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Biomedical subjects

T J Moore

Publications and source records attributed to T J Moore.

At least 109 records · Page 6Linked to original sources
PubMed1982

Indicators of response to a mass media CPR recruitment campaign.

Respondents to a mass media cardiopulmonary resuscitation (CPR) recruitment campaign in Harris County, Texas were more likely than non-respondents to be White, female, and under 45 years of age, to have had previous CPR training, experienced an incident in which knowledge of CPR might have been useful, or to have a friend or relative with a relevant medical history. The majority of the respondents were housewives, and professionals or technical workers, particularly in the health field. Findings can be used to identify audiences for future mass media CPR campaigns.

Adolescent↗
PubMed1982

Increase in jammed word intelligibility due to training of listeners.

Data are presented on the effect of training on naive subjects' ability to listen to voice communications under conditions of simulated cockpit noise and active jamming. The results indicate that training improved the performance of listeners under all conditions tested. Suggestions are made for further research to quantify increases in performance of communicators in jammed environments due to training.

Aerospace Medicine↗
PubMed1981

Plasma angiotensin II concentration regulates vascular but not adrenal responsiveness to restriction of sodium intake in normal man.

1. Sodium restriction increases adrenal and decreases vascular sensitivity to angiotensin II (ANG II). These responses may be mediated either by the circulating level of ANG II or other mechanisms also modified by a change in sodium balance. To assess the importance of the ANG II level, captopril, an oral converting enzyme inhibitor, was used to lower the plasma ANG II level to the sodium-loaded range while maintaining subjects in low sodium balance. 2. Normal volunteer subjects received an infusion of ANG II in increasing doses in three states: high sodium intake, low sodium intake and low sodium intake after pretreatment with captopril. 3. Basal levels of ANG II on high-sodium diet and low-sodium diet plus captopril were similar. In the ANG II infusion studies the slope of the aldosterone--ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. After the addition of captopril the slope was not decreased, indicating that the endogenous ANG II concentration is not necessary to maintain adrenal sensitivity during sodium restriction. 4. In the ANG II infusion studies the slope of the mean blood pressure--ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. The addition of captopril to sodium-restricted subjects caused the slope of the regression relationship to increase significantly, consistent with an enhanced vascular responsiveness when endogenous ANG II levels were lowered. However, the slope on low sodium plus captopril did not increase to the level of subjects on a high-sodium diet, suggesting that factors in addition to the circulating ANG II level are also important in regulating the vascular responsiveness to ANG II.

Adrenal Glands↗
PubMed1981

Alterations in aldosterone biosynthesis in essential hypertensives.

We studied hypertensives with decreased adrenal responsiveness to infused angiotensin II (AII) to assess their responsiveness to other aldosterone secretagogues, ACTH and potassium, which are thought to stimulate aldosterone synthesis in sites different from one another and from AII. All subjects, following sodium restriction, received an infusion of AII in increasing doses (0.1-3 ng/kg per min). The increment in aldosterone between control and the highest infusion dose divided by the increment in plasma AII was used as the index of adrenal responsiveness. All normotensive controls (NC) had a ratio greater than 0.5. Hypertensives with a normal ratio were designated normal responders (NR) and those with a lower ratio were abnormal responders (AbR). The slope of the regression line between aldosterone and AII was significantly less for the AbR (0.02 +/- 0.04) than for the NR (1.20 +/- 0.02, P less than 0.001) and the NC (1.00 +/- 0.03, P less than 0.001) groups. During infusion of cosyntropin in increasing doses (0.05-1.5 mIU/kg per 30 min), the aldosterone response of the AbR was significantly less than that of the NR (P less than 0.016) or the NC (P less than 0.05) groups. Similarly, after infusion of potassium (0.33 mEq/min), the increment in aldosterone in the AbR group (7.6 +/- 2.2 ng/dl) was significantly less than that in the NR (14.2 +/- 2.5 ng/dl, P less than 0.05) and the NC (18 +/- 5 ng/dl, P less than 0.05) groups. Thus hypertensives with decreased aldosterone responsiveness to infused AII also had decreased responsiveness to infused ACTH and potassium, suggesting that their defect lies in the intracellular aldosterone biosynthetic pathway.

Adrenocorticotropic Hormone↗
PubMed1980

Increase in prostaglandins during converting enzyme inhibition.

1. Because changes in the plasma concentration of angiotensin II and bradykinin appear inadequate to account completely for the hypotensive response to captopril, we measured changes in plasma prostaglandins in response to increasing doses of captopril in nine supine normal male subjects studied on both a high (200 mol/l) and low (10 mol/l) sodium intake. 2. On both the high and low sodium diets, captopril induced significant (P < 0.01) increments in the 13,14-dihydro-15-keto metabolite of the vasodilatory prostaglandin E2, which correlated significantly with the fall in blood pressure (P < 0.0001). 3. No significant changes were noted in the plasma levels of 6-keto-prostaglandins F1 alpha or thromboxane B2, the stable products of prostacyclin and thromboxane A2 respectively.

Adult↗
PubMed1980

Captopril-induced changes in prostaglandin production: relationship to vascular responses in normal man.

Captopril is a potent hypotensive agent whose efficacy has hitherto been attributed to its ability to alter either angiotensin II formation or kinin degradation. Our purpose was to examine captopril's acute effect on prostaglandin production, because changes in neither the renin-angiotensin nor the kallikrein-kinin systems appear adequate to account for the fall in arterial pressure. The plasma levels of angiotensin II, kinins, and prostaglandins were determined in response to increasing doses (5, 12.5, and 25 mg) of captopril and these responses were compared with the change in arterial pressure observed in nine supine normal male subjects studied on both a high (200 meq) and low (10 meq) sodium intake.Captopril significantly (P < 0.01) increased the levels of the 13,14-dihydro-15-keto metabolite of prostaglandin E(2) (PGE(2)-M), a potent vasodilator, with similar responses being observed on both a high and a low sodium intake. No significant changes in the plasma levels of 6-keto-prostaglandin F (1)alpha, or thromboxane B(2), the stable products of prostacyclin and thromboxane A(2), respectively, occurred. The depressor response to captopril correlated with the change in PGE(2)-M (r = 0.52, t = 5.44, P < 0.0001). On the other hand, although significant (P < 0.02) decrements in angiotensin II and increments in plasma kinins accompanied the hypotensive response in sodium-restricted subjects, in sodium-loaded subjects where the renin-angiotensin system was suppressed, no change in angiotensin II, and only a modest change in kinins was noted, even though significant (P < 0.01) decrements in diastolic blood pressure occurred (-10+/-2 mm Hg).Thus, changes in depressor prostaglandin production can better account for the hypotensive response to captopril, thereby extending to yet another vasoactive system an influence by this class of drugs and providing a new approach to dissecting the abnormality in the control of vascular tone in patients with hypertension.

Adult↗
PubMed1980

Primacy of the renin-angiotensin system in mediating the aldosterone response to sodium restriction.

The primacy of angiotensin II as the mediator of the adrenal's response to sodium restriction is controversial. We administered the oral converting enzyme inhibitor, captopril (SQ 14225), to test whether reduction of angiotension II generation for 26 h in sodium-restricted subjects would lower plasma aldosterone levels to values observed in subjects on a high sodium intake. Accordingly, plasma angiotensin II and aldosterone levels were measured in nine recumbent normal subjects on high (200 meq) and low (10 meq) sodium intakes and low sodium intake with captopril (12.5--25 mg four times a day for 26 h). Captopril reduced the sodium-restricted angiotensin II levels from 31 +/- 6 to 13 +/- 2 pg/ml, which was indistinguishable from that measured on the high sodium intake (11 +/- 2 pg/ml). Concomitantly, aldosterone levels were reduced from 25 +/- 4 to 7 +/- 1 ng/dl, which was similar to the high sodium value (8 +/- 1 ng/dl). There were no significant changes in serum sodium, cortisol, or potassium at the three sampling times. Thus, the complete suppression of the sodium-restricted levels of both angiotensin II and aldosterone into the high sodium range by captopril provides strong support for the hypothesis that the renin-angiotensin system is the prime mediator of the adrenal's response to sodium restriction.

Adult↗
PubMed1979

The adrenal receptor for angiotensin II is altered in essential hypertension.

To determine the mechanism underlying altered adrenal responsiveness in patients with essential hypertension, the renin-angiotensin-aldosterone axis was assessed in normotensive and hypertensive subjects using three pharmacological probes: SQ 20881, a converting enzyme inhibitor; saralasin, a competitive angiotensin antagonist with prominent agonist properties; and angiotensin itself. All subjects were studied while supine and in balance on a 10 meq Na/100 meq K intake. The decrement in plasma aldosterone with SQ 20881 in 26 hypertensive subjects (15+/-3 ng/dl) was normal (13+/-4 ng/dl), suggesting that the altered adrenal responsiveness in hypertensives is not because of a change in a postreceptor event or in the relative contribution of angiotensin to the control of aldosterone secretion. Saralasin at a dose (0.1 mug/kg per min) that reduced aldosterone levels in all normals produced a normal aldosterone decrement (14+/-3 ng/dl) in 19 patients with renovascular hypertension (12+/-4 ng/dl). The same dose, however, had no net effect on plasma aldosterone levels in 70 patients with normal or high renin essential hypertension (-1+/-1 ng/dl) despite identical metabolic balance and control renin and angiotensin levels. The altered response could be explained by an agonist effect, aldosterone rising in 45 of the essential hypertensives. There were no significant differences between normal and abnormal responders in pre- and postcortisol, -potassium, -renin and -angiotensin concentrations. Angiotensin was infused (0.1-3 ng/kg per min) in 15 patients with normal renin essential hypertension, previously studied with saralasin. A probit transformation defined the dose required to induce a 50% increase in aldosterone (ED50). In the patients in whom aldosterone rose with saralasin, the dose required to induce a 50% increase was significantly greater (P < 0.001) than in those in whom aldosterone fell normally (1.02+/-0.06 [SD] vs. 0.38+/-0.07 ng/kg per min). Vascular responses were similar in the various groups. We conclude that altered adrenal responsiveness to angiotensin in some essential hypertensive patients is secondary to a change in the interaction of angiotensin with its adrenal receptor.

Adrenal Glands↗
PubMed1979

Abnormal adrenal responsiveness and angiotensin II dependency in high renin essential hypertension.

Adrenal responsiveness to angiotensin II (AII) and the diastolic blood pressure responses to saralasin were studied in 19 patients with high renin essential hypertension (HREH) on a 10-meq Na(+)/100 meq K(+) diet. The increment in plasma renin activity (PRA) between supine and upright positions was used as an estimate of the acute stimulation of the adrenal gland by endogenous AII; the normal increment in plasma aldosterone divided by the increment in PRA was >3.8. 7 of 19 had abnormal upright posture responses with significantly greater mean PRA increments (24+/-6 ng/ml per h) and significantly smaller plasma aldosterone increments 47 +/- 16 ng/dl) (P < 0.036) compared to the increments observed in HREH patients with normal adrenal responsiveness (PRA = 15 +/- 1 ng/ml per h; plasma aldosterone = 87 +/- 17 ng/dl). When AII was infused at doses of 0.1-3 ng/kg per min, only patients with normal posture responses had normal plasma aldosterone increments; plasma aldosterone levels failed to significantly increase even at the highest infusion rate in the patients with the abnormal upright posture responses. The AII competitive inhibitor, saralasin (0.3-30 mug/kg per min) was then infused to study the occurrence of angiotensinogenic hypertension in both HREH subgroups. The mean decline in diastolic blood pressure to saralasin in the subnormal adrenal responsive patients (-15 +/- 3 mm Hg) was significantly greater than in the normal adrenal responsive group (-3 +/- 2 mm Hg) (P < 0.02).It is concluded that patients with HREH are not a homogeneous population; approximately one-third have AII-dependent hypertension. In these patients, the mechanism responsible for the elevated renin and blood pressure could be a compensatory increase secondary to decreased adrenal responsiveness to AII. In the remainder, the high PRA levels have little, if any, causal role in the pathogenesis of the hypertension but could reflect a marker of other pathophysiologic processes.

Adrenal Cortex↗
PubMed1978

Failure of renin suppression by angiotensin II in hypertension.

Angiotensin II was infused at rates varying from 0.1 to 10 ng/kg per minute into 49 subjects with hypertension and 26 normotensive subjects and changes in blood pressure, plasma angiotensin II, and plasma renin activity (PRA) were determined after 20 and 30 minutes at each dose. Similar dose-related increases in angiotensin II and blood pressure occurred with a threshold of 1 ng/kg per minute in the normotensive and hypertensive subjects. Whereas angiotensin II induced a significant, dose-related decrement in renin activity in the normotensive subjects, with a threshold of 1.0 ng/kg per minute, no significant change in renin activity occurred in either the normal-renin or high-renin hypertensive subjects. In a separate study, nine normotensive and six hypertensive sodium-restricted subjects were given a converting enzyme inhibitor, SQ 20881, 30 microgram/kg. Despite a significantly greater fall in blood pressure (P less than 0.006) and angiotensin II concentration (P less than 0.045) in the hypertensive subjects, they did not have a greater rise in plasma renin activity. We conclude that angiotensin II reduces renin release in normal man at infusion rates that yield plasma angiotensin II levels within the physiological range but has a strikingly reduced influence on renin release in hypertension. In high-renin hypertension due to renal artery stenosis or nephrosclerosis, renin release is presumed to be relatively autonomous because of a dominant, intrarenal mechanism. The mechanism in normal-renin essential hypertension is not clear, but the abnormality could well be related to the pathogenesis of the hypertension.

Adult↗
PubMed1978

Stimulation of 18-hydroxy-11-deoxycorticosterone secretion by angiotensin II and potassium.

The control of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) secretion is incompletely understood: ACTH seems to be the dominant regulator, the importance of angiotensin II (A-II) is uncertain, and the effect of potassium has not been investigated. The purpose of this study was to evaluate the 18-OH-DOC response to these three stimuli in vitro. Suspensions of isolated rat adrenal glomerulosa or fasciculata cells were stimulated with either alpha-1-24 ACTH (0.04 mU/ml), A-II (25 ng/ml), or potassium (5.9 mEq/liter), and 18-OH-DOC production was measured. In glomerulosa cells, ACTH produced the greatest 18-OH-DOC response but A-II and potassium also produced significant (P less than 0.001) 18-OH-DOC increases (control, 162 +/- 14 (SE) ng/10(6) cells incubated; A-II, 368 +/- 39; potassium, 380 +/- 37; ACTH, 1544 +/- 165). In fasciculata cells, 18-OH-DOC production increased with ACTH but not with A-II or potassium. These results document that A-II and potassium, as well as ACTH, can stimulate 18-OH-DOC production by glomerulosa but not by fascicuata cells. The response to A-II may provide an explanation for the reported increase in 18-OH-DOC production after sodium restriction.

18-Hydroxydesoxycorticosterone↗