Hormone replacement therapy reduces mean 24-hour blood pressure and its variability in postmenopausal women with treated hypertension.

BACKGROUND: The rate and severity of hypertension increase dramatically after menopause. Complications seem to be more frequent and marked in hypertensive patients with greater blood pressure (BP) variability, and antihypertensive treatment does not easily reduce this variability. The effect of hormone replacement therapy (HRT) on BP and its variability is not well understood in moderate to severe hypertension, but estrogen may have calcium channel-blocking properties. Cardiovascular events occur more frequently in the morning, likely in part because of a rise in BP. DESIGN: We prospectively studied 34 postmenopausal women with treated hypertension (mean age = 53 years) and receiving a cyclic combination of estradiol and norgestrel for 19 weeks with 24-h ambulatory BP monitoring. RESULTS: Mean daily BP and its variability decreased significantly with HRT (149.3 +/- 6.1 mm Hg vs. 140.3 +/- 8.5 mm Hg [p < 0.001]; diastolic: 95.4 +/- 4.7 mm Hg vs. 92.4 +/- 7.2 mm Hg [p < 0.05]). There was also a significant decrease in the early morning BP values after HRT (154.0 +/- 6.9 mm Hg vs. 145.6 +/- 11.0 mm Hg [p < 0.001]; diastolic: 98.0 +/- 4.8 mm Hg vs. 95.1 +/- 10.0 mm Hg [p < 0.05]). Subjects who were taking calcium channel blockers (n = 11) had only half the reduction in 24-h systolic BP compared with those who were not taking calcium channel blockers (5.3 mm Hg vs. 10.5 mm Hg), and the reduction in those who were taking calcium channel blockers failed to reach statistical significance. CONCLUSIONS: Our results demonstrate that HRT may have a role in decreasing the severity of hypertension, and the mechanism of its action might be through calcium channels.

Zinc, copper and manganese in serum, urine and stones.

Serum zinc, copper and manganese levels were estimated in normal subjects (NS) and stone formers (SF). There was no significant difference in the serum levels of Zn, Cu, and Mn in NS and SF, the values being 101.5 +/- 35.1 micrograms% and 94.3 +/- 45.6 for Zn; 91.75 +/- 27.0 micrograms% and 88.5 +/- 34.1 for Cu; and 87.0 +/- 36.7 micrograms% and 79.6 +/- 35.5 for Mn, respectively. Zinc excretion was relatively high in NS (790.08 +/- 172.88 micrograms/dl) as compared to other populations and was significantly higher in SF (1154.92 +/- 290.17 micrograms%, p less than 0.001). Copper and manganese excretions in SF were significantly lower than in NS (p less than 0.001). Zinc was present in substantial quantities in renal (2.52 +/- 3.98 g%), ureteric (0.75 +/- 0.51 g%) and vesical (1.71 +/- 3.20 g%) stones. Manganese was present in traces in all the stones and copper in two-thirds of the stones.

Sodium is neither a risk nor a protective factor in urolithiasis?

The effect of changes in urinary sodium, induced by dietary manipulation in normal subjects (NS) and in stone formers (SF) was studied by observing crytalluria qualitatively and by determining calcium, oxalate and phosphate crystallization quantitatively in an experimental model. In SF the calcium crystallization was significantly higher than in NS at all the three levels of urinary sodium studied. However, no difference was observed in oxalate and phosphate crystallization rates between these two groups. Calcium and oxalate (p less than 0.05) and oxalate and phosphate (p less than 0.001) were found to be correlated in NS but were non-significant in SF. The wide changes in the urinary sodium induced by dietary changes did not influence the crystallization rate of calcium, nor of oxalate and phosphate in NS as well as in SF. The results suggested that a sodium intake with lower and upper limits of 124 mg and 6,009 mg respectively did not act as "inhibitor" of crystallization rate nor did it induce hypercalciuria severe enough to pose a "risk" of stone formation. The results did not suggest that a high urinary sodium increases the solubility of calcium phosphate.