Central Stimulation of Renin Secretion through Serotonergic, Noncardiovascular Mechanisms

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.

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CENTRAL STIMULATION OF RESPIRATION DURING HYPOXIA

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1942.136.1.13 ◽

1942 ◽

Vol 136 (1) ◽

pp. 13-21 ◽

Cited By ~ 16

Author(s):

Carl A. Moyer ◽

Henry K. Beecher

Keyword(s):

Central Stimulation ◽

Stimulation Of

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Effect of acute stimulation of renin secretion on renal renin content in vivo

Kidney International ◽

10.1038/ki.1990.224 ◽

1990 ◽

Vol 38 (3) ◽

pp. 440-446 ◽

Cited By ~ 5

Author(s):

John A. Opsahl ◽

Paul A. Abraham ◽

Stephen A. Katz

Keyword(s):

Renin Secretion ◽

Renin Content ◽

Stimulation Of

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Stimulation of renin secretion by ethacrynic acid is independent of Na(+)-K(+)-2Cl- cotransport

AJP Renal Physiology ◽

10.1152/ajprenal.1990.259.4.f539 ◽

1990 ◽

Vol 259 (4) ◽

pp. F539-F544 ◽

Cited By ~ 1

Author(s):

C. S. Park ◽

P. S. Doh ◽

R. E. Carraway ◽

G. G. Chung ◽

J. C. Fray ◽

...

Keyword(s):

Loop Diuretic ◽

Ethacrynic Acid ◽

Inhibitory Effect ◽

Renin Secretion ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Specific Membrane ◽

Cortical Slices ◽

Stimulation Of

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.

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