Time-course of the change in blood pressure level in magnesium-deficient Wistar rats.
The aim of the present study was to determine whether a severely Mg-deficient diet can modify blood pressure in rats and whether these alterations in blood pressure are associated with a change in in vivo cardiovascular reactivity, alteration in plasma lipids and modification of the production of hormones involved in blood pressure regulation. Weanling male Wistar rats were pair-fed for 40 weeks with control (960 mg Mg/kg) and Mg-deficient (80 mg Mg/kg) diets. At 2 weeks, blood pressure was lower in Mg-deficient rats, while heart rate was greater than in controls. Mg-deficiency-induced hypotension was transitory and the administration of antihistamine agents inhibited the appearance of this hypotensive phase, suggesting that histamine may play a role in lowering blood pressure. Until 15 weeks, blood pressures were similar for control and Mg-deficient rats. Thereafter, blood pressure rose gradually until the end of the experiment in Mg-deficient rats. Heart rate remained higher in hypertensive Mg-deficient rats. After 21 weeks, in vivo cardiovascular reactivity to noradrenaline was lower and reactivity to angiotensin II was unchanged in hypertensive Mg-deficient rats. At 2 and 21 weeks, hypomagnesaemia was accompanied by higher plasma levels of Ca, triacylglycerols and cholesterol. Plasma renin activity was higher at week 2, whereas levels of plasma angiotensin converting enzyme were lower at 2 and 21 weeks in Mg-deficient rats. The plasma aldosterone level was higher at 2 and 21 weeks while the vasopressin level did not change. Plasma corticosterone levels were lower at 2 weeks and higher at 21 weeks. It is concluded that Mg deficiency induced a transitory hypotension followed by a sustained hypertension in rats. The release of vasodilator inflammatory agents may contribute to the early hypotension. The hypertensive phase may be explained by the increased sympathetic nervous activity induced by Mg deficiency even though the contribution of several hormonal systems implicated in blood pressure regulation remains to be elucidated.
Laurant
P
P
Laboratoire Physiologie, Pharmacologie et Nutrition Préventive Expérimentale, UFR Médecine et Pharmacie, Besançon, France.
Dalle
M
M
Berthelot
A
A
Rayssiguier
Y
Y
D000450:Aldosterone / Q000097:blood; D000704:Analysis of Variance; D000804:Angiotensin II; D000818:Animals; D001835:Body Weight; D002118:Calcium / Q000097:blood; D002316:Cardiotonic Agents; D002784:Cholesterol / Q000097:blood; D003345:Corticosterone / Q000097:blood; D006339:Heart Rate; D006634:Histamine H1 Antagonists / Q000627:therapeutic use; D007022:Hypotension / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D008275:Magnesium Deficiency / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D008297:Male; D009638:Norepinephrine; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D014662:Vasoconstrictor Agents
D002316:Cardiotonic Agents; D006634:Histamine H1 Antagonists; D014280:Triglycerides; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D000450:Aldosterone; D002784:Cholesterol; D007703:Peptidyl-Dipeptidase A; D002118:Calcium; D003345:Corticosterone; D009638:Norepinephrine