Drugs targeting CB1R, CB2R, TRPV1 and PPARs are proven effective in animal models mimicking cardiovascular disorders such as hypertension, atherosclerosis and myocardial infarction.
The results obtained in the codominant and overdominant models for the <i>PPAR-y</i> polymorphism showed a tendency to statistical significance (the C/G genotype inclined to hypertriglyceridemia), and were statistically significant in the codominant, dominant, and recessive models (the C/C genotype predisposed to increased blood pressure).
The biological actions of PPARα and PPARγ and their potential as a cardiovascular therapeutic target have been extensively reviewed, whereas the biological actions of PPARβ/δ and its effectiveness as a therapeutic target in the treatment of hypertension remain less investigated.
Importantly, TAFIa inhibitor and peroxisome proliferator-activated receptor-α agonists significantly reduced TAFIa and ameliorated animal models of pulmonary hypertension in mice and rats.
These data suggest that increased PPARalpha expression is a protective mechanism in hypertensive renal injury induced by nitric oxide withdrawal/high salt diet and that siRNAs targeting the DNA-binding domain of PPARalpha gene elicited differential effects on hypertension and kidney injury.
These data suggest that increased PPARalpha expression is a protective mechanism in hypertensive renal injury induced by nitric oxide withdrawal/high salt diet and that siRNAs targeting the DNA-binding domain of PPARalpha gene elicited differential effects on hypertension and kidney injury.
Making the THM animals deficient in Peroxisome proliferator-activated receptor-alpha (THM/PPARKO) totally abolished hypertension and myocardial hypertrophy.
Thus, apart from inhibition of ET-1 production, PPARalpha activation exerts protective actions in hypertension via a mechanism that involves NO production and/or inhibition of NAD(P)H oxidase activity.
Therefore, chronic PPAR-alpha agonist treatment reduces salt-dependent hypertension produced by ETB receptor blockade in male and female Sprague-Dawley rats.
Thus, apart from inhibition of ET-1 production, PPARalpha activation exerts protective actions in hypertension via a mechanism that involves NO production and/or inhibition of NAD(P)H oxidase activity.
We demonstrate that variation in the PPARalpha gene influences human left ventricular growth in response to exercise and hypertension, indicating that maladaptive cardiac substrate utilization can play a causative role in the pathogenesis of LVH.
We demonstrate that variation in the PPARalpha gene influences human left ventricular growth in response to exercise and hypertension, indicating that maladaptive cardiac substrate utilization can play a causative role in the pathogenesis of LVH.