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 minerals, on arterial responses in vitro in mineralocorticoid-NaCl hypertension.


METHODS
Forty young Wistar rats were allocated to four groups: Wistar, Whey-Wistar, deoxycorticosterone (DOC), and Whey-DOC. DOC (10 mg kg-1 s.c.) was given twice a week and these rats drank 0.7% NaCl solution, while the others received equal volumes of vehicle (sesame oil) and drank tap water. The supplementation was performed by adding 25% whey mineral concentrate to the chow, which in particular increased the intake of potassium and also that of calcium and magnesium in the rats. Responses of mesenteric arterial rings were examined in standard organ chambers after 10 study weeks.


RESULTS
During the 10 week study the DOC-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 relaxation induced by nitroprusside was attenuated in the DOC-treated rats, but was significantly shifted towards that of controls in the Whey-DOC group. Interestingly, endothelium-dependent relaxation to acetylcholine (ACh), which was clearly impaired in the DOC group, was comparable in the Whey-DOC and Wistar groups. Moreover, only in the DOC group the relaxation was improved by diclofenac suggesting that ACh was releasing cyclo-oxygenase-derived contractile factors from the endothelium, and the response was completely abolished by NG-nitro-L-arginine methyl ester (L-NAME). In contrast, diclofenac had a negligible effect on the response in the other groups which also showed distinct relaxations to ACh in the presence of L-NAME. This remaining response to ACh in Wistar rats was inhibited by the addition of apamin and glibenclamide, inhibitors of calcium-activated and ATP-sensitive potassium channels, respectively, suggesting that it was mediated by endothelium-dependent hyperpolarization. In the Whey-Wistar group arterial function did not differ from control Wistars.


CONCLUSIONS
Supplementation with whey mineral concentrate had a protective effect on endothelium-mediated control of arterial tone in experimental DOC-NaCl hypertension.
Wu
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X
Department of Pharmacology, University of Tampere, Medical School, Finland.
Mäkynen
H
H
Korpela
R
R
Pörsti
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I
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003900:Desoxycorticosterone; D004008:Diclofenac / Q000494:pharmacology; D006973:Hypertension / Q000178:diet therapy* / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000503:physiopathology; D008892:Milk; D008903:Minerals / Q000008:administration & dosage*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012965:Sodium Chloride; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
D016861:Cyclooxygenase Inhibitors; D008903:Minerals; D014665:Vasodilator Agents; D004008:Diclofenac; D009599:Nitroprusside; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D011189:Potassium Chloride; D019001:Nitric Oxide Synthase; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester