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Biomedical subjects

G R Van Loon

Publications and source records attributed to G R Van Loon.

At least 19 recordsLinked to original sources
PubMed1996

Effects of beta-FNA on sympathoadrenal, cardiovascular, and analgesic responses to DAMPGO at rest and during stress.

To elucidate further the role of mu-opioid receptors in mediating analgesia and cardiovascular function at rest and during stress, rats were pretreated ICV with either saline (5 microliters) or beta-funaltrexamine (beta-FNA, 5 nmol/5 microliters), a noncompetitive opioid receptor antagonist that inactivates irreversibly mu receptors, 2 days prior to [D-Ala2, N MePhe4, Gly5-ol]enkephalin (DAMPGO, 1 nmol, ICV) administration. Pretreatment with beta-FNA blocked DAMPGO-induced analgesia as measured by the tail-flick test. DAMPGO also produced an increase in blood pressure (BP), sympathoadrenal outflow, and a bradycardia. Pretreatment with beta-FNA converted the DAMPGO-induced bradycardia to a tachycardia, significantly reduced the DAMPGO-induced increase in epinephrine by 60%, and the norepinephrine response by 45%, and attenuated mildly the increase in BP due to DAMPGO. In saline-treated rats, restraint stress evoked an increase in HR, BP, and plasma catecholamines. Pretreatment with beta-FNA partially attenuated the increase in HR in response to stress. In the presence of DAMPGO, restraint stress resulted in a further bradycardia, which was significantly blocked by pretreatment with beta-FNA. Stress also produced increases in BP and plasma catecholamines, which were not prevented by pretreating rats with beta-FNA. These results indicate that beta-FNA may not have inactivated all the receptors accessible to DAMPGO which control BP, or alternatively, beta-FNA may selectively inactivate a subtype of mu receptors. In addition, brain mu opioid receptors appear to be significantly involved in mediating supraspinal analgesia and regulating parasympathetic outflow to the heart and sympathoadrenal release of catecholamines.

Adrenal Glands↗
PubMed1996

Endogenous opioid peptide mediation of hypoalgesic response in long-term diabetic rats.

This study was designed to examine the role of endogenous opioid peptide mediation of elevated pain threshold in adult male Sprague-Dawley rats with long-term diabetes mellitus induced by streptozotocin (STZ). Diabetes resulted in a significant elevation in pain threshold as measured by the tail-flick and/or hotplate latency tests. The hypoalgesic response in diabetic rats to hotplate testing developed gradually over a 4-6 week period after a transient hyperalgesia during the first two weeks of diabetes. The elevation of pain threshold achieved peak level by the fourth week after STZ administration, and remained at that level throughout the experimental period (up to 13 weeks). This hypoalgesic state in diabetic animals is thought to be mediated by opioid receptors (i.e. mu and delta). The involvement of the mu receptor is supported by the effect of naltrexone on the STZ-diabetic rats; naltrexone significantly attenuated the increase in tail-flick and hotplate latencies, compared to that of the non-diabetic controls. Furthermore, the concentration of native (free) Met-enkephalin in the spinal cord of STZ-diabetic rats was about 5-fold higher than that of non-diabetic animals. Such high levels of Met-enkephalin suggest the involvement of delta opioid receptors in the hypoalgesic response observed in STZ-diabetic rats. Seven weeks of insulin treatment, initiated after development of the hypoalgesic response, normalized not only plasma glucose level and body weight of diabetic rats, but also returned their antinociceptive latency toward normal. The results of this study showed that long-term diabetes is associated with altered pain threshold and further support the hypothesis for endogenous opioid peptide mediation of hypoalgesia in chronically diabetic rats that can be prevented by insulin treatment.

Analysis of Variance↗
PubMed1994

Effects of nicotine on the concentration of native and cryptic Met- and Leu-enkephalin in peripheral tissues.

The distribution of the native pentapeptides, Met- and Leu-enkephalin, and their cryptic forms (larger enkephalin-containing peptides) in adrenal medulla, spleen, lung, salivary gland, vas deferens, heart, duodenum and jejunum were determined by radioimmunoassay. The proportion of total Met- and Leu-enkephalin represented by native pentapeptide varied markedly among these tissues. Also, the distribution of native and cryptic Met-enkephalin was distinct from that of Leu-enkephalin. Repeated short-term administration of nicotine, 0.1 mg/kg i.p. six times at 30 min intervals, produced significant changes in native and cryptic Met-enkephalin in adrenal medulla, jejunum, vas deferens, spleen and heart. This regimen of nicotine also affected the concentration of Leu-enkephalin in adrenal medulla, jejunum and spleen.

Animals↗
PubMed1992

Effect of diabetes on the levels of two forms of Met-enkephalin in plasma and peripheral tissues of the rat.

Levels of native and cryptic or peptidase-derivable (after being digested with trypsin and carboxypeptidase) Met-enkephalin were measured by a specific radioimmunoassay method in plasma, anterior and neurointermediate lobes of pituitary and various peripheral tissues of streptozotocin (STZ) diabetic rats. The results show that the highest concentration of native and cryptic Met-enkephalin were found in the neurointermediate lobe of pituitary. Streptozotocine-induced diabetes alters the concentration of either or both forms of Met-enkephalin in plasma, the anterior and neurointermediate lobes of the pituitary, heart, lung, spleen, liver, seminal vesicle, vas deferens, kidney, bladder detrusor, and duodenum. One of the most pronounced effects of diabetes observed in this study is seen in the seminal vesicles where native Met-enkephalin was depleted to less than 10% of the control value. The uneven distribution of Met-enkephalin in peripheral tissues may suggest that these tissues process and/or metabolize Met-enkephalin to different degrees. Our data also suggest that STZ-induced diabetes alters the enkephalinergic activity in some of these tissues. It is suggested that some of the peripheral pathophysiological symptoms associated with diabetes may be attributed, in part, to altered activity of enkephalinergic systems.

Animals↗
PubMed1992

Plasma Met-enkephalin and catecholamine responses to intense exercise in humans.

Native and cryptic Met-enkephalin and catecholamines are coreleased in response to stress. However, it is not known whether Met-enkephalin and catecholamines exhibit concurrent temporal relationships in response to exercise. The purpose of this investigation was to examine the corelease of catecholamines and Met-enkephalin in endurance-trained (n = 6) and untrained (n = 6) male subjects during a 6-min bout of exercise: 4 min at 70% of maximal O2 uptake (VO2max) followed by 2 min at 120% VO2max. Peak catecholamine levels were found at 1 min of recovery. In trained subjects, native Met-enkephalin peaked during exercise at 70% VO2max, declined during exercise at 120% VO2max, and returned to basal levels by 1 min of recovery. In the untrained subjects, native Met-enkephalin peaked at 120% VO2max (6 min) and returned to baseline by 5 min of recovery. In both groups, cryptic Met-enkephalin peaked at 70% VO2max and returned to basal levels during exercise at 120% VO2max. These data demonstrate that during exercise there is a temporal dissociation in plasma levels of Met-enkephalin and catecholamines.

Adult↗
PubMed1991

Desensitization of central nicotinic cardiovascular effects by nicotine isomers and a quaternary analogue.

Nicotine produces potent cardiovascular and sympathoadrenal effects. Furthermore, repeated administration of nicotine is associated with development of tolerance for many responses. We sought to compare the effects of initial intracerebral administration of nicotine isomers and a quaternary analogue on cardiovascular and sympathoadrenal responses and to compare the desensitizing properties of these nicotinic compounds on subsequent responses to nicotine. Thus we examined the effects of (-)-nicotine, (+)-nicotine, N'-methylnicotinium iodide (N'MN), a quaternary analogue of (-)-nicotine, and saline vehicle, administered into a lateral cerebral ventricle, on heart rate (HR), systolic, diastolic and mean arterial blood pressure (BP), and plasma concentrations of epinephrine and norepinephrine in conscious, freely moving, adult, male rats. (-)-Nicotine (120 nmol, ICV) produced decrease in HR and increases in all other parameters. (+)-Nicotine at this dose produced only small effects on HR, BP and plasma catecholamines. An equimolar dose of N'MN produced similar effects on these parameters, quantitatively intermediate between those of the two nicotine isomers. Thirty min after administration of these nicotinic agonists, all parameters had returned to baseline. At this time, the effects of subsequent ICV administration of (-)-nicotine 120 nmol was studied in all animals. Prior administration of either (-)-nicotine or (+)-nicotine markedly attenuated the bradycardic response to (-)-nicotine, and N'MN was less effective in this regard. In contrast, neither (-)-nicotine nor N'MN inhibited the pressor response to subsequent (-)-nicotine, whereas (+)-nicotine did produce some attenuation of this pressor response. Similarly, only (+)-nicotine, was found to inhibit the plasma norepinephrine response to subsequent (-)-nicotine when this drug dose and timing of administration were used. The epinephrine response to subsequent (-)-nicotine was not affected by this dose (120 nmol) and timing of treatment with any of these ligands. These data support the concept that desensitization of the intracerebral effects of nicotine on cardiovascular and sympathoadrenal function may be mediated at binding sites other than those producing nicotinic responses.

Animals↗
PubMed1991

Nicotine-induced alterations in peripheral tissue concentrations of native and cryptic Met- and Leu-enkephalin.

This study examined the peripheral tissue distribution of native and cryptic Met- and Leu-enkephalin, and regulation of tissue enkephalins by nicotine. Met- and Leu-enkephalin concentrations showed widespread variation in tissue concentration and degree of processing. HPLC characterization of homogenate of spleen revealed that both native and cryptic immunoreactive Met-enkephalin are comprised of two peaks, one representing authentic Met-enkephalin pentapeptide and the other its sulfoxide. Subacute repeated administration of nicotine 0.1 mg/kg ip, six times at 30 min intervals, increased native Met- and Leu-enkephalin in adrenal medulla without affecting cryptic Met- and Leu-enkephalin concentrations, consistent with increased processing of larger peptides to Met- and Leu-enkephalin. Subacute nicotine decreased splenic concentrations of native and cryptic Met-enkephalin and native Leu-enkephalin, consistent with increased release of Met- and Leu-enkephalin from spleen and decreased synthesis of proenkephalin A or inadequate processing of larger peptides to enkephalin pentapeptides in spleen to compensate for the increased release during this period. HPLC characterization revealed that nicotine-induced decrease in native Met-enkephalin in spleen resulted from reductions in both pentapeptide and its sulfoxide. Nicotine also increased native Met-enkephalin in jejunum, decreased cryptic Met-enkephalin in heart atrium, increased native Leu-enkephalin in anterior pituitary and decreased cryptic Leu-enkephalin in jejunum. Nicotine may produce some of its effects through alterations in release of enkephalins from peripheral tissues.

Animals↗
PubMed1990

Nicotine protects against mu-opioid receptor antagonism by beta-funaltrexamine: evidence for nicotine-induced release of endogenous opioids in brain.

We have hypothesized that some effects of nicotine are mediated through endogenous opioids. This study was designed to demonstrate in rats that nicotine releases endogenous opioids in brain. In the control group, subcutaneous morphine (8 mg/kg) produced analgesia or antinociception as measured by prolongation of tail flick latency. Intracerebroventricular administration 24 h earlier of beta-funaltrexamine (beta-FNA, 2.5 micrograms), an antagonist which irreversibly alkylates opioid receptors, markedly reduced (66%) morphine analgesia. Subcutaneous administration of nicotine (0.1 mg/kg) prior to beta-FNA attenuated (31%) the inhibitory effect of beta-FNA on morphine analgesia. These data support our hypothesis that endogenous opioids released by nicotine bind to mu-opioid receptors in brain and protect them against inactivation by beta-FNA.

Analgesia↗
PubMed1990

Tolerance to nicotine-induced sympathoadrenal stimulation and cross-tolerance to stress: differential central and peripheral mechanisms in rats.

Nicotine stimulates the secretion of catecholamines from sympathetic nerve endings and adrenal medulla by acting on peripheral nicotinic cholinergic receptors. Nicotine is also a potent stimulant in the central nervous system but the significance of nicotinic receptors in brain in mediating cardiovascular and sympathoadrenal responses to nicotine is unclear. The responses of resting plasma catecholamines, blood pressure and heart rate were compared in rats receiving nicotine, administered either systemically or intracerebroventricularly (i.c.v.). Sympathoadrenal stress responses were also studied in rats rendered tolerant to nicotine from repeated systemic or intraventricular injections. Nicotine, given either intraventricularly or systemically, produced dose-related increases in the concentration of epinephrine in plasma. Little effect on norepinephrine in plasma was observed with nicotine given intraventricularly, indicating predominant stimulation of adrenomedullary pathways. In contrast, nicotine, given systemically, produced comparable increases in both epinephrine and norepinephrine. Blood pressure increased and heart rate fell in response to either intraventricular or systemic administration of nicotine. Rats exhibited tolerance to nicotine 24 hr after a single intraventricular injection; however, tolerance was not detected with systemically injected nicotine unless the injections were given at least every 30 min. Whereas rats rendered tolerant to systemic administration of nicotine were cross-tolerant to stress, with respect to sympathoadrenal stimulation, cross-tolerance with stress was not detected in rats treated with nicotine repeatedly by the intraventricular route. These results indicate that nicotinic receptors in brain modulate the central sympathetic outflow and adapt readily to nicotine stimulation with prolonged tolerance, but are probably not involved in sympathoadrenal stress responses. Peripheral nicotinic receptors, regulating sympathoadrenal secretion of catecholamines, displayed much shorter-lasting tolerance.

Adrenal Medulla↗
PubMed1990

Haloperidol-induced increase in striatal concentration of the tripeptide, Tyr-Gly-Gly, provides an index of increased enkephalin release in vivo.

A sensitive and specific radioimmunoassay has been developed for the tripeptide, Tyr-Gly-Gly, which has been shown previously to be an extraneuronal metabolite of opioid peptides derived from proenkephalin A. Using this assay, we found a regional variation in Tyr-Gly-Gly immunoreactivity in rat brain, with highest levels in striatum and lowest in cerebral cortex. Intracerebroventricular administration of the aminopeptidase inhibitor, bestatin; produced a threefold increase in Tyr-Gly-Gly immunoreactivity in rat striatum, whereas thiorphan, an enkephalinase inhibitor, produced a 45% reduction in striatal Tyr-Gly-Gly immunoreactivity. These data suggest that the tripeptide, Tyr-Gly-Gly, is in a dynamic state in the brain, and provide further support for the hypothesis that its concentration in specific brain areas may reflect the release of endogenous enkephalins in these brain areas. Further confirmation of the validity of measurements of brain Tyr-Gly-Gly as indices of enkephalin release under conditions of altered neuronal activity was provided by our demonstration that chronic dopamine receptor blockade with haloperidol increased striatal concentrations of both Met-enkephalin and Tyr-Gly-Gly.

Animals↗
PubMed1990

Plasma native and peptidase-derivable Met-enkephalin responses to restraint stress in rats. Adaptation to repeated restraint.

Met-enkephalin and related proenkephalin A-derived peptides circulate in plasma at picomolar concentration as free, native pentapeptide and at nanomolar concentration in cryptic forms. We have optimized conditions for measurement of immunoreactive Met-enkephalin in plasma and for generation by trypsin and carboxypeptidase B of much greater amounts of total peptidase-derivable Met-enkephalin in plasma of rats, dogs, and humans. Free Met-enkephalin (11 pM) is constituted by native pentapeptide and its sulfoxide. Characterization of plasma total Met-enkephalin derived by peptidic hydrolysis revealed a small amount (38 pM) of Met-enkephalin associated with peptides of molecular mass less than 30,000 D, and probably derived from proenkephalin A, but much larger amounts of Met-enkephalin associated with albumin (1.2 nM) and with a globulin-sized protein (2.8 nM). Thus, plasma protein precursors for peptidase-derivable Met-enkephalin differ structurally and chemically from proenkephalin A. Met-enkephalin generated from plasma by peptidic hydrolysis showed naloxone-reversible bioactivity comparable to synthetic Met-enkephalin. Prolonged exposure of adult, male rats to restraint stress produced biphasic plasma responses, with peaks occurring at 30 s and 30 min in both free native and total peptidase-derivable Met-enkephalin. Repeated daily exposure to this 30-min stress resulted in adaptive loss of responses of both forms to acute restraint. Initial plasma responses of Met-enkephalin paralleled those of epinephrine and norepinephrine, but subsequently showed divergence of response. In conclusion, Met-enkephalin circulates in several forms, some of which may be derived from proteins other than proenkephalin A, and plasma levels of both free native, and peptidase-derivable Met-enkephalin are modulated physiologically.

Adaptation, Physiological↗
PubMed1990

Tolerance and cross-tolerance to stress-induced increases in plasma Met-enkephalin in rats with adaptively increased resting secretion.

Plasma concentrations of both native (pentapeptide plus its sulfoxide) and peptidase-derivable (trypsin followed by carboxypeptidase-B) Met-enkephalin showed brisk increases in response to the stresses of immobilization, hemorrhage, and electric footshock in conscious, freely moving, adult male rats. Daily exposure to 150-min periods of immobilization resulted in a maintained increase in baseline plasma concentrations of native Met-enkephalin 21.5 h after the sixth day and a further increase after 39 days. The plasma native Met-enkephalin response to acute immobilization was attenuated on day 7 and completely absent on day 40. Unstressed rats showed a plasma native Met-enkephalin response to hemorrhage of 15% blood volume and a further increase in response to 25% hemorrhage. Immediately after initial acute immobilization or 6 days of daily immobilization when plasma native Met-enkephalin was elevated but the response to acute immobilization was attenuated, plasma native Met-enkephalin responses to hemorrhage were also attenuated. Rats that had been immobilized daily for 40 days and showed no plasma native Met-enkephalin response to acute immobilization also showed no responses to hemorrhage. After 39 days of immobilization when there was no plasma native Met-enkephalin response to acute immobilization, there was also no response to footshock. Thus, development of tolerance or adaptive loss of plasma native Met-enkephalin response to immobilization with repeated exposure to this stressor is associated with cross-tolerance or adaptive loss of the responses to the stresses of hemorrhage or electric footshock. Development of tolerance and cross-tolerance of plasma responses of peptidase-derivable Met-enkephalin paralleled that of native Met-enkephalin. Thus, adaptation of plasma Met-enkephalin responses to repeated exposure to a stressor included both increased resting secretion and decreased acute responses to homotypic or novel stressors.

Adaptation, Physiological↗
PubMed1989

Opioid mediation of cocaine-induced hyperactivity and reinforcement.

The mechanisms by which cocaine produces hyperactivity and reinforcement remain poorly understood. Since reinforcement is also a property of other drugs of abuse including opiates, we examined the possible mediation of these cocaine-induced behaviors by endogenous opioid peptides. In this study, we have confirmed reports that cocaine increases locomotor activity and conditioned place preference in rats. We have also demonstrated that opioid receptor blockade with naloxone antagonizes completely the locomotor-activating effect of cocaine and attenuates the strength of the place preference conditioning produced by cocaine. These data support the thesis that endogenous opioids are involved in mediation of cocaine-induced behavior.

Animals↗
PubMed1989

Role of sympathoadrenomedullary system in cardiovascular response to stress in rats.

Sympathetic nerve and/or adrenal medulla contributions to stress-induced cardiovascular responses were investigated by factoring out their influence using adrenal demedullation (DMED) and/or chemical sympathectomy with guanethidine (GUAN). Rats divided into 4 groups [sham-operated/saline (SHAM/SAL), SHAM/GUAN, DMED/SAL and DMED/GUAN] were injected i.p. over 4 weeks with either saline or GUAN (25 mg/kg/day). At the end of this treatment period, blood pressure (BP) and heart rate (HR) were monitored via carotid catheter prior to and during restraint in conscious rats. Treatments did not alter basal BP or HR when compared to controls. Restraint increased HR (delta 72 bpm) and systolic, diastolic and mean BP (delta approximately 20 mm Hg) in control animals. Restraint-induced HR change was significantly greater in DMED/SAL animals (delta 88 bpm), but less in SHAM/GUAN animals (delta 40 bpm) than in controls. DMED/GUAN was not different from SHAM/GUAN alone in altering HR response to stress, supporting the greater influence of sympathetic nerves over adrenal medulla in controlling HR. Chronic GUAN abolished normal pressor responses to restraint stress. DMED increased diastolic blood pressure response to stress. However, in DMED/GUAN rats, not only did stress fail to increase blood pressure but rather stress produced hypotension (delta - 34 mm Hg MAP), demonstrating the role of adrenal medulla in maintaining BP during stress. Differential effects of the various treatments on diastolic and systolic pressure suggest that the treatments had effects on peripheral vasculature. These results demonstrate that sympathetic nerves and adrenal medulla have important influences on cardiovascular function during stress and that in the absence of either, the other system may partially compensate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1989

Effect of transdermal clonidine on the endocrine responses to insulin-induced hypoglycemia in essential hypertension.

Clonidine hydrochloride via the central nervous system lowers blood pressure, inhibits ACTH and catecholamine release, and stimulates growth hormone secretion. To evaluate the effect of this drug on the release of glucoregulatory hormones during hypoglycemia, we studied the responses to insulin-induced hypoglycemia (0.1 units/kg) in 10 patients with mild essential hypertension before and after treatment for 16 weeks with transdermal clonidine. Clonidine significantly lowered blood pressure, basal plasma norepinephrine levels, and epinephrine and renin activity but did not affect basal growth hormone concentrations. Clonidine significantly reduced the norepinephrine and epinephrine responses to hypoglycemia (norepinephrine AUC from 207 +/- 16 SE to 156 +/- 25 nmol/L/min, epinephrine from 157 +/- 28 to 99 +/- 29 nmol/L/min; both p less than 0.05) and increased the growth hormone response (AUC from 763 +/- 148 ng/min/ml to 1164 +/- 292 ng/min/ml; p less than 0.05) but did not affect the cortisol response or the magnitude or rate of glucose recovery from hypoglycemia. Thus transdermal clonidine has several effects on glucose counterregulatory hormones that do not significantly alter insulin sensitivity or impair recovery from hypoglycemia.

Administration, Cutaneous↗
PubMed1989

Prior immobilization stress alters adrenal hormone responses to hemorrhage in rats.

The effect of prior immobilization stress (IMO) on the plasma epinephrine (EPI), norepinephrine (NE), adrenocorticotropic hormone (ACTH), and corticosterone (CS) responses to acute hemorrhage was studied in conscious male rats with chronic catheters in tail artery, using two combinations of IMO and hemorrhage. IMO per se led to significant increases of EPI, NE, ACTH, and CS in all animals. Hemorrhage of 25% of estimated blood volume (EBV) performed immediately after 150 min IMO caused exaggerated release of EPI and NE, whereas CS remained unchanged at the level previously elevated by IMO. ACTH response to initial blood loss of 12.5% was diminished in previously immobilized rats. Hemorrhage of 35% EBV after 60 min IMO and a 10-min recovery period also resulted in potentiated increases in EPI and NE, suppressed ACTH secretion, and no further change in stress-elevated CS concentration. No differences between groups were observed in relative mean arterial blood pressure, plasma protein, and lactate responses to 35% hemorrhage. Posthemorrhagic increase of plasma concentration of several tissue enzyme activities was significantly higher in prestressed rats. Furthermore, 24-h mortality rate increased by 49%. In summary, our results indicate that prior IMO potentiated activation of the sympathoadrenomedullary system and suppressed ACTH response to subsequent hemorrhage. Altered neuroendocrine responsiveness and stress-induced prehemorrhagic tissue damage may play roles in the increased susceptibility of the organism to blood loss.

Adrenocorticotropic Hormone↗
PubMed1989

mu-Opioid peptide modulation of cardiovascular and sympathoadrenal responses to stress.

The effects of mu- and delta-opioid receptor activation on sympathoadrenal and cardiovascular responses to stress were examined in conscious rats. The mu-selective agonist [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAGO) or the delta-selective agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) was injected into a lateral cerebral ventricle, then rats were stressed by restraint. Plasma catecholamines were measured, and arterial blood pressure and heart rate were recorded continuously. Restraint stress evoked increases in plasma catecholamines and heart rate in saline-pretreated rats. Both DAGO and DPDPE increased basal plasma levels of catecholamines and blood pressure, and DAGO, 5 nmol, produced bradycardia. DAGO, 5 nmol, but not DPDPE, potentiated the plasma catecholamine responses to restraint. However, the presence of DAGO or DPDPE during restraint resulted in decreases in heart rate and blood pressure. The effects of DAGO and DPDPE on plasma catecholamines, heart rate, and blood pressure were blocked by a mu-selective dose of naloxone but were not reversed by the delta-selective antagonist ICI 174864. These results indicate that mu-receptor stimulation during restraint stress facilitates sympathoadrenal and parasympathetic outflow and results in vasodilatation of some peripheral vascular beds.

Animals↗