WHEY MINERAL SUPPLEMENTATION AND ARTERIAL TONE IN MINERALOCORTICOID-NACL HYPERTENSION

Objective: The aim was to study the effects of supplementation of rat chow diet with whey mineral concentrate (Whey), a diet rich in milk mi nerals, on arterial responses in vitro in mineralocorticoid-NaCl hyper tension. Methods: Forty young Wistar rats were allocated to four group s: Wistar, Whey-Wistar, deoxycorticosterone (DOG), and Whey-DOG. DOG ( 10 mg kg(-1) s.c.) was given twice a week and these rats drank 0.7% Na Cl solution, while the others received equal volumes of vehicle (sesam e oil) and drank tap water, The supplementation was performed by addin g 25% whey mineral concentrate to the chow, which in particular increa sed the intake of potassium and also that of calcium and magnesium in the rats. Responses of mesenteric arterial rings were examined in stan dard organ chambers after 10 study weeks. Results: During the 10 week study the DOG-NaCl treatment had a marked hypertensive effect in rats, while the whey mineral supplementation was without significant effect on blood pressure in the Whey-DOC and Whey-Wistar groups. Arterial re laxation induced by nitroprusside was attenuated in the DOC-treated ra ts, but was significantly shifted towards that of controls in the Whey -DOc group. Interestingly, endothelium-dependent relaxation to acetylc holine (ACh), which was clearly impaired in the DOG group, was compara ble in the Whey-DOG and Wistar groups. Moreover, only in the DOG group the relaxation was improved by diclofenac suggesting that ACh was rel easing cyclo-oxygenase-derived contractile factors from the endotheliu m, and the response was completely abolished by N-G-nitro-L-arginine m ethyl ester (L-NAME). In contrast, diclofenac had a negligible effect on the response in the other groups which also showed distinct relaxat ions to ACh in the presence of L-NAME. This remaining response to ACh in Wistar rats was inhibited by the addition of apamin and glibenclami de, inhibitors of calcium-activated and ATP-sensitive potassium channe ls, respectively, suggesting that it was mediated by endothelium-depen dent hyperpolarization. In the Whey-Wistar group arterial function did not differ from control Wistars. Conclusions: Supplementation with wh ey mineral concentrate had a protective effect on endothelium-mediated control of arterial tone in experimental DOC-NaCl hypertension.