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Biomedical subjects

J H Mersey

Publications and source records attributed to J H Mersey.

31 records · Page 2Linked to original sources
PubMed1986

Long-term experience with terazosin for treatment of mild to moderate hypertension.

Two hundred twenty-six patients with mild to moderate hypertension were treated with terazosin in an open, multicenter study to determine the drug's long-term efficacy and safety. All patients had previously received terazosin in a short-term study; 66 patients entered from later short-term studies and had experienced a 7 mm Hg decrease in supine diastolic blood pressure in response to terazosin. Terazosin was administered once or twice daily either alone or in combination with a diuretic and/or a beta blocker. Supine systolic and diastolic blood pressures were significantly decreased from baseline during time intervals ending at 90, 180, 360, and 720 days of long-term therapy. No clinically significant trends were observed in pulse rate, clinical laboratory test results, physical examinations, or electrocardiograms. Patients had a tendency toward a slight weight gain. The most common adverse experiences attributed to terazosin monotherapy were dizziness and asthenia (9.7 percent and 6.6 percent, respectively). Adverse experiences were usually of mild or moderate severity. Of the 226 patients who underwent long-term therapy, 29 (13 percent) withdrew because of adverse experiences, and three (1 percent) withdrew because of uncontrolled blood pressure. This study demonstrates that terazosin is effective and safe for long-term treatment of hypertension.

Adrenergic alpha-Antagonists↗
PubMed1986

Adrenal insufficiency due to invasion by lymphoma: documentation by CT scan.

We have presented the first documented description of the induction of adrenal failure from invasion by a lymphoma. Although adrenal involvement may be common in this disease, which often involves the retroperitoneum, adrenal failure is still unusual. Our case suggests that clinical suspicion must be heightened when lymphoma is present. In particular, adrenal function tests are indicated for patients who have CT evidence of bilateral adrenal invasion from any source, including lymphoma.

Adrenal Gland Neoplasms↗
PubMed1984

The use of the plasma epinephrine response in the diagnosis of idiopathic postprandial syndrome.

Patients with idiopathic postprandial syndrome (IPS) report recurrent postprandial episodes that resemble the clinical manifestations of hypoglycemia. In an effort to find objective criteria for diagnosis of IPS, we studied a group of patients with IPS and controls during an oral glucose tolerance test. Patients with IPS had a significantly lower mean glucose nadir and higher hypoglycemic index than controls. Although 74% of patients with IPS had glucose nadirs higher than 50 mg/dL, their responses of epinephrine, cortisol, growth hormone, glucagon, and norepinephrine were significantly higher than the respective changes in the controls. Of the five hormones, only the epinephrine response separated the patients from the controls without overlap. The epinephrine response may represent a valuable diagnostic criterion for this disorder.

Adolescent↗
PubMed1984

Withdrawal phenomena in subjects with essential hypertension on clonidine or tiamenidine.

The incidence and pathogenesis of withdrawal phenomena with the centrally acting drugs clonidine (CLON) and tiamenidine (TIAM) were evaluated. Thirty subjects with hypertension on hydrochlorothiazide (HCTZ) were randomized to TIAM or CLON. Blood pressure and integrated plasma catecholamine levels fell equally in response to both drugs. On withdrawal, blood pressure and pulse rose in both groups with no difference between them. Three subjects had symptoms of withdrawal, four had blood pressure overshoot above pretreatment levels of 10 mm Hg or more, and eight had a rise in blood pressure of 30 mm Hg systolic or 20 mm Hg diastolic. There was no difference between TIAM and CLON in these effects. There was a direct correlation between blood pressure rise and increase in integrated plasma norepinephrine levels. We conclude that the incidence of withdrawal phenomena in subjects on TIAM or CLON is infrequent and that there is a direct relationship between the rise in blood pressure and the loss of suppression of catecholamines by these drugs.

Adult↗
PubMed1983

Plasma norepinephrine and epinephrine responses to glucagon in patients with suspected pheochromocytomas.

Plasma norepinephrine and epinephrine levels were measured before and after glucagon administration in 28 patients suspected of having a pheochromocytoma: three patients were subsequently found to have tumors. The norepinephrine response predicted the presence or absence of a tumor in 27 of the 28 patients. Epinephrine levels doubled, on the average, in patients who did not have pheochromocytomas, and were not useful in distinguishing the patients with or without tumors. A comparison of the response to glucagon and a placebo indicated that changes in plasma catecholamine levels were hormone-related and not the result of side-effects accompanying injection. The glucagon provocation test, with measurement of plasma norepinephrine and epinephrine levels, may be a useful adjunctive tool for evaluating patients suspected of having a pheochromocytoma when performed according to a standardized protocol and interpreted in relation to appropriate controls.

Adolescent↗
PubMed1982

Adrenal vein epinephrine levels: a useful aid in venous sampling for primary aldosteronism.

We evaluated the usefulness of adrenal vein epinephrine levels as an indicator of adrenal venous dilution in seven patients with primary aldosteronism who had venous sampling. In six patients adrenal vein epinephrine levels greater than 1500 pg/mL confirmed that relatively undiluted adrenal efflux had been obtained. In another patient a low value of left adrenal vein epinephrine indicated that the sample was markedly diluted with nonadrenal blood. Measurement of epinephrine levels appears to be a useful tool for verifying successful venous sampling, particularly when cortisol and aldosterone levels from the same adrenal vein are not elevated or when deep adrenal vein cannulation cannot be confirmed radiologically.

Adenoma↗
PubMed1981

Thyroid hormone levels after acute L-thyroxine loading in hypothyroidism.

While extrathyroidal conversion of T4 to T3 sustains circulating T3 blood levels in patients receiving maintenance doses of L-T4, the serum T3 rise after the acute administration of large doses of L-T4 may involve an additional mechanism, T3 contamination in L-T4 preparations. L-T4 (1000 micrograms; Synthroid) was given orally to four noncompliant hypothyroid individuals (mean T4, 1.0 micrograms/dl; mean T3, 28 ng/dl). Continuously withdrawn blood sampling revealed a mean rise in serum T4 to 7.7 micrograms/dl at 4 h and a parallel rapid mean rise in serum T3 to 66 ng/dl (136% over baseline) at 4 h. RIA analysis of the experimental batches of Synthroid revealed 0.7-0.9% T3 contamination. Oral administration of 5 or 10 micrograms Cytomel (T3; corresponding to 0.5% and 1% T3 contamination in 1000 micrograms Synthroid) to two of the hypothyroid subjects at a later date resulted in T3 serum elevations 12% and 68% as great as post 1000 micrograms L-T4. To eliminate basal hormone changes between these experiments, a third subject received 7.5 micrograms Cytomel on day 1 (corresponding to the measured T3 contamination in 1000 micrograms Synthroid), followed by 1000 micrograms Synthroid on day 2. Resulting peak T3 levels were identical. In summary, hypothyroid individuals rapidly absorb acute L-T4 loads, with parallel increases in T4 and T3 blood levels. The major source of this T3 elevation is the contaminant in L-T4 preparations. This degree of T3 contamination becomes clinically significant in acute large dose T4 regimens and results in euthyroid levels of T3.

Fasting↗
PubMed1981

The effect of prostaglandin inhibition on renin release. A comparison of furosemide and low-sodium stimulation tests.

Furosemide administration is considered comparable to sodium restriction and upright posture as a stimulation test of PRA. This view can be questioned if different mechanisms of renin release are involved. Prostaglandins appear to be an important mediator of renin release. Using a prostaglandin antagonist, indomethacin, we attempted to assess the relative role of prostaglandins in the two renin stimulation tests. Eleven healthy volunteers on a high-sodium intake had PRA and PA measured in response to furosemide stimulation before and during indomethacin administration and then in response to sodium restriction combined with upright posture before and during indomethacin. Supine PRA was 0.41 ng/ml/hr on high sodium and 0.19 after indomethacin (p less than 0.05). On low sodium, the supine PRA was 2.07 ng/ml/hr and 0.98 after indomethacin (p less than 0.05). The increase in PRA (delta PRA) was 3.26 ng/ml/hr with furosemide stimulation and 1.23 after indomethacin (p less than 0.025). The PRA was 3.71 ng/ml/hr with low-sodium stimulation and upright posture and 2.53 after indomethacin (NS). PA paralleled PRA except that there was no suppression of supine values with indomethacin. We conclude that prostaglandins mediate baseline renin secretion and renin stimulation in response to furosemide. However, no comparable prostaglandin mediation could be demonstrated during renin stimulation secondary to sodium restriction. The two standard renin stimulation tests appear to involve different mechanisms of renin release.

Adult↗
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

Adrenal responses to pharmacological interruption of the renin-angiotensin system in sodium-restricted normal man.

We assessed the role of the renin-angiotensin system in the control of aldosterone secretion in response to sodium restriction in 62 normal subjects. Both saralasin, an angiotensin II antagonist, and SQ 20881, a converting enzyme inhibitor, induced a dose-related decrease in plasma aldosterone levels when the renin-angiotensin system was activated by restriction of sodium intake. Two types of experiments were performed with saralasin. In the first set, a dose-response relationship was established 20 min after beginning infusions ranging from 0.03-1.0 microgram/kg/min. The optimal dose was 0.1 microgram/kg/min, with a reduction in aldosterone levels of -10.1 +/- 3.8 ng/dl (P less than 0.025). Higher doses induced smaller reductions in aldosterone levels. In the second set, a 3-h infusion was given. The results were qualitatively similar but the magnitude was greater (-15 +/- 4 ng/dl; P less than 0.01). The aldosterone response 20 min after administration of SQ 20881 paralleled the angiotensin II response, with the first significant decrement (-6.5 +/- 1.5 ng/dl; P less than 0.01) occurring at 0.1 mg/kg and maximum (-10 +/- 3 ng/dl) occurring at 0.3 mg/kg. Thus, both agents produced qualitatively similar changes in aldosterone secretion in sodium-restricted normal subjects. However, neither reduced sodium restricted aldosterone levels to that measured in sodium-loaded subjects because of the intrinsic limitation of each agent. Saralasin is a partial agonist. SQ 20881 induces an increase in plasma renin activity via interruption of the short feedback loop, which probably limits its action. Yet, these data do support the hypothesis that angiotensin mediates the adrenal's response to sodium restriction in normal man.

Adolescent↗
PubMed1977

Relationship between aldosterone and bradykinin.

To assess relationships between plasma bradykinin and the individual elements of the renin-angiotensin-aldosterone system 11 normal subjects and five subjects with adrenal insufficiency were studied on an intake of 200 mEq sodium/100 mEq potassium. In adrenal insufficiency subjects, plasma bradykinin did not change when angiotensin II levels were increased by an infusion rate of 3 ng/kg per min for 30 minutes; plasma aldosterone remained undetectabel. In normal subjects, angiotensin II at 3 ng/kg per min or potassium at 20 mEq/hour infused intravenously for 2 hours both significantly increased plasma aldosterone levels, yet neither stimulus altered plasma bradykinin. Thus, acute elevations in angiotensin II and plasma aldosterone were not associated with changes in the levels of plasma bradykinin. In five additional normal subjects on an intake of 10 mEq sodium/100 mEq potassium, a threshold dose of converting enzyme inhibitor (SQ 20881) at 30 microng/kg was given intravenously. Five minutes after administration of the drug, blood pressure and plasma angiotensin II levels had significantly declined and plasma bradykinin levels had significantly increased (P is less than 0.02). Within 10-20 minutes, however, all had returned to control accompanied by a sustained increase in plasma renin activity, and a decrement in plasma aldosterone. Plasma renin activity, which had increased by more than 2-fold after the administration of the converting enzyme inhibitor, remained elevated until the completion of the study at 320 minutes. Eighty minutes after beginning the infusion, plasma aldosterone levels returned to control. Thus, the results suggest that plasma bradykinin correlates more closely with acute changes in plasma renin activity (and angiotensin I) than plasma aldosterone or angiotensin II, suggesting a role for converting enzyme in the regulation of both plasma renin activity and plasma bradykinin. Furthermore, the declines in blood pressure observed with converting enzyme inhibition may be attributable to both changes in plasma angiotensin II and plasma bradykinin concentrations. However, it is emphasized that these short-term studies may not reflect the role of bradykinin in the long-term control of blood pressure.

Adrenal Insufficiency↗