Vasoactive Intestinal Peptide Stimulates Renin Secretion in vitro:Evidence for a Direct Action of the Peptide on the Renal Juxtaglomerular Cells

ABSTRACT Treatment with a high dose of oestradiol for 6 months caused hyperprolactinaemia and pituitary hyperplasia in female Wistar–Furth rats. Changes in the vasoactive intestinal peptide (VIP) and dopamine content of the hypothalamus and pituitary were also found. The hypothalamic dopamine concentration was only slightly reduced and, although the concentration of dopamine in the pituitary was less in treated animals, the total pituitary content was increased. The concentration of VIP in the pituitary was increased by oestradiol treatment but decreased in the non-median eminence hypothalamus. In the median eminence the VIP content was increased by oestradiol treatment and the amount present correlated positively and significantly with pituitary wet weight in animals treated with both oestradiol and fluphenazine. In Fischer 344 rats, oestradiol produced greater incremental changes in pituitary wet weight and plasma concentrations of prolactin than in Wistar controls and the increase in the pituitary concentration of VIP was five times greater. Although peptide turnover has not been measured, these results suggest that oestradiol, as well as having a direct action, stimulates pituitary lactotrophs by increasing pituitary concentrations of VIP. J. Endocr. (1988) 116, 259–265

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Do Calcium-Activated Chloride Channels Control Renin Secretion?

Physiology ◽

10.1152/physiologyonline.1990.5.2.43 ◽

1990 ◽

Vol 5 (2) ◽

pp. 43-46 ◽

Cited By ~ 1

Author(s):

A Kurtz

Keyword(s):

Chloride Channels ◽

Renin Secretion ◽

Volume Control ◽

Juxtaglomerular Cells ◽

Epithelioid Cells ◽

Intracellular Ca ◽

Cl Channels

The rate of renin secretion from renal juxtaglomerular epithelioid cells appears to be inversely correlated to intracellular Ca activity. Such a dependency of renin secretion on Ca activity could be controlled by Ca-activated Cl channels that may be involved in the volume control of juxtaglomerular cells.

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Calcium in the control of renin secretion: Ca2+ influx as an inhibitory signal

AJP Renal Physiology ◽

10.1152/ajprenal.1981.240.1.f70 ◽

1981 ◽

Vol 240 (1) ◽

pp. F70-F74 ◽

Cited By ~ 2

Author(s):

C. S. Park ◽

D. S. Han ◽

J. C. Fray

Keyword(s):

Incubation Temperature ◽

Inhibitory Effect ◽

Renin Secretion ◽

Juxtaglomerular Cells ◽

Stimulatory Action ◽

Inhibitory Signal ◽

Ca Antagonist ◽

K Concentration ◽

Energy Dependent

The mechanism for the inhibition of renin secretion in vitro from renal cortical slices by angiotensin II, antidiuretic hormone, ouabain, and high K+ concentration was studied. The inhibitory effect of these agents was blocked by a Ca antagonist, verapamil. In addition, epinephrine stimulated renin secretion and its stimulatory action was blocked by ouabain. These results support the hypothesis that Ca2+ influx into juxtaglomerular cells plays a role as an inhibitory signal whereas Ca2+ efflux is a stimulatory signal for renin secretion. Renin secretion was greatly stimulated by lowering incubation temperature, indicating that renin secretion is not energy dependent. The possibility is discussed that Ca2+ of juxtaglomerular cells might activate an enzyme(s) that then modulates some sequential steps of renin secretory processes, thereby controlling the rate of renin secretion.

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Immunohistochemical localization of atrial natriuretic peptide binding sites in juxtaglomerular cells and vascular walls of rat kidney

Acta Endocrinologica ◽

10.1530/acta.0.1190235 ◽

1988 ◽

Vol 119 (2) ◽

pp. 235-239 ◽

Cited By ~ 5

Author(s):

Mitsuhide Naruse ◽

Kohsaku Nitta ◽

Tsutomu Sanaka ◽

Kiyoko Naruse ◽

Hiroshi Demura ◽

...

Keyword(s):

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Binding Sites ◽

Direct Action ◽

Rat Kidney ◽

Complex Method ◽

Juxtaglomerular Cells ◽

Vascular Walls ◽

Sites Of Action ◽

Atrial Natriuretic

Abstract. Since the kidney is one of the major sites of action for atrial natriuretic peptide (ANP) and immunoreactive ANP has been detected in tissue extract by radioimmunoassay, we have applied the immunohistochemical technique by using the avidin-biotin complex method to investigate ANP binding sites in the rat kidney. Although no immunostaining was observed in the kidney of control rats, immunoreactive ANP was present in the juxtaglomerular cells, the vascular walls of interlobular arteries, arcuate arteries, arterioles including vas afferens and vas efferens, and the medullary peritubular capillary of ANP-pretreated rats. In contrast, no tubular structure was stained. These results suggest that ANP may affect renin secretion via its direct action on the juxtaglomerular cells and that it predominantly induces natriuresis by its effects on renal hemodynamics.

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Regulation of in vitro renin secretion by ANG II feedback manipulation in vivo in the ovine fetus

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.277.4.r1230 ◽

1999 ◽

Vol 277 (4) ◽

pp. R1230-R1238 ◽

Cited By ~ 4

Author(s):

Carlos E. Giammattei ◽

Jack W. Strandhoy ◽

James C. Rose

Keyword(s):

Feedback Regulation ◽

Late Gestation ◽

Renin Secretion ◽

Juxtaglomerular Cells ◽

Fetal Life ◽

Ang Ii ◽

Active Renin ◽

Age Related

The renin-angiotensin system is critically important to fetal cardiovascular function and organ development. The feedback regulation of renin secretion by ANG II develops early in gestation yet does not linearly progress from fetal life to adulthood. Renin secretion is elevated in late gestation compared with earlier or postnatal time periods, which suggests that some component of the negative feedback regulation of renin secretion is less sensitive in late gestation. We examined in fetal sheep the age-related consequence of chronic in vivo manipulation of ANG II on renal renin secretion measured in vitro. Immature (101–103 days of gestation) and mature (130–133 days of gestation) fetuses were treated for 72 h with enalaprilat, ANG II or vehicle. Content and basal and isoproterenol-stimulated secretion of prorenin (PR) and active renin (AR) from fetal kidney cortical slices were determined. Enalaprilat pretreatment in vivo increased renal renin content and basal and stimulated secretion of PR and AR in vitro even in immature animals. Immunohistochemical localization showed that enalaprilat treatment caused an age-related recruitment of renin-containing juxtaglomerular cells. Conversely, ANG II pretreatment decreased basal and stimulated PR and AR secretion from immature fetal kidneys, but only inhibited PR secretion from mature kidneys. It also caused an age-related decrease in the percentage of renin-containing juxtaglomerular cells. These results suggest that ANG II feedback modulates not only the synthesis and content of renin, but the sensitivity of the coupling between stimulus and secretion. A critical observation of our study is that the higher renal tissue concentrations of prorenin and active renin in late gestation may be a consequence of reduced sensitivity to ANG II feedback; this is consistent with the increased plasma concentrations of renin found in near-term mammals.

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Do osmotic forces play a role in renin secretion?

AJP Renal Physiology ◽

10.1152/ajprenal.1988.255.1.f1 ◽

1988 ◽

Vol 255 (1) ◽

pp. F1-F10 ◽

Cited By ~ 8

Author(s):

O. Skott

Keyword(s):

Secretory Granules ◽

Proton Gradient ◽

Renin Secretion ◽

Renin Release ◽

Juxtaglomerular Cells ◽

Proton Gradients ◽

Low Calcium ◽

Release In Vitro

Secretory granules swell during exocytosis. Swelling may follow fusion and assist in extrusion of the granular content, or swelling may cause granular fusion with the plasmalemma. A granular proton gradient has been suggested to be involved in such preexocytic granular swelling. Exocytosis of renin from juxtaglomerular cells of isolated preparations is very sensitive to changes in the extracellular osmolality. Extracellular hyposmolality causes swelling of secretory granules, fusions between peripherally located granules and plasmalemma, and an increased number of release episodes. Induction of granule swelling at constant extracellular osmolality also stimulates renin release. Newly recruited renin granules are osmosensitive, and a high extracellular osmolality blocks secretion induced by other means (low calcium). Dissipation of granular proton gradients inhibits renin release without affecting the osmosensitivity. Thus, in renin release in vitro, a granular swelling precedes fusion and exocytosis, and a granular proton gradient may contribute to preexocytic swelling when extracellular osmolality is constant. The osmosensitivity may be important for macula densamediated renin release.

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