s):  
Peter A. Rittenhouse ◽  
Erica A. Bakkum ◽  
Andrew D. Levy ◽  
Qian Li ◽  
Joseph M. Yracheta ◽  
...  

1990 ◽  
Vol 38 (3) ◽  
pp. 440-446 ◽  
Author(s):  
John A. Opsahl ◽  
Paul A. Abraham ◽  
Stephen A. Katz

1990 ◽  
Vol 259 (4) ◽  
pp. F539-F544 ◽  
Author(s):  
C. S. Park ◽  
P. S. Doh ◽  
R. E. Carraway ◽  
G. G. Chung ◽  
J. C. Fray ◽  
...  

This study investigated the cellular mechanism of stimulation of renin secretion by the loop diuretic ethacrynic acid (EA) in rabbit renal cortical slices. The diuretic rapidly stimulated renin secretion reversibly and in a concentration-dependent manner. The stimulation was independent of the presence of Na+, Cl-, Ca2+, or other loop diuretics (furosemide and bumetanide) in the incubation media, suggesting that the stimulation in vitro was not dependent on the inhibitory effect of the diuretic on Na(+)-K(+)-2Cl-cotransport. The findings do not support the macula densa hypothesis. The stimulation by the diuretic was prevented and reversed by thiols such as cysteine and dithiothreitol, which also prevented and reversed the stimulation of renin secretion by the nondiuretic sulfhydryl reagent P-chloromercuriphenyl-sulfonate (PCMPS). These results suggest that EA stimulates renin secretion in vitro via reversible chemical reactions with specific membrane sulfhydryl groups that may have no functional role in the Na(+)-K(+)-2Cl- cotransport.


1957 ◽  
Vol 190 (2) ◽  
pp. 350-355 ◽  
Author(s):  
Edgar Haber ◽  
Kurt W. Kohn ◽  
S. H. Ngai ◽  
D. A. Holaday ◽  
S. C. Wang

Medulla oblongata of 80 vagotomized cats was explored with microelectrodes. Spontaneous respiratory neuronal activities and chest movements were recorded simultaneously with a twin beam cathode ray oscilloscope. It was found that inspiratory discharges are concentrated in the reticular formation between 3 mm rostral and 1 mm caudal to the level of the obex, which corresponds approximately to the inspiratory region of Pitts, Magoun and Ranson. On the other hand, expiratory discharges are not obtained in Pitts' expiratory area, but are found in a circumscribed region in the reticular formation from the level of the obex to 3 mm caudally. Electric stimulation of this region has been found recently by Ngai and Wang to yield marked expiratory spasm. It is concluded that the expiratory center is located caudally to the inspiratory center in the cat. The spontaneous respiratory neuronal discharges continue with no alterations of pattern of firing during drug-induced respiratory paralysis, and are increased both in number and in frequency during CO2 inhalation. Stimulation of the vagus nerve with 50 shocks/sec. reduces inspiratory discharges and prolongs the duration of expiratory discharges.


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