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Biomedical subjects

R A Mueller

Publications and source records attributed to R A Mueller.

At least 163 records · Page 9Linked to original sources
PubMed1977

An unsuccessful attempt to treat hypertension with acupuncture.

The effectiveness of 5 sets of acupuncture loci in decreasing systemic blood pressure was compared with chlorthalidone and propranolol in patients with essential hypertension. No statistically significant acute or long-term changes in plasma catecholamines, renin activity, or blood pressure and pulse rate were observed as a result of acupuncture treatment. The decrease in blood pressure was significantly less than that observed with propranolol, but not significantly less than that produced by chlorthalidone. Because of the poor patient acceptance of acupuncture and in the absence of a beneficial response, we feel acupuncture as employed in this study is of limited value in the management of patients with essential hypertension.

Acupuncture Therapy↗
PubMed1975

Effect of hypophysectomy on cAMP changes in rat adrenal medulla evoked by catecholamines and carbamylcholine.

It was the aim of this study to investigate the mechanisms responsible for changes in 3',5'-cyclic adenosine monophosphate (cAMP) in the rat adrenal medulla occuring after administration of carbamylcholine, histamine, ACTH and various phenylethylamines. Carbamylcholine, ACTH, histamine, noradrenaline and dopamine produced marked (500-900%) increases in adrenal cAMP which were very similar in both adrenal cortex and medulla both with respect to time-course and relative extent. Interestingly isoprenaline and adrenaline did not influence cAMP levels even at excessively high doses. In all cases studied transsection of the splanchnic fibers supplying the adrenals reduced the increase in medullary cAMP by not more than 25--30%, suggesting that cAMP levels in the adrenal medulla are predominantly regulated by non-neuronal mechanisms. This assumption was strongly supported by the observation that hypophysectomy completely abolished the 500--600% increase in cAMP produced by 50 mumol/kg of dopamine and reduced the 700% increase resulting from 4.4 mumol/kg of carbamylcholine to 70%. In spite of the marked increase in cAMP produced by single and repeated doses of dopamine in the adrenal medulla there was no subsequent induction of tyrosine hydroxylase (TH). Moreover carbamylcholine (8.2 mumol/kg) evoked TH induction only in innervated adrenals whereas after denervation, in spite of the large (+ 500%) and prolonged (more than 90 min) increase in cAMP, no TH induction could be observed. It is concluded that adrenal medullary cAMP is predominantly regulated by the pituitary gland via the adrenal cortex and only to a much smaller extent--if at all--by direct cholinergic mechanisms, which are responsible for the initiation of TH induction.

Adrenal Cortex↗
PubMed1975

Central monaminergic neuronal effects on minimum alveolar concentrations (MAC) of halothane and cyclopropane in rats.

The effect of interference with central catecholamine- or serotonin-containing neurons on the response of rats to inhalation anesthetics were explored. Interference with catecholaminergic function by inhibition of amine synthesis with alpha-methyltyrosine alone or combined with destruction of these neurons by 6-hydroxydopamine reduced brain concentrations of norepinephrine and dopamine without altering serotonin concentrations. These alterations decreased the minimum alveolar concentration (MAC) of halothane when tail-clamping was used as the test stimulus. Similar small reductions of halothane MAC were produced in rats given 5,6-dihydroxytryptamine and p-chlorophenylalanine, which decreased brain serotonin without altering noreopinephrine or doapamine concentrations. When catecholaminergic or serotoninergic neuronal function was similarly disrupted in rats later exposed to cyclopropane, no alternation in MAC was observed. It is suggested that disruption of central amine-containing neurons may lower the MAC's of depressant anesthetics only, and not excitatory anesthetics.

Amines↗
PubMed1975

Effects of acute unilateral renal denervation in the rat.

Studies were undertaken to characterize the renal responses to acute unilateral renal denervation and the mechanisms involved in these responses. Denervation was produced in anesthetized nondiuretic rats by application of phenol to the left renal artery. Studies were also performed in sham-denervated nondiuretic rats. Whole kidney and individual nephron studies were performed before and after denervation or sham denervation. Denervation increased urine volume from the left kidney to about twice its control value (P less than 0.001) and increased urinary sodium excretion from 332 neq min minus -1 to 1,887 neq min minus -1 (P less than 0.001). Glomerular filtration rate (GFR) and renal plasma flow (RPF) remained unchanged in both kidneys after the procedure. The innervated right kidney showed no changes in urine volume or in sodium excretion. After denervation, late proximal ratio of tubular fluid inulin concentration to that of plasma [(F/P)In] decreased from 2.23 to 1.50 (P less than 0.001) while single nephron GFR remained unchanged. Absolute reabsorption decreased from 16.5 to 9.9 n. min minus -1 (P less than 0.001). (F/P)In ratios were also decreased in early distal (from 6.21 to 3.18, P less 0.001) and late distal convolutions (from 16.41 to 8.33, P less than 0.001) during the experimental period. (F/P)Na ratios remained unchanged in the early distal convolutions, but increased from 0.18 to 0.38 (P less than 0.01) in late distal convolutions after denervation. Absolute Na reabsorption after denervation increased in the loop of Henle, distal convolution, and collecting ducts. Any changes in intrarenal hydrostatic pressures after denervation were always small. There were no changes in GFR, RPF, urine volume, urinary sodium excretion, or late proximal (F/P)In after sham denervation. We conclude that the diuresis and natriuresis seen after acute renal denervation were caused by a marked depression of sodium and water reabsorption in the proximal tubule with partial compensation in more distal nephron segments. These responses appeared to be unrelated to systemic or intrarenal hemodynamic changes. The results demonstrate an effect of the renal nerves on proximal tubular function.

Aminohippuric Acids↗
PubMed1975

The placement of long-term "criminally insane" patients in open settings.

Twenty long-term psychiatric patients with criminal charges against them were transferred from the Iowa Security Medical Facility to open hospitals and aftercare settings between 1969 and 1971. Staff prepared the patients for transfer and persuaded authorities to permit the placements. Follow-up shows 19 have adapted to the new settings. The authors speculate that age is a factor in predicting aftercare adjustment; 18 of the 19 patients were at least 44 years old. The authors also feel that clinical staff must take the initiative to reduce the needless confinement of such patients.

Adult↗
PubMed1974

Location of an isoproterenol-responsive cyclic AMP pool in adrenergic nerve cell bodies and its relationship to tyrosine 3-monooxygenase induction.

To decide whether adenosine 3':5'-cyclic monophosphate (cyclic AMP) plays a role as a second messenger in the trans-synaptic induction of tyrosine 3-monooxygenase (EC 1.14.16.2), it is desirable to discriminate between neuronal and extraneuronal changes in cyclic AMP concentration. Treatment of newborn rats with nerve growth factor antiserum or 6-hydroxydopamine, leading to destruction of 61-85% of the adrenergic nerve cell bodies in the superior cervical ganglion, led to a decrease in cyclic AMP of only 16-28%. This observation demonstrates that a relatively small portion of cyclic AMP is localized in the adrenergic neurons. However, administration of isoproterenol produced an increase (12-fold) in cyclic AMP only in this neuronal pool. Neither single nor repeated injections of isoproterenol led to induction of tyrosine monoxygenase. This, together with previous observations that experimental conditions leading to induction of the enzyme do not produce significant increases of cyclic AMP in the whole ganglion, is taken as an indication that cyclic AMP is not acting as a second messenger in the trans-synaptic induction of tyrosine monooxygenase in the rat superior cervical ganglion. In the rat adrenal medulla, treatment with reserpine led to both a shortlasting (60-90 min) increase in cyclic AMP and a subsequent induction of tyrosine monooxygenase. However, the increase in cyclic AMP was almost completely prevented (40 compared to 320%) by pretreatment of the rats with propranolol while the induction of tyrosine monooxygenase was not diminished. This observation also argues against an exclusive key-function of cyclic AMP in trans-synaptic induction of tyrosine monooxygenase in the adrenal medulla.

Adrenal Medulla↗
PubMed1974

Evidence for involvement of 5-hydroxytryptamine in the actions of amphetamine.

1 Pargyline treatment, 1 h before (+)-amphetamine (1 mg/kg), reduced amphetamine-stimulated motor activity. This inhibition was reversed in animals pretreated with p-chlorophenylalanine (PCPA).2 Following treatment with PCPA or 5,6-dihydroxytryptamine (5,6-DHT), amphetamine-induced locomotor activity was significantly potentiated. The increased response to amphetamine in PCPA-treated rats was reversed in animals pretreated with 5-hydroxytryptophan.3 The inhibition of amphetamine-stimulated locomotor activity by treatment with 6-hydroxydopamine was not reversed by PCPA treatment.4 Stereotypies produced by amphetamine were not found to be altered by depletion of 5-hydroxytryptamine.5 Induction of adrenal tyrosine hydroxylase activity produced by chronic amphetamine administration was significantly potentiated by PCPA, emphasizing the involvement of a 5-hydroxytryptamine inhibitory system in more than one action of amphetamine.

Adrenal Glands↗