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Biomedical subjects

J W Conn

Publications and source records attributed to J W Conn.

At least 19 recordsLinked to original sources
PubMed1982

Double-blind comparison of doxepin and desipramine in patients with primary affective disorder.

A double-blind comparison of doxepin versus desipramine was performed in carefully defined patients with research diagnosis of Primary Affective Disorder. While both drugs showed equal efficacy after 4 weeks, doxepin demonstrated a more rapid onset of action and surprisingly few side effects. Desipramine did not prove to be "activating" and did not worsen agitated depression. Although doxepin showed few autonomic side effects, it was nevertheless sedating, indicating that tricyclics with more anticholinergic effects are not necessarily more sedating drugs.

Adult↗
PubMed1979

17 alpha-Hydroxylase deficiency. A combination of hydroxylation defect and reversible blockade in aldosterone biosynthesis.

We have studied the hormonal secretion and excretion patterns in a patient with the XX type of 17 alpha-hydroxylase deficiency. In the untreated state, the patient's urine contained only those steroids which do not require 17-hydroxylation in their biosynthesis. Aldosterone was not produced in the patient and the metabolic product of its immediate precursor, 18-hydroxy-11-dehydro-tetrahydrocorticosterone, was excreted in markedly elevated amounts. This apparent complete block in 18 oxidation was reversible upon long-term ACTH suppression within 27 days. Direct in vitro incubation of the patient's adrenal gland removed at operation demonstrated, 1) the complete lack of 17 alpha-hydroxylase activity, 2) the functional block in the ability to oxidize the hydroxyl group at the 18 methyl side chain. The addition of physiological concentrations of angiotensin to the incubation medium further showed, 3) angiotensin mildly stimulated the entire aldosterone biosynthetic pathway, 4) angiotensin directly stimulated the conversion of 18-hydroxycorticosterone to aldosterone. We propose that in this patient, 17-hydroxylase deficiency produced a decreased plasma concentration of cortisol, followed by stimulation of deoxycorticosterone production by ACTH. The resultant increase in extracellular fluid volume suppressed plasma renin activity. This resulted in a low plasma concentration of angiotensin II which directly suppressed oxidation of 18-hydroxycorticosterone to aldosterone. This defect has been called corticosterone methyl oxidase defect type 2.

18-Hydroxycorticosterone↗
PubMed1977

Renin reactivity, renin activity and renin concentration in patients with normal and low renin essential hypertension.

Renin activity, concentration, substrate and reactivity were determined in normal subjects as well as in hypertensive subjects with suppressed and normal plasma renin activity. Renin substrate measurements were similar in all groups. Renin reactivity, a measure of circulating modifiers of the renin reaction, was significantly increased in both hypertensive groups. Reactivity was significantly greater in the normal renin hypertensive group than the low renin hypertensive group. Renin concentration was significantly suppressed in both hypertensive groups, but to a greater degree in the low renin hypertensives. These findings suggest that plasma renin concentration may be suppressed in most hypertensive subjects. Furthermore, plasma renin activity may be "normalized" in most hypertensive subjects by the effect of circulating modifiers of the renin reaction. While renin reactivity in the plasma of low-renin hypertensive subjects is accelerated to a lesser degree than that of the normal-renin hypertensives, this finding alone does not explain the low plasma renin activity.

Angiotensinogen↗
PubMed1977

Renin-renin substrate kinetic constants in the plasma of normal and estrogen-treated humans.

The renin-renin substrate Michaelis constant (Km) and maximal velocity (Vmax) were determined in the plasmas of normal subjects. The mean Km was 0.7 microgram/ml. Under these conditions, the in vitro reaction of renin with physiologic concentrations of renin substrate will proceed at only 70% of its maximal velocity. Following estrogen administration, Km doubled to a value of 1.3 microgram/ml. Vmas increased by 81%. Analysis of the changes induced in the in vitro reaction velocity demonstrated that estrogen-induced acceleration of the renin reaction is dependent upon both an increase in renin substrate concentration as well as an increase in Vmas. The latter appears to be quantitatively more important. These findings suggest the emergence of modifying factors in the renin-renin substrate interaction following estrogen administration.

Angiotensinogen↗
PubMed1976

The dexamethasone-modified adrenal scintiscan in hyporeninemic aldosteronism (tumor versus hyperplasia). A comparison with adrenal venography and adrenal venous aldosterone.

The dexamethasone-modified adrenal scintiscan, a noninvasive procedure, is described for the preoperative distinction between primary aldosteronism (aldosterone-producing ademona) and idiopathic aldosteronism (bilateral hyperplasia) and for the preoperative localization of aldostersone-producing adenomas. This procedure has been carried out on 17 subsequently proved cases of primary aldosteronism and nine cases (four unexplored) of idiopathic aldosteronism. In the tumor cases, it indicated correctly the side of the tumor in 88 per cent. It was correct in predicting the existence of bilateral hyperplasia in all of the five cases explored. It produced the same response in four more cases believed to have bilateral hyperplasia, in which surgical exploration has not been carried out. Many of the same patients had, in addition, standard adrenal scintiscans (SS), adrenal venography, and determinations of aldosterone in adrenal venous blood. These results are compared with those of the dexamethasone scintiscan (DS). In tumor localization, the 88 per cent figure for the DS was only moderately better than that of the other three (71 per cent, SS; 80 per cent, venography; 80 per cent, adrenal venous aldosterone levels). However, in predicting bilateral hyperplasia, the DS was 100 per cent correct, as were the levels of aldosterone in adrenal venous blood. The SS and adrenal venography failed in bilateral hyperplasia and gave many false-positive results indicating tumor. The DS, a relatively simple outpatient procedure, appears to be at least as effective, both in lateralizing tumors and distinguishing between tumor and bilateral hyperplasia, as the more difficult, expensive, and sometimes hazardous invasive procedure of bilateral adrenal vein catheterization.

Adolescent↗