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Biomedical subjects

L A Fisher

Publications and source records attributed to L A Fisher.

At least 19 recordsLinked to original sources
PubMed1991

Effects of exercise training on responses to central injection of CRF and noise stress.

The purpose of this study was to test the hypothesis that the cardiovascular and sympathoadrenal responses to acute environmental stress are attenuated by exercise training. Furthermore, we tested the hypothesis that the cardiovascular and sympathoadrenal responses to intracerebroventricular (ICV) administration of corticotropin-releasing factor (CRF) would be attenuated by training. Conscious, unrestrained, male Sprague-Dawley rats assigned to either a treadmill trained (16-26 m/min, 30-60 min/day, 5 days/week) or nontrained (16-26 m/min, 10 min/day, 1 day/week) group were studied. After 8-10 weeks of training, maximal oxygen uptake was significantly higher in the trained (108 +/- 3 ml/kg/min) vs. the nontrained (94 +/- 4 ml/min/kg) group. There were no significant differences in baseline mean arterial pressure, heart rate and plasma catecholamine levels associated with training. Trained rats exhibited significantly attenuated elevations in arterial pressure (20 +/- 3 vs. 36 +/- 2 mmHg for nontrained) and heart rate (-3 +/- 3 vs. 12 +/- 5 beats/min for nontrained) in response to acute noise stress. Twenty minutes after ICV administration of CRF, blood pressure (trained = 119 +/- 2 mmHg, nontrained = 127 +/- 2 mmHg), heart rate (trained = 408 +/- 8 beats/min, nontrained = 424 +/- 10 beats/min), plasma norepinephrine levels (trained = 757 +/- 54 pg/ml, nontrained = 775 +/- 100 pg/ml) and plasma epinephrine levels (trained = 266 +/- 29 pg/ml, nontrained = 225 +/- 42 pg/ml) were significantly elevated in both trained and nontrained groups. CRF-induced elevations of blood pressure, but not heart rate or plasma catecholamine levels, were significantly attenuated in the trained group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Differentiated hemodynamic responses to central versus peripheral administration of corticotropin-releasing factor in conscious rats.

Corticotropin-releasing factor (CRF) modifies cardiovascular function and hemodynamic status after administration into the central nervous system and into the peripheral circulation. The mechanisms by which CRF alters arterial pressure and heart rate have been examined in detail whereas little information exists regarding the processes mediating CRF-induced changes in regional blood flow. Therefore, studies were performed in conscious, unrestrained Sprague-Dawley rats to examine potential mechanisms underlying the regional hemodynamic effects of intracerebroventricular versus intravenous administration of CRF. Intracerebroventricular administration of CRF increased arterial pressure, heart rate, and mesenteric vascular resistance while decreasing iliac vascular resistance. Intravenous pretreatment with the CRF receptor antagonist, alpha-helical CRF9-41, did not alter the cardiovascular and hemodynamic responses to central administration of CRF. In contrast, prior ganglionic blockade prevented CRF-induced responses except for the reduction in iliac vascular resistance. Intravenous administration of CRF reduced arterial pressure and mesenteric vascular resistance, elevated heart rate, and transiently increased iliac vascular resistance. Intravenous pretreatment with alpha-helical CRF9-41 completely abolished the cardiovascular and hemodynamic responses to peripheral administration of CRF. Ganglionic blockade prior to intravenous administration of CRF augmented the reductions in arterial blood pressure and mesenteric vascular resistance, prevented the increase in heart rate, and unmasked a decrease in iliac vascular resistance. The divergent actions and mechanisms of action of CRF on regional hemodynamics when administered peripherally, as opposed to centrally, indicate that this peptide produces different hemodynamic effects that are specific to its site of action.

Animals↗
PubMed1991

Central regulation of stress responses: regulation of the autonomic nervous system and visceral function by corticotrophin releasing factor-41.

Our understanding of the role of CRF in mediating integrated endocrine, autonomic and visceral stress responses is rudimentary at best. Delineating the large number of neurochemical factors that influence the activity of CRF-containing hypophyseotrophic neurones offers one direction for future research in this area. Another approach might be to examine the neuropharmacological actions of transmitters which are co-localized within CRF-containing neurones. For example, CRF and dynorphin-related peptides coexist within a subpopulation of paraventricular neurones (Roth et al, 1983), suggesting the potential for their simultaneous release and possible functional interactions between them. Interestingly, CRF and dynorphin-related peptides exhibit reciprocal actions on the release of each other in vitro and in vivo. CRF stimulates the release of immunoreactive dynorphin from rat hypothalamic slices (Nikolarakis et al, 1986) while dynorphin A1-17 inhibits the basal secretion of immunoreactive CRF from rat hypothalami (Yajima et al, 1986). In vivo experiments demonstrate that i.c.v. administration of dynorphin A1-13 reduces basal and hypotension-induced secretion of CRF into hypophyseal portal blood (Plotsky, 1986). Recent studies suggest that, in addition to their interactions at the level of release, these peptides may also modify the CNS actions of each other on autonomic and cardiovascular function (Overton and Fisher, 1989b). Thus, CRF-induced elevations of arterial pressure, heart rate and plasma catecholamine levels are attenuated by co-administration of low doses of dynorphin A1-17. The reciprocal release actions and neuropharmacological interactions between CRF and dynorphin A1-17 suggest that local integration or perhaps feedback regulation of stress-induced autonomic and cardiovascular responses may be achieved by the co-release of multiple neurotransmitters from a single source. In summary, the combined anatomical, pharmacological and physiological data provide support for the involvement of CRF neuronal systems in mediating the integration of endocrine, autonomic, and visceral functions, particularly in response to stress. Future research in this area may contribute to our understanding of the neurobiology of CRF as well as the CNS mechanisms governing homeostasis.

Animals↗
PubMed1991

Central and peripheral injections of the 5-HT2 agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane, modify cardiovascular function through different mechanisms.

The mechanisms underlying the cardiovascular effects of central and peripheral administration of the 5-HT2 (serotonin) receptor agonist (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI) were studied in conscious rats. Intravenous (10-1000 nmol/kg) and i.c.v. (3-300 nmol) administration of DOI produced dose-related elevations of arterial pressure without altering heart rate except after injection of the highest doses. Pretreatment with xylamidine tosylate, a 5-HT2 receptor antagonist that does not cross the blood-brain barrier, blocked the pressor response to i.v., but not i.c.v., administration of equivalent doses of DOI. Pretreatment with the vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP significantly reduced the pressor response to i.c.v., but not i.v., administration of DOI. Prior ganglionic blockade with chlorisondamine amplified the pressor response to both i.v. and i.c.v. administration of DOI. Pretreatment with a combination of chlorisondamine, xylamidine and d(CH2)5Tyr(Me)AVP abolished the pressor response to i.c.v. administration of DOI. Thus, the pressor response to i.v. administration of DOI was mediated at sites outside the blood-brain barrier, most likely at vascular 5-HT2 receptors, and was not secondary to vasopressin release. Inappropriate heart rate changes attended the pressor responses to i.v. administration of DOI, suggesting an action at extravascular sites. The pressor response to i.c.v. administration of DOI resulted from a combination of vasopressin release, modulation of autonomic nervous outflow and some leakage into the periphery.

Amidines↗
PubMed1991

Central nervous actions of serotonin and a serotonin1A receptor agonist: cardiovascular excitation at low doses.

Studies were performed in conscious unrestrained rats to compare the cardiovascular effects of i.c.v. administration of serotonin (5-HT) and the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). Low doses (less than 10 nmol) of 5-HT and 8-OH-DPAT elicited significant elevations of arterial pressure and heart rate. At doses greater than 10 nmol, 5-HT produced pressor responses attended by significant reductions of heart rate whereas 8-OH-DPAT produced significant depressor and bradycardiac responses. Concurrent i.c.v. administration of the nonselective 5-HT receptor antagonist, methiothepin, abolished the cardiovascular responses to a low (1 nmol) and a high (100 nmol) dose of 5-HT and a low (3 nmol) dose of 8-OH-DPAT. In contrast, methiothepin cotreatment did not prevent the reductions of arterial pressure and heart rate induced by a high (100 nmol) dose of 8-OH-DPAT. These results suggest that stimulation of central nervous system 5-HT1A receptors with low doses of 8-OH-DPAT produces cardiovascular activation.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1990

Gastrointestinal motor effects of corticotropin-releasing factor in mice.

The present investigation examined the effects of centrally and peripherally administered corticotropin-releasing factor on gastric emptying and gastrointestinal transit in mice. Corticotropin-releasing factor, given either intracerebroventricularly or intrathecally, caused a dose-dependent inhibition of gastric emptyping and gastrointestinal transit. Intravenous or intraperitoneal administration of corticotropin-releasing factor, while 5- to 7-fold less potent than after central injection, produced an equivalent level of effect. alpha-Helical corticotropin-releasing factor, a corticotropin-releasing factor receptor antagonist, blocked the effects of intracerebroventricularly administered corticotropin-releasing factor when the antagonist was given concurrently by the intracerebroventricular, but not by the intraperitoneal, route. Conversely, corticotropin-releasing factor, when given peripherally, was antagonized equally well by intracerebroventricular or intraperitoneal administration of the antagonist. The inhibition of gastric emptying induced by corticotropin-releasing factor was reduced by pretreatment with the ganglionic blocking agent, chlorisondamine, and in adrenalectomized mice, but this effect was not antagonized by naloxone. These findings provide evidence for an action of corticotropin-releasing factor within the central nervous system, as well as a peripheral site of action, to inhibit gastric emptying in the mouse. The gastrointestinal motor effects of corticotropin-releasing factor are not mediated through opioid mechanisms although their full expression may require intact autonomic innervation and adrenal function.

Adrenalectomy↗
PubMed1990

Central nervous system cardiovascular actions of CRF in sinoaortic-denervated rats.

Studies were performed in unrestrained conscious Sprague-Dawley rats to examine the central nervous system (CNS) mechanism by which corticotropin-releasing factor (CRF) produces simultaneous elevations of arterial pressure and heart rate. To test the hypothesis that CRF inhibits ongoing impulse transmission through and/or transmitter release from the CNS terminations of baroreceptor afferents, the cardiovascular effects of intracerebroventricular administration of CRF were compared in rats subjected to prior sham surgery (Sham) or sinoaortic denervation (SAD). Resting levels of arterial pressure and heart rate were elevated after SAD. In addition, SAD resulted in greater chronotropic sympathetic tone and reduced chronotropic parasympathetic tone as assessed by intravenous injections of atropine methyl nitrate and DL-propranolol. Intracerebroventricular administration of CRF in both surgical groups elicited significant increases in arterial pressure and heart rate, although a tendency for reduced tachycardic responses after SAD was apparent. Pretreatment with atropine or propranolol revealed that both the parasympathetic and sympathetic nervous systems contribute to CRF-induced heart rate responses in both surgical groups. These results suggest that ongoing baroreceptor afferent transmission is not requisite for the expression of CRF-induced cardiovascular changes. Thus it is unlikely that CRF elevates arterial pressure and heart rate through an exclusive action at the CNS terminations of baroreceptor sensory fibers.

Analysis of Variance↗
PubMed1990

Cardiovascular responses to exercise in the rat: role of corticotropin-releasing factor.

The effects of intracerebroventricular (icv) administration of a corticotropin-releasing factor (CRF) receptor antagonist, alpha-helical CRF, on systemic and regional hemodynamic adjustments to exercise were studied in conscious rats. On consecutive days, rats received saline icv, alpha-helical CRF icv, and no treatment 30 min before treadmill exercise (TMX). Increases in heart rate (HR) and mean arterial pressure (MAP) in response to TMX (16.1-28.6 m/min) were similar after icv administration of saline or no treatment. In rats receiving saline icv or no treatment, estimated vascular resistance increased in the mesenteric and renal regions and declined in the iliac (hindlimb) region. After icv administration of alpha-helical CRF9-41, HR and MAP responses during TMX were significantly attenuated. In addition, TMX-induced elevations of estimated mesenteric vascular resistance and iliac blood flow velocity were blunted after CRF receptor blockade. These altered cardiovascular and hemodynamic responses were ultimately reflected in the animals' compromised ability to run. The results suggest that the central nervous system actions of endogenous CRF are necessary for the full expression of the cardiovascular adjustments to TMX in the conscious rat.

Animals↗
PubMed1990

Central nervous effects of CRF and angiotensin II on cardiac output in conscious rats.

Studies were performed to determine whether the central nervous system actions of corticotropin-releasing factor (CRF) and angiotensin II (ANG II) on systemic arterial pressure are mediated, in part, through changes in cardiac output (CO). Changes in CO after intracerebroventricular administration of ANG II and CRF were assessed in conscious unrestrained rats bearing pulsed Doppler flow probes on the ascending aorta. Intracerebroventricular injection of CRF (0.15 nmol) increased arterial pressure (15-20 mmHg), heart rate (70-100 beats/min), and CO (25-35%) without significantly affecting total peripheral resistance. Intracerebroventricular injection of ANG II (0.1 nmol) produced similar elevations of arterial pressure (15-20 mmHg). However, the ANG II-induced pressor response was attended by significant decreases in heart rate (20 beats/min) and CO (10-15%) and significant increases in total peripheral resistance (30-40%). The results of these studies demonstrate that CO, as assessed by pulsed Doppler flow probe methodology, may be influenced significantly and differentially by central nervous system administration of CRF and ANG II.

Angiotensin II↗
PubMed1989

Modulation of central nervous system actions of corticotropin-releasing factor by dynorphin-related peptides.

Corticotropin-releasing factor (CRF) and dynorphin-related peptides are co-localized within a subset of hypothalamic neurons suggesting the possibility of their co-release. Therefore, studies were performed in conscious unrestrained rats to examine whether dynorphin-related peptides modify the central nervous system (CNS) actions of CRF on sympathetic nervous activity and cardiovascular function. Intracerebroventricular (i.c.v.) administration of dynorphin A1-8 (0.1 and 1.0 nmol) did not alter arterial pressure (AP) or heart rate (HR). I.c.v. injection of dynorphin A1-13 (0.1, 0.3 and 1.0 nmol) produced transient elevations of HR but did not significantly affect AP. I.c.v. administration of dynorphin A1-17 (0.1, 0.3 and 1.0 nmol) elicited delayed (10-15 min) and transient elevations of AP and HR. CRF (0.15 nmol, i.c.v.) produced immediate and sustained elevations of AP, HR and plasma catecholamine levels. Upon simultaneous administration, 0.1 nmol of dynorphin A1-17, but not 0.1 nmol of dynorphin A1-8 or dynorphin A1-13, markedly attenuated CRF-induced elevations of AP, HR, and plasma catecholamine levels. The results suggest that selected dynorphin-related peptides may modify the CNS actions of CRF.

Animals↗
PubMed1989

Corticotropin-releasing factor: endocrine and autonomic integration of responses to stress.

Corticotropin-releasing factor, a 41-residue peptide, is established as the principal physiological regulator of the pituitary-adrenal axis. The neuroanatomic distribution of corticotropin-releasing factor and its receptors suggests that this peptide may be a neurotransmitter in pathways outside the hypophysiotropic zone. Indeed, corticotropin-releasing factor demonstrates potent neuropharmacological actions that are independent of its pituitary effects. Laurel Fisher reviews the combined anatomical, pharmacological and physiological evidence that supports a role for corticotropin-releasing factor in mediating the integrated endocrine, autonomic and cardiovascular responses to stress.

Animals↗
PubMed1989

Family cigarette smoking and test performance by adolescents.

This research considers test performance by adolescents as a correlate of cigarette smoking by their families. Scores obtained by adolescents on the California Achievement Test decreased as the amount of cigarette smoking by other members of their families increased. The relationship was not accounted for by active cigarette smoking of the adolescent or by 20 other social and psychological variables.

Achievement↗
PubMed1989

Central autonomic modulation of cardiac baroreflex by corticotropin-releasing factor.

The effects of intracerebroventricular administration of corticotropin-releasing factor (CRF) on baroreflex control of heart rate were studied in conscious, unrestrained rats. Stimulus-response curves relating mean arterial pressure (MAP) to pulse interval were constructed for assessment of baroreflex function. CRF, intracerebroventricularly injected, elicited dose-related reductions of resting pulse interval, response range, and reflex gain and elevations of resting arterial pressure and MAP50 (arterial pressure at midrange). Earlier peripheral blockade of cardiac vagal influences with atropine methyl nitrate greatly attenuated the effects of CRF on resting pulse interval, response range, and reflex gain. In contrast, earlier blockade of cardiac sympathetic influences with intravenous propranolol treatment did not alter the ability of CRF to reduce resting pulse interval, response range, and reflex gain. The central nervous system effects of CRF on cardiac baroreflex function were qualitatively similar to the actions of atropine methyl nitrate. It is concluded that CRF alters transmission in central nervous system pathways mediating baroreceptor-induced activation of cardiac vagal motor neurons.

Animals↗
PubMed1989

Use of smokeless tobacco by age, race, and gender in ten standard metropolitan statistical areas of the southeast United States.

Most surveys of smokeless tobacco use have been limited to young people, and in the few studies of adults, researchers have not considered age, race, and gender simultaneously, although broad age groups have been used. Data on smokeless tobacco use by race and gender for 5-year age groups up to age 70 and older were compiled from 21,203 households in 10 Standard Metropolitan Statistical Areas of the southeastern United States.

Adolescent↗
PubMed1988

Autonomic and cardiovascular effects of corticotropin-releasing factor in the spontaneously hypertensive rat.

Corticotropin-releasing factor (CRF) administered intracerebroventricularly (i.c.v.) produced a greater increase of plasma epinephrine and glucose concentrations in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto (WKY) or Sprague-Dawley (SD) rats. In contrast, CRF given i.c.v. produced significant elevations of mean arterial pressure (MAP) and heart rate (HR) in WKY and SD rats, but not in SHRs. To determine whether the prominent rise of plasma epinephrine levels following CRF administration to SHRs was a unique response to this peptide, two other stimuli for epinephrine secretion were evaluated, i.e. bombesin given i.c.v., and insulin given intravenously (i.v.). In contrast to the apparent enhanced responsiveness of the SHR to CRF, plasma epinephrine levels following either bombesin or insulin administration were similar in SHR, WKY and SD rats. These results demonstrate that the adrenomedullary response to CRF administration in the SHR is of greater magnitude than in WKY or SD rats. In an effort to identify the mechanisms responsible for the differential cardiovascular and adrenomedullary responses to CRF in the SHR versus WKY rat, CRF binding studies were performed. No difference in binding affinity of [125I]CRF or CRF receptor number could be identified in brains from SHR and WKY rats. Thus, CRF influences cardiovascular and adrenomedullary functions in a qualitatively dissimilar fashion in SHR and WKY rats. These differences are not secondary to any measurable alteration in CRF receptor affinity and number in SHR and WKY rats.

Animals↗
PubMed1988

Corticotropin-releasing factor: central nervous system effects on baroreflex control of heart rate.

The effects of intracerebroventricular injections of corticotropin-releasing factor on baroreflex control of heart rate were examined in conscious, unrestrained rats. Baroreflex control of heart rate was tested by generating stimulus-response curves relating arterial pressure to pulse interval over a wide range of arterial pressures. Administration of corticotropin-releasing factor produced dose-related alterations of pressure-dependent curve parameters, e.g., range, gain and pressure at midrange. These results suggest that corticotropin-releasing factor alters transmission in neural pathways that process baroreceptor information.

Animals↗
PubMed1988

Three mass media campaigns to prevent adolescent cigarette smoking.

This article describes behavioral science theory and formative research used to develop television and radio campaigns for preventing the initiation of cigarette smoking among adolescents. It also presents the content and form of the messages, the plans, and the costs for national implementation of the campaigns.

Adolescent↗