Magnesium metabolism in hypertension and type 2 diabetes mellitus.

The increasing evidence for the clinical relevance of altered magnesium metabolism to states of altered insulin resistance confirms the role of magnesium deficit as a possible underlying common mechanism of the "insulin resistance" of hypertension and altered glucose tolerance. The pioneer work of Lawrence M. Resnick and his group using the cellular ion-based approach that we are only partially presenting here has consistently contributed to the progress of the field, demonstrating (a) the critical importance of magnesium metabolism in regulating insulin sensitivity as well as vascular tone, and blood-pressure homeostasis; (b) that magnesium deficiency, defined on the basis of intracellular free magnesium levels, and or serum ionized magnesium is a common feature of both diabetic and hypertensive states as well as various other cardiovascular and metabolic processes and aging; (c) the ability of environmental factors such as dietary nutrient-sugar and mineral content to alter the set point of steady-state cell ion activity; and (d) that magnesium supplementation is indicated in conditions associated with magnesium deficit although well-designed therapeutic trials of magnesium in essential hypertension and type 2 diabetes mellitus are needed in the near future.

Interaction between ferric ions, phospholipid hydroperoxides, and the lipid phosphate moiety at physiological pH.

Iron-catalyzed lipid peroxidation was examined using 1H NMR in a biphasic aqueous-chloroform system. At physiological pH (7.4), mole ratios of phospholipids/Fe3+ as low as 1300:1 catalyzed the rapid disappearance of endogenous lipid hydroperoxides with a loss of two of the four double bonds in PC containing palmitic (16:0) and arachidonic (20:4) acids in the sn-1 and sn-2 positions, respectively.

Cellular-free magnesium depletion in brain and muscle of normal and preeclamptic pregnancy: a nuclear magnetic resonance spectroscopic study.

Preeclampsia is a pregnancy disorder of unknown origin, characterized by vasospasm, elevated blood pressure, and increased neuromuscular irritability, features common to syndromes of magnesium deficiency. Evidence of serum and ionized magnesium metabolism disturbances have been observed in women with preeclampsia. This and the therapeutic utility of magnesium in preeclampsia led us to investigate the extent to which an endogenous tissue magnesium deficiency might be present in and contribute to its pathophysiology.

Acute vascular effects of the angiotensin II receptor antagonist olmesartan in normal subjects: relation to the renin-aldosterone system.

The extent to which the clinical effects of angiotensin receptor blockers (ARB) are related to ambient renin system activity remains poorly defined. Therefore, we measured blood pressure (BP), large (C1) and small (C2) arterial compliance, systemic vascular resistance (SVR), plasma renin activity (PRA), and the 24-h urinary excretion of sodium (UNaV) and aldosterone before and 1, 2, 4, and 24 h after administration of single doses of placebo, and 5, 20, and 40 mg of the ARB olmesartan medoximil to 12 unmedicated normotensive subjects. In the basal state, SVR was inversely related to UNaV (r = -0.

Differential effects of antihypertensive drug therapy on arterial compliance.

Although vascular compliance, deltaV/deltaP, is abnormal in essential hypertension and can be improved by antihypertensive drug therapy, it is not clear whether drug-induced changes in compliance are attributable solely to lower achieved blood pressure (BP), and thus equally likely with different drugs possessing similar antihypertensive efficacy. Therefore, we used computerized arterial pulse waveform analysis (CAPWA) to measure capacitive (C1) and oscillatory (C2) components of arterial compliance in essential hypertensive subjects (n = 39) before, and 1 and 3 months after achieving normotensive BP values with administration of either dihydropyridine calcium channel antagonists (CaBl, n = 11), converting enzyme inhibitors (CEI, n = 9), angiotensin receptor blockers (ARB, n = 9), or beta-blockers (BBl, n = 10). Despite equivalent effects on BP (CABL: -19 +/- 4/-15 +/- 2 mm Hg; CEI: -12 +/- 3/-13 +/- 2 mm Hg; ARB: -10 +/- 3/-12 +/- 2 mm Hg; and BBl: -14 +/- 3/-12 +/- 2 mm Hg; P <.

Arterial elasticity among normotensive subjects and treated and untreated hypertensive subjects: influence of race.

Objectives: To determine arterial elasticity in normotensives and in treated and untreated hypertensive Black and White subjects.

Methods: A prospective multicenter, controlled clinical trial evaluated large (C-) and small (C2) artery elasticity indices among 3 groups: 1) normotensive subjects with or without a family history of hypertension; 2) controlled and treated hypertensive subjects; and 3) untreated and uncontrolled hypertensive subjects. Blood pressure was measured using a mercury manometer and arterial compliance or elasticity was determined using a CVProfilor DO-2020 CardioVascular Profiling System (Hypertension Diagnostics, Inc, Eagan, Minn).

Vascular Effects of Progesterone : Role of Cellular Calcium Regulation.

-Vascular actions of progesterone have been reported, independently of estrogen, affecting both blood pressure and other aspects of the cardiovascular system. To study possible mechanisms underlying these effects, we examined the effects of P in vivo in intact rats and in vitro in isolated artery and vascular smooth muscle cell preparations. In anesthetized Sprague-Dawley rats, bolus intravenous injections of P (100 µg/kg) significantly decreased pressor responses to norepinephrine (0.