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Biomedical subjects

R B McCall

Publications and source records attributed to R B McCall.

At least 73 records · Page 4Linked to original sources
PubMed1983

Developmental changes in head-circumference and mental-performance growth rates: a test of Epstein's phrenoblysis hypothesis.

Epstein's phrenoblysis hypothesis states that brain growth and mental growth occur in correlated spurts at 3-10 months and 2-4, 6-8, 10-12 or 13, and 14-16 or 17 years of age. The present study was the first to test statistically such spurts in head-circumference and mental-age growth rates and to assess any correspondence in individual differences between spurts in the two variables in a single sample of children measured serially between 2.5 and 17 years of age. While the statistically significant spurts observed in each variable did fall within the hypothesized age periods, the chance rate for such theoretical concordance was high and several hypothesized spurts were not supported. Moreover, no relationship existed within individuals between head-circumference and mental-age growth-rate patterns.

Adolescent↗
PubMed1983

Interactions between baroreceptor and sympathetic pathways.

The interactions between baroreceptor and sympathetic pathways were determined in anesthetized cats using computer summation techniques. Electrical stimuli applied to baroreceptor afferent nerves produced an early and late period of inhibition of sympathetic nervous discharge (SND) recorded from the external carotid or inferior cardiac nerves. The late period of baroreceptor-induced inhibition summated algebraically with the cardiac-locked slow wave of SND during all phases of the cardiac cycle. Increases in the intensity of baroreceptor stimulation resulted in an increase in the amplitude and duration of the late inhibition. Alterations in the periodicity of SND failed to effect the late phase of inhibition. Picrotoxin blocked the late period of baroreceptor-induced inhibition but enhanced the cardiac locking of SND. These data indicate that the late period of inhibition reflects the ability of afferent nerves to modulate the amplitude of central sympathetic outflow, regardless of its periodicity. In addition, the central baroreceptor pathways involved in amplitude modulation and temporal locking of SND to the cardiac cycle are distinct and are located at the level of the brain stem. A spinal component of baroreceptor-induced sympathoinhibition is also described.

Afferent Pathways↗
PubMed1983

Evidence for a central sympathoexcitatory action of alpha-2 adrenergic antagonists.

The effect of alpha-2 adrenergic receptor antagonists on sympathetic nerve discharge (SND) recorded from the external carotid and splanchnic nerves were studied in baroreceptor-denervated cats. Low i.v. doses of piperoxane and rauwolscine dramatically increased SND and produced a concomitant rise in mean arterial pressure and heart rate. High doses of piperoxane also resulted in an increase in SND. High doses of rauwolscine, however, markedly reduced mean arterial pressure, heart rate and SND. The pressor response to i.v. norepinephrine was greatly attenuated by high doses of rauwolscine and slightly reduced by piperoxane. Piperoxane failed to alter SND in catecholamine-depleted animals. In vitro binding experiments indicated that piperoxane and rauwolscine bound selectively to the alpha-2 adrenergic receptor and had little affinity for alpha-1 receptor sites. In addition, rauwolscine displaced [3H]LSD binding. These data indicate that low doses of the alpha-2 receptor antagonist piperoxane and rauwolscine act centrally to increase SND. In addition, the nature of the interactions between central noradrenergic neurons and neurons involved in the genesis of sympathetic nerve activity is discussed.

Adrenergic alpha-Antagonists↗
PubMed1983

U-54,669F: a novel hypotensive agent.

U-54,669F, a new antihypertensive agent, administered orally was associated with dose-related hypotensive responses in conscious, spontaneously hypertensive, and normotensive rats (0.015-0.5 mg/kg) and in supine conscious monkeys (1-10 mg/kg). No loss of hypotensive efficacy of U-54,669F was observed after 1 wk of daily repetitive treatment. U-54,669F did not alter electrical postganglionic sympathetic nerve activity or postsynaptic sympathetic function. Hypotensive responses to U-54,669F were blunted in spinal cats. U-54,669F was associated with dose-related decreases in norepinephrine (NE) levels in plasma and in cardiac and splenic tissue, whereas brain NE was unaltered. U-54,669F attenuated vascular responses associated with electrical stimulation of sympathetic nerves. However, at hypotensive doses, U-54,669F did not impair the ability of monkeys to withstand orthostatic stress, or contraction of the nictitating membrane secondary to sympathetic stimulation in the cat. U-54,669F appears to alter peripheral sympathetic neurogenic function, but apparently does not enter the central nervous system and does not impair the ability to withstand orthostatic stress at effective hypotensive doses.

Angiotensin II↗
PubMed1983

Environmental effects on intelligence: the forgotten realm of discontinuous nonshared within-family factors.

The author argues that environmental variation that occurs within families but is not shared by siblings--nonshared within-family environmental variation--is a major influence on general mental performance and has largely been ignored. Data are presented from longitudinal studies that reveal that intraindividual variation over age in IQ accounts for as much or more variability than has been estimated to be the nonshared within-family environmental variation in IQ. Given these results, the author speculates that such factors may account for 15%-25% of all variability in IQ and 30%-50% of environmental variability in IQ. The implications of this type of environmental factor are considered from conceptual and methodological perspectives.

Age Factors↗
PubMed1982

Neurophysiological effects of hallucinogens on serotonergic neuronal systems.

Low intravenous doses of the hallucinogen d-lysergic acid diethylamide (LSD) markedly suppress the discharge of serotonin (5-HT)-containing neurons in the dorsal raphe nucleus of the rat. Microiontophoretically applied LSD also inhibits the firing of 5-HT neurons, indicating that the inhibitory effect is mediated directing on 5-HT neurons. Forebrain neurons receiving a major serotonergic input are relatively insensitive to LSD. Other indole hallucinogens (i.e., psilocin, dimethyltryptamine, and 5-methoxydimethyltryptamine) also preferentially inhibit raphe firing as compared to postsynaptic forebrain neurons. These observations led to the hypothesis that hallucinogens produce their psychoactive effects by acting preferentially upon 5-HT autoreceptors in the dorsal raphe allowing postsynaptic neurons to escape from the tonic inhibitory action of 5-HT neurons. However, problems exist with the concept that hallucinogens produce their psychoactive effects by disinhibiting postsynaptic neurons. First, the time course of the behavioral and neuronal effects of LSD do not correlate. Second, 5-HT neurons do not become tolerant to the inhibitory actions of LSD. Third, the hallucinogen mescaline fails to directly inhibit 5-HT neurons. Finally, the nonhallucinogen lisuride markedly suppresses the discharges of 5-HT neurons. These observations suggest that postsynaptic actions of hallucinogens may be of prime importance in producing their psychedelic effects. Evidence is presented to suggest that the hallucinogens may act postsynaptically to sensitize both serotonergic and noradrenergic receptors. It is suggested that a mechanism of receptor sensitization, in distinction to disinhibition, might account for the altered perceptual reactivity produced by these drugs.

Animals↗
PubMed1982

A rat model for predicting orthostatic hypotension during acute and chronic antihypertensive drug therapy.

An experimental model has been developed to determine postural hypotension in chloralose-urethane-pentobarbital (CUP) anesthetized rats. Using this technique, mean arterial pressure, heart rate, and blood pressure compensation to 60 degree tilt were examined in rats treated acutely and chronically with a spectrum of standard antihypertensive agents. The results closely parallel the orthostatic profiles seen clinically with these drugs. Significant orthostatic hypotension was seen with the acute intravenous administration of the alpha-adrenergic antagonists phenoxybenzamine, phentolamine, and prazosin, the neuronal suppressant guanethidine, and the ganglionic blockers hexamethonium and chlorisondamine. The central antihypertensive clonidine displayed mild, acute orthostasis that dissipated by 1 hr. The vasodilator minoxidil was entirely free of postural effects. Chronically, guanethidine, the ganglionic blocker mecamylamine, and a high dose of reserpine all resulted in significant postural hypotension after 4 days of oral administration. Prazosin's acute orthostasis had largely dissipated by this time. Chronic minoxidil resulted in slight overcompensation to tilt. Based on the consistency to these data relative to the clinical profiles of these standard antihypertensive agents, it would appear that the CUP anesthetized rat is an accurate, efficient test model for identifying orthostasis in novel hypotensive agents under acute and chronic drug treatment conditions.

Anesthesia↗
PubMed1982

1-(alkylamino)isochromans: hypotensives with peripheral and central activities.

A series of 1-[1-(3,4-dimethoxy-1H-2-benzopyran-1-yl)alkyl]-4-arylpiperazines that shows hypotensive activity in the conscious rat has been investigated. Structure-activity relationships are described. A typical example that was investigated in greater detail is 1-[2-(3,4-dihydro-6,7-dimethoxy-1H-2-benzopyran-1-yl)ethyl]-4-(4-fluorophenyl)piperazine. This compound decreases sympathetic nerve activity recorded from the external carotid and splanchnic nerves of baroreceptor-denervated cats and, therefore, has a central component to its mechanism of action. It also blocks pressor effects of norepinephrine and phenylephrine and is thus an alpha-adrenergic antagonist. Binding data characterize this as alpha 1-adrenergic receptor blockade.

Adrenergic alpha-Antagonists↗
PubMed1982

Involvement of serotonin in the central regulation of blood pressure: evidence for a facilitating effect on sympathetic nerve activity.

The effects of serotonin (5-HT) receptor agonists and antagonists on sympathetic nervous discharge (SND) recorded from the external carotid and splanchnic nerves were studied in baroreceptor-denervated cats. Intravenous administration of the 5-HT antagonists methysergide (0.025-1.6 mg/kg), metergoline (0.01-0.32 mg/kg), cyproheptadine (0.05-1.6 mg/kg) and cinanserin (0.2-6.4 mg/Kg) was associated with a prolonged dose-related inhibition of SND. Maximum reductions in SND produced by methysergide, metergoline, cyproheptadine and cinanserin were 90, 72, 71 and 50%, respectively. In contrast, a progressive increase in SND was observed in vehicle control animals. Methysergide, metergoline and cyproheptadine failed to reduce SND in cats pretreated with the 5-HT synthesis inhibitor p-chlorophenylalanine. Clonidine (20 micrograms/kg i.v.) significantly inhibited SND (-73%) in p-chlorophenylalanine-treated cats. The selective 5-HT agonists 5-methoxydimethyltryptamine and lisuride also reduced SND in a dose-dependent manner. The time course of the depressor effects of 5-methoxydimethyltryptamine and lisuride correlate well to their ability to inhibit 5-HT cell firing. These data indicate that 5-HT agonists which act presynaptically to inhibit 5-HT cell firing and antagonists which act postsynaptically to block the effect of synaptically released 5-HT both mediate a central reduction in SND. It is concluded that central 5-HT neurons facilitate transmission in central sympathetic pathways.

Animals↗
PubMed1981

Evidence for a central depressor action of postsynaptic alpha 1-adrenergic receptor antagonists.

The effects of alpha-adrenergic receptor antagonists on sympathetic nervous discharge (SND) recorded from the external carotid and splanchnic nerves were studied in baroreceptor intact and denervated cats. Prazosin (50 microgram/kg, i.v.) produced a rapid fall in mean arterial pressure (MAP) and no significant change in heart rate (HR) in baroreceptor denervated cats. Prazosin administration was also associated with a prolonged inhibition of SND. Nerve activity was significantly reduced within 5 min of prazosin administration remained depressed throughout the 2 h observation period. Like prazosin, WB-4101 (0.5 mg/kg, i.v.) also produced significant reductions in MAP and SND. In addition, WB-4104 produced a transient bradycardia. The decreases in MAP and SND were reversed by piperoxane (0.5 mg/kg, i.v.). Both prazosin and WB-4101 inhibited the pressor response to i.v. norepinephrine. In baroreceptor intact cats, prazosin decreased MAP and SND, but did not affect HR. In contrast, phentolamine (1 mg/kg, i.v.) decreased MAP but increased SND and HR. These data indicate that the sympatholytic action of WB-4101 and prazosin results from a centrally mediated reduction in SND as well as a peripheral blockade of alpha-adrenergic receptors. These data further suggest that noradrenergic neurons normally facilitate the outflow of sympathetic nerve activity from the central nervous system.

Adrenergic alpha-Antagonists↗
PubMed1981

Tetrahydro-2-benzoxepins: a novel family of hypotensives.

A novel series of 1-(alkylamino)-1,3,4,5-tetrahydro-7,8-dimethoxy-2-benzoxepins shows hypotensive activity. A typical example is 1-[2-(1,3,4,5-tetrahydro-7,8-dimethoxy-2-benzoxepin-1-yl)ethyl]-4-(4-fluorophenyl)piperazine. This compound is an alpha blocker with peripheral and central activities.

Anesthesia↗
PubMed1980

Pharmacological characterization of serotonin receptors in the facial motor nucleus: a microiontophoretic study.

The effects of 'peripheral' serotonin (5-HT) antagonists on the facilitation of facial motoneuron excitation by 5-HT were investigated in the present study. Microiontophoretic application (5--10 aA) or intravenous administration of methysergide (0.5--1.0 mg/kg), cyproheptadine (0.5--1.0 mg/kg), cinanserin (0.5--1.0 mg/kg), or metergoline (50--100 micrograms/kg) antagonized the facilitating effect of 5-HT but not that of norepinephrine (NE) on facial motoneurons. Blockade developed within 1--2 min of the intravenous administration of methysergide, cyproheptadine and cinanserin and continued up to 30 min. The antagonism produced by intravenous metergoline took 8--15 min to develop and lasted for at least 6 h. Chronic administration of metergoline resulted in supersensitivity to 5-HT and NE in the facial nucleus. The putative 5-HT antagonists chlorpromazine, propranolol, and methiothepin failed to block the facilitating effect of 5-HT; however, methiothepin did block NE. The results are discussed in relation to a two-component model of the 5-HT mediated motor syndrome consisting of : (1) patterned excitatory inputs to motor nuclei; (2) 5-HT facilitation of these excitatory inputs. The 'peripheral' 5-HT antagonists appear to directly block the latter component.

Animals↗
PubMed1980

Subjective uncertainty, variability of experience, and the infant's response to discrepancies.

4-month-old infants were assessed in a habituation/discrepancy paradigm using random shapes to test several propositions deduced from the discrepancy hypothesis. First, an inverted-U distribution of attention was found for discrepancies produced by random shapes which differ in the density of contours or spatial frequencies rather than in terms of specific overt pattern. Second, the distribution of attention was more similar for discrepancies defined by increases and by decreases in contour density for random shapes than for checkerboard stimuli. This result supported the role of the hypothesized intervening variable of subjective uncertainty, because while simple checkerboards are subsets of more complex checkerboards, simple random shapes are not unmodified portions of more complex shapes. Third, greater variability of experience with stimuli about a given level of standard stimulation reduced attention to simple discrepancies but increased attention to larger magnitudes of more complex discrepancies.

Attention↗
PubMed1979

Serotonergic facilitation of facial motoneuron excitation.

The effect of serotonin (5-HT) on motoneurons located in the facial nucleus of the rat was investigated in the present study. Microiontophoretic application of 10--200 nA pulses of 5-HT lasting from 1 to 10 min failed to excite facial motoneurons. However, small amounts of 5-HT facilitated the subthreshold and threshold excitatory effects of iontophoretically applied glutamate on these cells. Typically, the current of glutamate required to produce an activation of facial motoneurons was reduced by at least 50% in the presence of 5-HT. In addition, 5-HT markedly shifted to the left the cumulative dose-response curve of glutamate-induced excitation of motoneurons. The 5-HT releasing agent p-chloroamphetamine (PCA) facilitated the excitatory effects of glutamate on montoneurons in control animals, but not in those pretreated with the 5-HT also facilitated the subthreshold and threshold excitation of motoneurons produced by stimulation of the motor cortex and the red nucleus. The facilitating effect of 5-HT was blocked by methysergide. Norepinephrine also facilitated facial motoneuron excitation but this effect was not blocked by methysergide. It is concluded that 5-HT in the facial nucleus functions in a manner that is not analagous to direct excitation, but rather acts as a gain setter to enhance the effects of excitatory afferent inputs.

Animals↗