Resveratrol treatment was beneficial in preventing the development of concentric hypertrophy and cardiac dysfunction in SHR. The cardioprotective effect of resveratrol in SHR may be partially mediated by a reduction in oxidative stress. Thus, resveratrol may have potential in preventing cardiac impairment in patients with essential hypertension.

The ability of resveratrol to limit the increase in compliance of SHR arteries is likely related to inhibitory effects on remodeling and pro-growth ERK signaling rather than blood pressure or arterial wall component stiffness.

Collectively, these findings show that the anti-hypertrophic actions of PPARs require DGKζ. Thus, within the cardiomyocyte, there exists a PPAR-DGK signalling axis that underpins the ability of PPAR ligands to inhibit ET1-dependent hypertrophy.

Background: Consumption of high-glycemic index foods contributes to the development of hypertension in some patients. Likewise, in spontaneously hypertensive rats (SHR), high sucrose promotes a secondary rise in systolic blood pressure (SBP). Chromium (III) (Cr³⁺) prevents sucrose-induced hypertension, but leaves the basal hypertension that characterizes SHR intact. Methods: Since hypertension entails increased peripheral resistance, we compared effects of Cr³⁺ on resistance arteries from SHR fed low-glycemic (starch) versus high-glycemic (sucrose) index diets. Subgroups of SHR also received Cr³⁺. Structure, stiffness, and vasodilation of mesenteric resistance arteries were studied using pressurized myography. Results: Sucrose increased SBP in SHR and, exclusively in sucrose-fed SHR, Cr³⁺ reduced SBP and augmented acetylcholine or nitroprusside-dependent vasodilation. Neither sucrose nor Cr³⁺ affected artery structure or stiffness. Since Cr³⁺ enhanced vasodilation, we assessed endothelial NO synthase (eNOS), guanylate cyclase, cGMP-dependent protein kinase (PKG-1α and 1β), and PKG activity by immunoblotting. Sucrose reduced eNOS, PKG-1β, and PKG activity. Cr³⁺ prevented the effects of sucrose on NO signaling. Conclusion: In hypertension exacerbated by high-glycemic index diet, Cr³⁺ reduces SBP. The BP-lowering effect of Cr³⁺, selectively on sucrose-induced but not basal hypertension in SHR, involves at least in part, improving vasodilatory function vis-à-vis restoration of NO signaling in resistance arteries.

Polyunsaturated fatty acids (PUFAs) have significant, cardioprotective effects against ischemia. Hempseed contains a high proportion of the PUFAs linoleic acid (LA) and alpha-linolenic acid (ALA), which may have opposing effects on postischemic heart performance. There are no reported data concerning the cardiovascular effects of dietary hempseed intake. A group of 40 male Sprague-Dawley rats were distributed evenly into four groups that were fed for 12 wk a normal rat chow supplemented with hempseed (5% and 10%), palm oil (1%), or a 10% partially delipidated hempseed that served as a control. Plasma ALA and gamma-linolenic acid levels were significantly elevated in the rats that were fed a 5% or 10% hempseed-supplemented diet, but in heart tissue only ALA levels were significantly elevated in the rats fed these diets compared with control. After the dietary interventions were completed, postischemic heart performance was evaluated by measuring developed tension, resting tension, the rates of tension development and relaxation, and the number of extrasystoles. Hearts from rats fed a hempseed-supplemented diet exhibited significantly better postischemic recovery of maximal contractile function and enhanced rates of tension development and relaxation during reperfusion than hearts from the other groups. These hearts, however, were not protected from the occurrence of extrasystoles, nor were the increases in resting tension altered during ischemia or reperfusion as a function of any dietary intervention. Our data demonstrate that dietary hempseed can provide significant cardioprotective effects during postischemic reperfusion. This appears to be due to its highly enriched PUFA content.