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Hormone replacement therapy (HRT) reduces the incidence of cardiovascular disease (CVD) in postmenopausal women (PMW). Recently, it has been reported that HRT declines angiotensin converting enzyme (ACE) activity, which may be one of the factors protecting against CVD. We measured the plasma levels of bradykinin, which would be expected to increase because the bradykinin-degrading enzyme (kinase II) is the same as ACE. Treatment with conjugated estrogens (0.625 mg/day) and medroxyprogesterone (2.5 mg/ day) was given for 3 months as HRT to 19 hypertensive and 19 normotensive PMW. Plasma bradykinin and ACE activity levels were measured at baseline and after 3 months of HRT. The plasma levels of ACE activity in both the hypertensive and normotensive PMW were significantly reduced by HRT. The plasma levels of bradykinin in the hypertensive PMW were significantly increased by HRT, whereas the administration of HRT tended to increase plasma levels of bradykinin in the normotensive PMW. The increased bradykinin levels with a concomitant decrease of plasma ACE activity by HRT in hypertensive PMW seem to be beneficial for reducing the risk of CVD.

We investigated whether endothelial dysfunction might contribute to the exaggerated vasoconstriction that was induced by the administration of norepinephrine at the early stage of one-kidney, one-clip renal hypertension (1K1C) in rats. We also studied the role of the renin-angiotensin system in this phenomenon. Male Wistar rats were killed 48 hours after the induction of renal artery stenosis or sham operation, and ring preparations of the thoracic aorta were obtained. The isometric contraction and relaxation of aortic strips produced by norepinephrine and acetylcholine, respectively, were recorded with a force-displacement transducer. The aorta of 1K1C rats showed a significantly (P<.05) exaggerated contractile response to norepinephrine as compared with that of control rats. Rubbing the endothelium and treatment with methylene blue or N0-monomethyl L-arginine acetate augmented the contractile responses to norepinephrine to a greater extent in Although an increased vascular reactivity to vaso-L.1 constrictor substances has been observed both in clinical hypertension",2 and in animal models of hypertension,3-9 the mechanisms are not completely understood. Folkow et al10 suggest that this hyperresponsiveness in hypertension is due to vascular wall hypertrophy or medial hypertrophy that results in an increased vessel wall to lumen ratio. Findings of other investigators4,5"11 indicate that such mechanisms are not the only explanation. For instance, Prewitt et al"l reported that no vascular wall hypertrophy was observed in resistance vessels of one-kidney, one-clip renal hypertensive (iKiC) rats, despite a structural reduction in the size of the lumen. Others45 have reported that an exaggerated pressor response and increased sensitivity (change in threshold) to norepinephrine occur in rabbits with renal artery stenosis at an early stage, even before the onset of hypertension. These studies4,5"11 indicate that the exaggerated pressor response may be due to some alteration in the responsiveness of the vessels without hypertrophy of the vascular wall and suggest that the responsiveness of the vascular smooth muscle cells itself may be enhanced. However, confirmatory evidence is lacking.Received February 18, 1993; accepted October 8, 1993 Our objective was to determine the role of depressed synthesis and/or release of EDRF on the exaggerated vasoconstrictive response to norepinephrine at the early stage of hypertension before the development of vascular wall hypertrophy or an increased vascular wall to lumen ratio. The present study was designed to clarify the role of the renin-angiotensin system in endothelial by guest on

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The level of nitric oxide (NO) in exhaled air fluctuates in normal individuals depending on the physiological conditions. We evaluated the effects of duration of exhalation and breath-holding on the exhaled concentrations of NO in 16 normal human volunteers. Exhaled gas corresponding to vital capacity was collected in 6-liter Tedlar bags and analyzed by chemiluminescence. The NO concentration in exhaled gas increased significantly in proportion to the duration of exhalation [P = 0.009 +/- 0.011 (SD)] and was increased after breath-holding. There was no significant difference in the exhaled NO concentration among 10-s phases of a 30-s exhalation, as determined from multiple breath collections. The NO released from the airways is presumably unaffected by fluctuation of exhalation speed. The NO release rate, calculated from a single regression analysis between the NO concentration and the duration of exhalation, was 39 +/- 29 pmol/s, a value which was about fourfold greater in nine patients with bronchial asthma.

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Background and Aim:  A cut‐off value of 2.5‰ for the 13C‐urea breath test (UBT) is recommended in Japanese persons, based on the result of a multicenter trial in patients prior to treatment for eradication of Helicobacter pylori. The cut‐off value of 2.5‰ has also been used in the assessment of eradication after treatment. The 6–8‐week evaluation after treatment is recommended in the guidelines of the Japanese Society of Gastroenterology. The present study aimed to prospectively re‐assess the cut‐off value of the 13C‐UBT at 6 weeks after treatment by using the results obtained at 6 months as an indication of true positive or true negative H. pylori infection status. Methods:  One hundred and ninety patients who were positive for H. pylori underwent eradication treatment, and 177 patients of these patients who were assessed as having true positive or true negative H. pylori status  at  6 months  after  treatment  were  evaluated  in  this  study.  Eradication  was  assessed  by 13C‐UBT,  culture,  and  histology  at  6 weeks  and  at  6 months  after  treatment,  and  the  cut‐off  value  of 13C‐UBT at 6 weeks was re‐assessed. Results:  A cut‐off value of 3.5‰. at 6 weeks after treatment showed 97.2% diagnostic accuracy, while a cut‐off value of 2.5‰ at 6 weeks showed 96.0% diagnostic accuracy. For a 3.5‰ cut‐off value, only five patients were positive by 13C‐UBT and were negative by culture and histology at 6 weeks, and three patients were true positive and two were false positive by the 13C‐UBT at 6 months. Conclusion:  A cut‐off value of 3.5‰ for the 13C‐UBT is recommended at 6 weeks after eradication treatment in Japanese persons.