Study summary · research use only
Vasoactive intestinal peptide infusion reverses existing myocardial fibrosis in the rat
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study in Wistar Kyoto rats on a high (4.4%) salt diet, the authors examined whether infusion of vasoactive intestinal peptide (VIP) affects myocardial fibrosis. Rats were randomised to zero time control, 4 week infusion of VIP (5 pmol/kg/min), or vehicle control infusion. Myocardial VIP concentration, measured by radioimmunoassay, increased significantly in VIP-treated rats compared with vehicle-treated controls (P<0.01), while fibrosis, quantitated by computerised histomorphometry, was significantly lower in VIP-treated rats than in both the zero time control (P<0.05) and vehicle infused control (P<0.0005). Of six profibrotic mediators measured, VIP infusion was associated with significantly decreased mRNA expression of angiotensinogen (Agt, P<0.01) and angiotensin receptor type 1a (AT1a, P<0.01) versus vehicle infused controls.
Abstract
Congestive cardiac failure has become one of the major health challenges of the 21st century and new therapies are needed to address this problem. The concentration of vasoactive intestinal peptide (VIP) in the heart has been shown to decrease as fibrosis (the pathology leading to heart failure) increases and to become undetectable in end stage cardiomyopathy. We sought to determine whether replenishment of myocardial VIP might treat myocardial fibrosis and therefore represent a new therapeutic target. Wistar Kyoto rats on a high (4.4%) salt diet were randomised to zero time control, 4 week infusion of VIP (5 pmol/kg/min) or vehicle control infusion. Myocardial VIP concentration was measured by radioimmunoassay, fibrosis was quantitated by computerised histomorphometry and changes in pro-fibrotic mediators were measured by quantitative rt-PCR. Myocardial VIP increased significantly in VIP treated rats compared with vehicle treated controls (P < 0.01) while fibrosis in the VIP treated rats was significantly lower than in both the zero time control (P < 0.05) and the vehicle infused control (P < 0.0005). Although all six profibrotic mediators which were measured increased over the 4 week experimental period VIP infusion only affected angiotensinogen (Agt) and angiotensin receptor type 1a (AT1a) expression. In both instances VIP caused a significant decrease in messenger rna expression (Agt P < 0.01 and At1a P < 0.01) compared with vehicle infused controls. We conclude that VIP infusion increased myocardial VIP concentration and was able to reverse existing myocardial fibrosis suggesting a possible therapeutic role for a VIP based therapy in cardiac failure.
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