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Amiloride normalizes arterial pressure in Cyp1a1ren‐2 transgenic rats without significant effects on small artery function
Author(s) -
Grisk Olaf,
Rohsius Robert,
Schmid Catherina,
Schlüter Torsten,
Rettig Rainer
Publication year - 2009
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.23.1_supplement.605.2
Subject(s) - amiloride , medicine , endocrinology , blood pressure , renin–angiotensin system , transgene , vasodilation , vasoconstriction , epithelial sodium channel , plasma renin activity , artery , nifedipine , angiotensin ii , sodium , chemistry , calcium , biochemistry , organic chemistry , gene
Activation of the vascular and renal epithelial sodium channel (ENaC) may contribute to arterial hypertension. Cyp1a1ren‐2 transgenic rats carry a renin transgene the expression of which can be induced by feeding an inductor. During transgene induction, these rats show high plasma aldosterone and tissue angiotensin II levels. We tested if hypertension is sensitive to amiloride in these rats and if transgen activation causes amiloride‐sensitive alterations in small arteries that may contribute to hypertension. Cyp1a1ren‐2 transgenic rats (n = 6‐8 per group) were randomized to control (ctr), three weeks transgene induction (ind) and three‐weeks transgene induction + amiloride (amil) during the last week. At the end of the experiment, mean arterial pressure (MAP) was 118 ± 2 (ctr); 153 ± 8 (ind) and 118 ± 2 mmHg (amil). With MAP as effective transmural pressure, third order mesenteric and renal arteries did not show differences in lumen diameter. There was no difference in vascular compliance, α 1 ‐adrenoceptor‐ or depolarisation‐induced vasoconstriction and endothelium‐dependent vasodilation. Amiloride‐induced arterial pressure reduction in transgen‐induced rats was accompanied by increased renal sodium excretion. We conclude that amiloride normalizes arterial pressure in Cyp1a1ren2 transgenic rats likely by stimulating renal sodium excretion but without appreciable effects on small artery function.