Effect of light-percentage, stimulus-luminance, exposure-duration and their interactions upon the CFF threshold.
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Adolescent↗
Biomedical subjects
T J Moore
Publications and source records attributed to T J Moore.
Converting enzyme inhibition in essential hypertension: the hypotensive response does not reflect only reduced angiotensin II formation.
To determine the relative importance of hormonal factors in mediating the hypotensive response to converting enzyme inhibition (CEI), plasma renin activity (PRA), angiotensin II, and bradykinin responses to SQ20,881 were measured in 20 supine patients with essential hypertension in balance on a 10 mEq sodium diet. Patients were divided into two groups according to their diastolic blood pressure response: responders had a decrement in diastolic pressure which exceeded 9 mm Hg, the upper value of the 95% confidence limits for normotensive patients studied under similar conditions; nonresponders did not. Compared to the nonresponders, responders not only had a higher control PRA (8.7 +/- 1.7 ng/ml/hr vs 4.8 +/- 2.1, p < 0.05) and larger decrement in plasma angiotensin II (18.7 +/- 4.9 pg/ml vs 3.2 +/- 1.7, p < 0.01), but also had a higher control bradykinin (3.2 +/- 0.7 ng/ml vs 1.1 +/- 0.2, p < 0.05) and larger increment in bradykinin (4.5 +/- 1.3 ng/ml vs 1.0 +/- 0.4, p < 0.05) following SQ20,881. Because SQ20,881 altered both angiotensin II and bradykinin concentrations, we assessed the contribution of blockade of angiotensin II formation by administering angiotensin II infusions to seven responders during coverting enzyme blockade, with the angiotensin II dose adjusted to restore diastolic pressure to control levels. The plasma angiotensin II level required to return blood pressure to control was 45 +/- 15 pg/ml higher than the control plasma angiotensin II level (p < 0.01), suggesting that some other factor(s), perhaps bradykinin, are also responsible for the hypotensive response to converting enzyme inhibition.
Adolescent↗
Differences in response to the peptidyldipeptide hydrolase inhibitors SQ 20,881 and SQ 14,225 in normal-renin essential hypertension.
We compared vascular and hormonal responses to teprotide (SQ 20,881) and captopril (SQ 14,225) in patients with normal renin essential hypertension given a 10 mEq sodium diet. In 10 patients receiving SQ 20,881, significant changes occurred in diastolic blood pressure (DBP, -13 +/- 2.5 mm Hg), angiotensin II (-7.1 +/- 2.1 pg/ml), and plasma renin activity (PRA, +6.6 +/- 1.9 ng/ml/hr) (p < 0.01 in all cases). Twenty-one patients receiving SQ 14,225 had significant changes in mean DBP (-18 +/- 1.5 mm Hg), angiotensin II (-6.6 +/- 1.5 pg/ml), and PRA (+7.8 +/- 2.4 ng/ml/hr) (all p values < 0.01). In spite of a significantly greater hypotensive response (p < 0.02), patients receiving SQ 14,225 showed increments in PRA and decrements in angiotensin II that did not differ significantly from those seen after SQ 20,881. Moreover, there was a significant change in plasma kinins in patients receiving SQ 20,881 (+2.0 +/- 0.9 ng/ml, p < 0.01) but no change in kinins in patients receiving SQ 14,225 (0.0 +/- 0.1, ns). We conclude that there are important differences in the mechanism mediating the hypotensive response to SQ 20,881 and SQ 14,225 in normal renin essential hypertension.
Adult↗
Contribution of prostaglandins to the antihypertensive action of captopril in essential hypertension.
To determine whether prostaglandins contribute to the depressor response to the converting enzyme inhibitor, captopril, we measured the plasma prostaglandin levels by radioimmunoassy before and after captopril administration, and then examined the effect of prostaglandin synthetase inhibition on captopril's antihypertensive effect. When a single oral captopril dose (25-100 mg) was given to 31 sodium-restricted patients with essential hypertension, the levels of the stable transformation product of prostacyclin remained unmeasurable and that of thromboxane A2 did not change, while the metabolite of PGE2 (PGE-M) increased by 53% (34 +/- 4pg/ml pre-captopril, 52 +/- 5 pg/ml after; p less than 0.001). As expected, blood pressure (BP) and angiotension II (AII levels fell, and kinin levels rose (all changes p less than 0.001). We then blocked prostaglandin synthesis in 18 of these subjects for 24 hours with either indomethacin (n = 10) or aspirin (n = 8) before repeating the captopril dose, to assess the importance of these PGE-M increments. The PGE-M responses to captopril were effectively blocked in nine of 10 subjects receiving indomethacin and four of eight receiving aspirin. In these 13 patients, the depressor response to captopril was significantly blunted (-20 +/- 3mm Hg pre-synthetase inhibition vs - 13 +/- 2 mm Hg post; p less than 0.05). When these agents did not block the PGE-M response to captopril, the BP response was also unchanged (-15 +/- 4mm Hg pre, -18 +/- 5mm Hg post). Neither indomethacin nor aspirin changed the AII or kinin responses to captopril. We conclude that the prostaglandins may be important mediators of captopril's antihypertensive effect in the sodium-restricted state.
Adult↗
Converting-enzyme inhibition corrects the altered adrenal response to angiotensin II in essential hypertension.
Of patients with essential hypertension, 30% to 50% do not modulate adrenal and renovascular responsiveness to angiotensin II (AII) with changes in sodium intake. To define the role of AII in mediating these altered responses, the adrenal and renal vascular responses to AII infusion (0.3, 1.0, 3.0 ng/kg/min) were assessed on a sodium-restricted intake in 31 patients with essential hypertension and 13 normotensive controls before and after 72 hours of converting-enzyme inhibition. Forty percent of the hypertensive patients had a subnormal adrenal response to AII. There were no differences between the normal and abnormal responding hypertensive patients in a number of clinical and biochemical factors except that the "abnormal responders" had a significantly (p less than 0.03) greater control AII level (37 +/- 3 vs 29 +/- 3 pg/ml) and lower control plasma aldosterone level (14 +/- 2 vs 22 +/- 3 ng/dl) than the "normal responders." When a converting-enzyme inhibitor was administered, no change in adrenal responsiveness to AII occurred in the normotensive controls or the hypertensive normal responders. In the hypertensive abnormal responders, both the threshold sensitivity and the entire dose response curve was significantly (p less than 0.01) enhanced following short-term converting-enzyme inhibition. This increased sensitivity could not be explained by differences in AII increment with AII infusions, in basal aldosterone levels, or in blood pressure or basal AII response to converting-enzyme inhibition. Since they occurred whether captopril or enalapril (MK 421) were used, this phenomenon is likely to be a specific effect of converting-enzyme inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Glands↗
Trauma of the ear from infrasound.
Twenty-eight chinchillas received continuous or intermittent infrasound (1, 10, 20 Hz) at 150, 160, or 170 dB SPL; there were 7 controls. Serial sections of the temporal bones were examined using light microscopy. Pathologies noted were tympanic membrane perforation, stapes subluxation, bleeding from the middle ear mucosa and tensor tympani, strial pathology, Reissner's membrane rupture, endolymphatic hydrops, saccular wall rupture, hair cell damage, and blood in the cochlear scalae. Continuous infrasound was more damaging than intermittent. Only continuous infrasound produced saccular pathology and perforations of the tympanic membrane. Of the other pathologies observed, continuous infrasound exposures produced 67% of the hair cell damage, 73% of the bleeding in the cochlear scalae, 83% of the strial pathology, and 78% of the cases of cochlear hydrops. 170-dB infrasound exposures produced the highest percentage of ears with pathologies of the three exposure intensities. As frequency increased the percentage of ears with pathologies decreased.
Animals↗
Health information sources of the poorly informed: implications for health educators and communicators.
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Attitude to Health↗
Metabolism and covalent binding of [14C]toluene by human and rat liver microsomal fractions and liver slices.
The in vitro metabolism of [14C]toluene by liver microsomes and liver slices from male Fischer F344 rats and human subjects has been compared. Rat liver microsomes produced only benzyl alcohol from toluene. Liver microsomes from human subjects metabolized toluene to benzyl alcohol, benzaldehyde, and benzoic acid. Liver microsomes from one human donor also produced p-cresol and o-cresol. The overall rate of toluene metabolism by human liver microsomes was 9-fold greater than by rat liver microsomes. Human liver microsomal metabolism of benzyl alcohol to benzaldehyde required NADPH and was inhibited by carbon monoxide and high pH (pH 10). but was not inhibited by ADP-ribose or sodium azide. These results suggest that cytochrome P-450, rather than alcohol dehydrogenase, was responsible for the metabolism of benzyl alcohol to benzaldehyde. Human and rat liver slices metabolized toluene to hippuric acid and benzoic acid. The overall rate of toluene metabolism by human liver slices was 1.3-fold greater than by rat liver slices. Cresols and cresol conjugates were not detected in human or rat liver slice incubations. Covalent binding of [14C]toluene to human liver microsomes and slices was 21-fold and 4-fold greater than to the comparable rat liver preparations. Covalent binding did not occur in the absence of NADPH, was significantly decreased by coincubation with cysteine, glutathione, or superoxide dismutase, and was unaffected by coincubation with lysine. Protease and ribonuclease digestion decreased the amount of toluene covalently bound to human liver microsomes by 78% and 27% respectively. Acid washing of human liver microsomes had no effect on covalent binding.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Drinking↗