The serotonin-4 receptor agonist cisapride and angiotensin-II exert additive effects on aldosterone secretion in normal man.

Suprarenal aortic constriction sufficient to reduce renal perfusion pressure by approximately 50% increased aldosterone secretion in anesthetized rats pretreated with dexamethasone. Bilateral nephrectomy under the same experimental conditions blocked the aldosterone response. Additionally, [1-sarcosine, 8-alanine]angiotensin II blocked the response in aldosterone secretion to aortic constriction in dexamethasone-treated rats. Finally, in rats hypophysectomized to exclude the influence of ACTH, the aldosterone response to aortic constriction was blocked by [1-sarcosine, 8-alanine]angiotensin II. The results indicate that angiotensin II increased aldosterone secretion during aortic constriction in the rat. These observations, along with those reported previously in sodium-depleted rats, point to an important overall role for the renin-angiotensin system in the control of aldosterone secretion in the rat.

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Angiotensin II-activated protein kinase D mediates acute aldosterone secretion

Molecular and Cellular Endocrinology ◽

10.1016/j.mce.2009.11.017 ◽

2010 ◽

Vol 317 (1-2) ◽

pp. 99-105 ◽

Cited By ~ 17

Author(s):

Brian A. Shapiro ◽

Lawrence Olala ◽

Senthil Nathan Arun ◽

Peter M. Parker ◽

Mariya V. George ◽

...

Keyword(s):

Angiotensin Ii ◽

Protein Kinase ◽

Protein Kinase D ◽

Aldosterone Secretion

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Role of tyrosine kinase and protein kinase C in the steroidogenic actions of angiotensin II, α-melanocyte-stimulating hormone and corticotropin in the rat adrenal cortex

Biochemical Journal ◽

10.1042/bj3050433 ◽

1995 ◽

Vol 305 (2) ◽

pp. 433-438 ◽

Cited By ~ 40

Author(s):

S Kapas ◽

A Purbrick ◽

J P Hinson

Keyword(s):

Protein Kinase C ◽

Angiotensin Ii ◽

Protein Kinase ◽

Tyrosine Kinase ◽

Zona Glomerulosa ◽

Aldosterone Secretion ◽

Melanocyte Stimulating Hormone ◽

Kinase C ◽

Stimulating Hormone

The role of protein kinases in the steroidogenic actions of alpha-melanocyte-stimulating hormone (alpha-MSH), angiotensin II (AngII) and corticotropin (ACTH) in the rat adrenal zona glomerulosa was examined. Ro31-8220, a potent selective inhibitor of protein kinase C (PKC), inhibited both AngII- and alpha-MSH-stimulated aldosterone secretion but had no effect on aldosterone secretion in response to ACTH. The effect of Ro31-8220 on PKC activity was measured in subcellular fractions. Basal PKC activity was higher in cytosol than in membrane or nuclear fractions. Incubation of the zona glomerulosa with either alpha-MSH or AngII resulted in significant increases in PKC activity in the nuclear and cytosolic fractions and decreases in the membrane fraction. These effects were all inhibited by Ro31-8220. ACTH caused a significant increase in nuclear PKC activity only, and this was inhibited by Ro31-8220 without any significant effect on the steroidogenic response to ACTH, suggesting that PKC translocation in response to ACTH may be involved in another aspect of adrenal cellular function. Tyrosine phosphorylation has not previously been considered to be an important component of the response of adrenocortical cells to peptide hormones. Both AngII and alpha-MSH were found to activate tyrosine kinase, but ACTH had no effect, observations that have not been previously reported. Tyrphostin 23, a specific antagonist of tyrosine kinases, inhibited aldosterone secretion in response to AngII and alpha-MSH, but not ACTH. These data confirm the importance of PKC in the adrenocortical response to AngII and alpha-MSH, and, furthermore, indicate that tyrosine kinase may play a critical role in the steroidogenic actions of AngII and alpha-MSH in the rat adrenal zona glomerulosa.

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Modulation of Ca2+ transients in neonatal and adult rat cardiomyocytes by angiotensin II and endothelin-1

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.270.3.h857 ◽

1996 ◽

Vol 270 (3) ◽

pp. H857-H868 ◽

Cited By ~ 5

Author(s):

R. M. Touyz ◽

J. Fareh ◽

G. Thibault ◽

B. Tolloczko ◽

R. Lariviere ◽

...

Keyword(s):

Angiotensin Ii ◽

Receptor Agonist ◽

Dependent Manner ◽

Induced Responses ◽

Ang Ii ◽

Binding Studies ◽

Vasoactive Peptides ◽

Adult Cardiomyocytes ◽

Etb Receptor ◽

Dose Dependent

Vasoactive peptides may exert inotropic and chronotropic effects in cardiac muscle by modulating intracellular calcium. This study assesses effects of angiotensin II (ANG II) and endothelin-1 (ET-1) on intracellular free calcium concentration ([Ca2+]i) in cultured cardiomyocytes from neonatal and adult rats. [Ca2+]i was measured microphotometrically and by digital imaging using fura 2 methodology. Receptor subtypes through which these agonists induce responses were determined pharmacologically and by radioligand binding studies. ANG II and ET-1 increased neonatal atrial and ventricular cell [Ca2+]i transients in a dose-dependent manner. ANG II (10(-11) to 10(-7) M) failed to elicit [Ca2+]i responses in adult cardiomyocytes, whereas ET-1 increased [Ca2+]i in a dose-dependent manner. The ETA receptor antagonist BQ-123 significantly reduced (P 7< 0.05) ET-1 induced responses, and the ETB receptor agonist IRL-1620 (10(-7) to 10(-5) M) significantly increased (P < 0.05) [Ca2+]i in neonatal and adult cardiomyocytes. ET-1 binding studies demonstrated 85% displacement by BQ-123 and approximately 15% by the ETB receptor agonist sarafotoxin S6c, suggesting a predominance of ETA receptors. Competition binding studies for ANG II failed to demonstrate significant binding on adult ventricular myocytes, indicating the absence or presence of very few ANG II receptors. These data demonstrate that ANG II and ET-1 have stimulatory [Ca2+]i effects on neonatal cardiomyocytes, whereas in adult cardiomyocytes, ANG II-induced effects are insignificant, and only ET-1-induced responses, which are mediated predominantly via ETA receptors, are preserved. Cardiomyocyte responses to vasoactive peptides may thus vary with cardiac development.

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