Pertussis toxin enhances the beta-adrenergic and blocks the alpha-adrenergic regulation of renin secretion in renal cortical slices

Life Sciences ◽  
1986 ◽  
Vol 38 (11) ◽  
pp. 1005-1011 ◽  
Author(s):  
José Pedraza-Chaverrí ◽  
M.Carmen Alatorre-González ◽  
JoséCarlos Peña ◽  
J.Adolfo García-Sáinz
Keyword(s):  
Pertussis Toxin ◽  
Renin Secretion ◽  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Cortical Slices

Localization and secretion of newly synthesized and stored renin: two compartments and secretory mechanisms

1988 ◽  
Vol 255 (1) ◽  
pp. F100-F107
Author(s):  
M. Kawamura ◽  
M. Parmentier ◽  
T. Inagami
Keyword(s):  
Isoelectric Focusing ◽  
Microsomal Fraction ◽  
Renin Secretion ◽  
Renin Activity ◽  
Beta Adrenergic ◽  
Granule Fraction ◽  
Adrenergic Mechanism ◽  
Intracellular Pathways ◽  
Rat Renal Cortical Slices ◽  
Cortical Slices

Intracellular pathways of renin secretion were examined by use of rat renal cortical slices. Renin was labeled with [35S]methionine by incubating the cortical slices for 2 h. The labeled immunoprecipitable renin was found in microsomal fraction (F1) but not in the renin granule fraction (F2). The newly synthesized and radiolabeled renin was secreted from the incubated slices into the medium. The rate of secretion of the labeled renin activity was not increased by 10(-6) M isoproterenol, whereas secretion of total renin activity was markedly stimulated. The isoelectric focusing patterns of renin in F1 and F2 were compared with those secreted with or without isoproterenol. The pattern of F1 was similar to that secreted in the medium without stimulation. These studies suggest that a constitutive pathway exists for renin secretion from the kidney and that the constitutive (nonstimulable) pathway is responsible for the secretion of newly synthesized renin and that it is not stimulated by a beta-adrenergic mechanism.

Ontogeny of neuronally released norepinephrine on renin secretion in sheep

1989 ◽  
Vol 257 (4) ◽  
pp. R765-R770 ◽  
Author(s):  
K. T. Nakamura ◽  
J. M. Klinkefus ◽  
F. G. Smith ◽  
T. Sato ◽  
J. E. Robillard
Keyword(s):  
Renin Secretion ◽  
Renal Nerves ◽  
Nerve Terminals ◽  
Norepinephrine Release ◽  
Fetal Sheep ◽  
Postnatal Maturation ◽  
Active Renin ◽  
Inactive Renin ◽  
Cortical Slices

The role of renal nerves and norepinephrine release on renin secretion during fetal and postnatal maturation has not been studied. Experiments were performed to determine the effect of veratridine, a substance known to promote norepinephrine release from nerve terminals, on active and inactive renin secretion from renal cortical slices of fetal (134-138 days gestation; term is 145 days), newborn (4-9 days of age), and adult nonpregnant sheep. Veratridine (10-300 microM) significantly increased active renin secretion and produced a small but nonsignificant rise in inactive renin secretion in all three groups of animals (P less than 0.05). The percent rise in active renin secretion during veratridine stimulation was similar among all groups. Veratridine-stimulated (300 microM) active renin secretion was antagonized by tetrodotoxin (0.5 and 5.0 microM) and DL-propranolol (1 microM) in fetal renal cortical slices. However, neither tetrodotoxin nor propranolol completely inhibited the stimulatory effect of veratridine on active renin secretion. These results suggest that 1) norepinephrine released from nerve terminals may regulate active renin secretion early during development; 2) the effect of veratridine on active renin secretion was similar in fetal, newborn, and adult sheep; 3) veratridine had no significant effect on inactive renin secretion; and 4) active renin secretion due to depolarization of nerve terminals in fetal sheep is dependent on activation of beta-adrenoceptors as it is in adults.

beta-Adrenergic regulation of adenosine 3',5'-monophosphate concentration in brain microvessels

Science ◽  
1979 ◽  
Vol 204 (4390) ◽  
pp. 330-332 ◽  
Author(s):  
T. Herbst ◽  
M. Raichle ◽  
J. Ferrendelli
Keyword(s):  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Brain Microvessels

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

1990 ◽  
Vol 259 (4) ◽  
pp. F539-F544 ◽  
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.

Age-related differences in beta-adrenergic regulation of repolarization in canine epicardial myocytes

1996 ◽  
Vol 271 (3) ◽  
pp. H1174-H1181 ◽  
Author(s):  
F. Charpentier ◽  
Q. Y. Liu ◽  
M. R. Rosen ◽  
R. B. Robinson
Keyword(s):  
Ventricular Myocardium ◽  
Control Site ◽  
Developmental Changes ◽  
Delayed Rectifier ◽  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Control Value ◽  
Age Related ◽  
Patch Technique ◽  
Epicardial Myocytes

Developmental changes occur in beta-adrenergic modulation of repolarization in canine. Purkinje fibers that may have important implications for rhythm and arrhythmias. No comparable data exist for ventricular myocardium. Therefore, we studied developmental changes in beta-adrenergic regulation of repolarization and delayed rectifier potassium current (IK) in canine ventricular epicardium. We first investigated the effects of isoproterenol (Iso) on action potentials (AP) recorded from epicardial slices with standard microelectrodes, and then we further determined the mechanisms of Iso action using the nystatin-perforated patch technique on isolated epicardial myocytes. In microelectrode studies Iso (10(-7) M) induced a shortening of the AP in preparations from adult dogs but not in those from dogs < 30 days old. These results were confirmed on AP recorded from single myocytes. Although the plateau was increased by Iso at all ages, the AP at 90% of repolarization was shortened (P < 0.05, n = 6) in adult but unchanged in < 30-day-old myocytes (NS, n = 6). Voltage-clamp studies showed that IK of adult cells was increased from a control value of 10.23 +/- 1.87 to 13.43 +/- 1.92 pA/pF with Iso (step to +50 mV, P < 0.05, n = 6), but IK was not modified in cells from young animals (6.49 +/- 2.72 pA/pF in control and 6.56 +/- 2.62 pA/pF with Iso, n = 4). Increasing the Iso concentration to 10(-5) M failed to increase IK significantly (n = 4). However, 10(-7) M Iso did increase L-type Ca2+ current from 172 +/- 31 to 262 +/- 42 pA (P < 0.05, n = 4), consistent with the effect to increase the AP plateau. These results show that there are developmental changes in beta-adrenergic regulation of repolarization in canine epicardium and that the control site of developmental changes is in the IK channel rather than the beta-adrenergic receptor cascade.

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