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Biomedical subjects

A U Waks

Publications and source records attributed to A U Waks.

10 recordsLinked to original sources

Role of insulin and norepinephrine in the hypertension of obesity.

The present study compares plasma norepinephrine (PNE), renin activity (PRA), aldosterone (PA), and insulin (RIAI) levels between 13 normotensive and 42 hypertensive obese subjects during weight maintenance, and in 19 of the 42 obese hypertensive subjects, these variables were measured during 16 weeks on a very low calorie diet (VLCD). Mean values for baseline RIAI and PNE were elevated in the 55 obese subjects compared to nonobese controls. However, when the normotensive and hypertensive groups were compared, mean values for PNE, PRA, PA, and RIAI were not different. In the 19 obese hypertensive subjects studied on the VLCD, there were significant reductions from baseline in mean body weight, blood pressure, RIAI, and PNE, but not for PRA or PA. Two phases of blood pressure, RAIA, and PNE responses to weight loss were noted. In the early phase (days 1-7), blood pressure and RAIA decreased dramatically, whereas PNE, PRA, and PA increased. During the late phase (weeks 2-16), further significant decreases in blood pressure and weight were accompanied by reductions in PNE (604 +/- 50 to 403 +/- 43 pg/mL, P < .01) and in RIAI (13.9 +/- 1.7 to 10.3 +/- 1.6 microU/mL, P < .05). As levels of insulin and norepinephrine were similar in normotensive and hypertensive obese individuals during weight maintenance, they may not contribute to the hypertension associated with obesity. During weight loss, however, the temporal changes in blood pressure, insulin, and norepinephrine suggest their mediation of the hypotensive response.

Adult↗

Cations in essential hypertension.

Sodium intake has been linked to the development and perpetuation of hypertension for almost a century. Nevertheless, considerable controversy over this relationship remain. More recently, the other major body cations, potassium, calcium and magnesium, have also been implicated. The evidence relating dietary sodium, potassium, calcium and magnesium intake to hypertension is summarized, and the present evidence for dietary modification of cation intake in the treatment of mild essential hypertension is evaluated.

Calcium↗

Cations and hypertension: sodium, potassium, calcium, and magnesium.

The association between sodium intake and hypertension has been studied for almost a century. More recently, it has been suggested that abnormalities in dietary intake of potassium, calcium, and magnesium may play a major role in the pathogenesis of hypertension. A critical analysis of selected data from animal and human studies is discussed.

Animals↗

Obesity and hypertension: long-term effects of weight reduction on blood pressure.

Long-term follow-up studies were conducted on massively obese hypertensive subjects during and after a successful protein supplemented fast (PSMF) in order to correlate blood pressure changes with caloric intake and body weight. The blood pressures in 43 subjects were compared during rapid weight loss and at identical weights during post-fast weight gain (Study A). Blood pressures and body weights in 50 subjects were compared prior to starting PSMF and prior to restarting the program 21 months later (Study B). One hundred twenty-five compliant subjects were observed after one month of weight maintenance (Study C-1), and 39 subjects were followed during six months of weight maintenance (Study C-2). In Study A, during subsequent weight gain on an unrestricted diet blood pressure was significantly higher than at identical weight during continuous weight loss on PSMF. However, this increase in blood pressure was only approximately 30 percent of the original decrease. In Study B, weight loss and blood pressure reduction were significantly correlated. After one month of weight maintenance following continuous weight loss of 73 lb, there was no increase in blood pressure (Study C-1). A small but significant increase in blood pressure after six months (Study C-2) was associated with similar small weight increment. However, all blood pressures remained well within the normotensive range and significantly lower than control values. In this study, long-term changes in blood pressure correlated with changes in body weight.

Blood Pressure↗

BP changes in obese hypertensive subjects during rapid weight loss. Comparison of restricted v unchanged salt intake.

A controlled prospective study compared two groups of obese hypertensive subjects during 12 weeks of a hypocaloric protein-supplemented fast containing 40 mEq of sodium daily. One group received additional sodium chloride sufficient to maintain baseline sodium intake measured prior to the fast (210 m/Eq/day). Sodium restriction resulted in greater weight loss and slightly greater BP reduction only during the initial week of fasting. Thereafter, despite sodium equilibrium, further substantial weight loss and BP reduction were identical in both groups, the decrement in weight being linear (1.89 kg/wk) and the BP reduction asymptotic. Although the initial reduction in BP during the first week of supplemented fast may be attributable to negative salt and water balance, the further reduction in BP during a period of constant sodium balance must be caused by weight loss per se or by the triggering of other antihypertensive mechanisms associated with weight reduction.

Blood Pressure↗

Error in blood-pressure measurement due to incorrect cuff size in obese patients.

Trained nurse-specialists obtained 84 000 blood-pressure measurements in 1240 obese subjects using cuffs of the three standard adult sizes in a randomised order. The differences in readings between the three cuffs were smallest in non-obese subjects and became progressively greater with increasing arm circumference (AC) in the obese population. The regular cuff (12 X 23 cm) showed the greatest bias in relation to AC. Formulae and a table have been derived to correct the measurement error caused by cuffs of inappropriate size at various ACs. The reported high prevalence of hypertension in obese subjects may be greatly overestimated.

Arm↗