Role of voltage-gated calcium channels in potassium-stimulated aldosterone secretion from rat adrenal zona glomerulosa cells

Uebele, Victor N.; Nuss, Cindy E.; Renger, John J.; Connolly, Thomas

doi:10.1016/j.jsbmb.2004.04.012

Cited by 16 publications

(12 citation statements)

References 53 publications

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“…Recently, some researchers have suggested that L-type or T-type CCBs can directly inhibit aldosterone secretion from glomerulosa cells triggered by angiotensin II or K + stimulation [20, 21]. Interestingly, Imagawa et al [21] demonstrated that T-type CCB leads to a reduction of aldosterone secretion from H295R cells, and that this effect is, at least partly, due to suppression of the expression of 11-β-hydroxylase and aldosterone synthase, which catalyze the final two steps in aldosterone synthesis.…”

Section: Discussionmentioning

confidence: 99%

Different Effects of L/N-Type and L-Type Calcium Channel Blockers on the Renin-Angiotensin-Aldosterone System in SHR/Izm

et al. 2009

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Background: The L/N-type calcium channel blocker (CCB) cilnidipine has been demonstrated to suppress sympathetic nerve activity. In the present study, we investigated the effects of cilnidipine on the renin-angiotensin-aldosterone system (RAAS) in SHR/Izm rats to confirm differences from the effects of L-type CCB. Methods: Male SHR/Izm rats received vehicle, cilnidipine (0.3, 3 mg/kg) or amlodipine (0.3, 3 mg/kg) by gavage for systolic blood pressure (SBP) measurement. For biochemical analyses, the experiments were performed under anesthesia. Results: Low doses of cilnidipine or amlodipine had no effect on SBP or RAAS parameters. A high dose of either drug produced similar effects on SBP levels. Although cilnidipine had no effect on plasma renin activity or the plasma angiotensin II level, amlodipine significantly increased these parameters as compared to levels in the vehicle group. The cilnidipine group had a significantly lower plasma aldosterone level and renal cortical tissue norepinephrine level than the vehicle group. Conclusions: Cilnidipine had effects different from those of L-type CCB on the RAAS in SHR/Izm rats. Our results indicate that suppression of RAAS hyperactivity by cilnidipine can be partly explained by its sympatholytic action.

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Section: Discussionmentioning

confidence: 99%

Different Effects of L/N-Type and L-Type Calcium Channel Blockers on the Renin-Angiotensin-Aldosterone System in SHR/Izm

et al. 2009

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“…More recently, the Ca 2+ influx via T-type channels has been shown to be necessary for the hCG-dependent progesterone synthesis via a G protein coupled receptor in granulosa cells of the ovary (Agoston et al 2004). In glomerulosa cells of the adrenal gland, the maximal aldosterone secretion in response to stimulus by 8-bromo-cAMP is only achieved in the presence of external calcium, and T-type calcium channels are clearly involved (Uebele et al 2004). Whatever the mechanism, the increase in intracellular Ca 2+ , either released from intracellular stores or induced by entry from the extracellular compartment, is known to play an important role in steroidogenesis (Cooke, 1999).…”

Section: Discussionmentioning

confidence: 99%

Intracellular calcium changes in mice Leydig cells are dependent on calcium entry through T‐type calcium channels

Costa

Varanda

2007

The Journal of Physiology

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“…This increase in intracellular Ca 2+ can be blocked by the L-type CCB nifedipine, though not completely in the case of the angiotensin II-induced intracellular Ca 2+ elevation [27], with a concomitant decrease in aldosterone production [28]. In addition, even verapamil and diltiazem, which are nondihydropyridine L-type Ca 2+ channel antagonists, exerted inhibitory actions on aldosterone production in rat's adrenal glands [29]. These findings indicate that the production of aldosterone may be stimulated by processes other than by Ca 2+ influx through the L-type calcium channel.…”

Section: Actions Of Dihydropyridine Ccbs On Adrenal Steroid Synthesismentioning

confidence: 99%

Suppression of Aldosterone Synthesis and Secretion by Channel Antagonists

Ikeda

Isaka

Fujioka

et al. 2012

International Journal of Endocrinology

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Aldosterone, a specific mineralocorticoid receptor (MR) agonist and a key player in the development of hypertension, is synthesized as a final product of renin-angiotensin-aldosterone system. Hypertension can be generally treated by negating the effects of angiotensin II through the use of angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin II type 1 receptor antagonists (ARBs). However, the efficacy of angiotensin II blockade by such drugs is sometimes diminished by the so-called “aldosterone breakthrough” effect, by which ACE-Is or ARBs (renin-angiotensin system (RAS) inhibitors) gradually lose their effectiveness against hypertension due to the overproduction of aldosterone, known as primary aldosteronism. Although MR antagonists are used to antagonize the effects of aldosterone, these drugs may, however, give rise to life-threatening adverse actions, such as hyperkalemia, particularly when used in conjunction with RAS inhibitors. Recently, several groups have reported that some dihydropyridine Ca2+ channel blockers (CCBs) have inhibitory actions on aldosterone production in in vitro and in the clinical setting. Therefore, the use of such dihydropyridine CCBs to treat aldosterone-related hypertension may prove beneficial to circumvent such therapeutic problems. In this paper, we discuss the mechanism of action of CCBs on aldosterone production and clinical perspectives for CCB use to inhibit MR activity in hypertensive patients.

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Role of voltage-gated calcium channels in potassium-stimulated aldosterone secretion from rat adrenal zona glomerulosa cells

Cited by 16 publications

References 53 publications

Different Effects of L/N-Type and L-Type Calcium Channel Blockers on the Renin-Angiotensin-Aldosterone System in SHR/Izm

Different Effects of L/N-Type and L-Type Calcium Channel Blockers on the Renin-Angiotensin-Aldosterone System in SHR/Izm

Intracellular calcium changes in mice Leydig cells are dependent on calcium entry through T‐type calcium channels

Suppression of Aldosterone Synthesis and Secretion by Channel Antagonists

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