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Deficiency of the T‐type Calcium Channel Ca v 3.1 attenuates Plasma Aldosterone and Cardiac Hypertrophy despite similar Ang II‐induced Hypertension
Author(s) -
Thuesen Anne,
Jensen Boye,
Hansen Pernille
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.957.6
Subject(s) - aldosterone , medicine , endocrinology , plasma renin activity , renin–angiotensin system , blood pressure , mineralocorticoid , chemistry , angiotensin ii , heart rate
Background T‐type calcium channels affect adrenal aldosterone stimulus‐secretion coupling. It was hypothesized that Ang II infusion led to an attenuated blood pressure increase and aldosterone response in Ca v 3.1 ‐/‐ mice. Method Mean arterial pressure was measured continuously with chronically indwelling catheters. Plasma aldosterone and renin were measured with RIA. Results Ang II increased significantly mean arterial pressure in Wt and Ca v 3.1 ‐/‐ mice with no differences between genotypes. Heart rate in Ang II‐infused Ca v 3.1 ‐/‐ mice was significantly lower compared to control. Plasma aldosterone was significantly lower in the Ca v 3.1 ‐/‐ mice compared to the Wt mice after Ang II infusion. At baseline, there was a tendency towards a lower aldosterone level in the in the Ca v 3.1 ‐/‐ mice compared to the Wt mice. The heart/body weight ratio was significantly higher after Ang II infusion in Wt mice compared to Ca v 3.1 ‐/‐ . The Ang II‐induced heart weight increase in Wt mice was inhibited by mineralocorticoid receptor blocker administration with no effect on MAP. Plasma renin was significantly lower after Ang II infusion in both groups. Summary; global deletion of T‐type Ca v 3.1 subtype attenuates AngII‐induced aldosterone plasma increase and heart rate. The attenuated plasma aldosterone impairs cardiac hypertrophy in Ang II induced hypertension. Conclusion Ca v 3.1 channels affect the plasma aldosterone levels but not Ang II induced hypertension. Aldosterone contributes significantly to cardiac hypertrophy in vivo independently of blood pressure and Ang II concentration. Foundation Danish Research Council and Danish Heart Foundation