Biomedical subjects

L C Keil

Publications and source records attributed to L C Keil.

At least 73 records · Page 4Linked to original sources

PubMed1989

Mechanism of inhibition of renin response to hypotension by atrial natriuretic factor.

We have reported that infusion of atrial natriuretic factor (ANF) inhibited the rise in plasma renin activity (PRA) in response to constriction of the abdominal aorta to cause a reduction in renal perfusion pressure (RPP). To evaluate the effect of ANF on neural control of renin release, acute thoracic inferior vena caval constriction (TIVCC) was performed in conscious dogs to reduce arterial pressure by 25% of control and stimulate PRA by a reflex increase in renal nerve activity and a reduction in RPP. Propranolol was used to block neural stimulation of renin release. TIVCC caused significant increases in PRA, plasma aldosterone, arginine vasopressin (AVP), and adrenocorticotropic hormone (ACTH) concentrations. The increase in PRA was significantly reduced by the infusion of either ANF at 20 ng.kg-1.min-1 or propranolol. The combined infusion of ANF and propranolol produced an additive and complete inhibition of the renin response to TIVCC; therefore the effect of ANF is independent of neural stimulation of renin release. ANF at 20 ng.kg-1.min-1 also inhibited increases in aldosterone, AVP, and ACTH, but ANF at 5 ng.kg-1.min-1 only affected the aldosterone response to TIVCC. Therefore ANF inhibits angiotensin II-stimulated aldosterone synthesis and/or secretion at very low doses and at higher doses attenuates reflex increases in AVP and ACTH caused by hypotension.

Adrenocorticotropic Hormone↗

PubMed1989

Lack of effect of vasopressin replacement on renin hypersecretion in Brattleboro rats.

To determine how the vasopressin deficiency in homozygous Brattleboro rats with diabetes insipidus produces increased renin secretion, homozygous and heterozygous Brattleboro rats were infused through subcutaneously implanted Alzet minipumps for 1 wk with a dose of arginine vasopressin that restored plasma vasopressin to normal in the homozygous animals. In the homozygous animals, plasma renin activity (PRA) and the PRA response to immobilization remained elevated compared with Long-Evans controls. Propranolol reduced PRA to normal and markedly reduced the PRA response to immobilization. PRA was normal in heterozygous Brattleboro rats. The data indicate that the increased renin secretion in homozygous rats is a result of increased sympathetic activity, and because circulating vasopressin does not cross the blood-brain barrier, it seems likely that the increased sympathetic activity is central in origin.

Animals↗

PubMed1989

Effect of baroreceptor denervation on vasopressin and cortisol responses to angiotensin II infusion in conscious dogs.

Recent studies suggest that the pressor response to exogenous angiotensin II infusion may, through baroreceptor-dependent mechanisms, counteract the stimulatory effect of the peptide on vasopressin and adrenocorticotropic hormone (ACTH) secretion. To test this hypothesis, the effect of combined cardiac and sinoaortic baroreceptor denervation on the increases in plasma concentrations of vasopressin and cortisol (used as an index of ACTH secretion) produced by angiotensin II infusion was studied in conscious dogs. In eight intact dogs, 30-min angiotensin II infusions at 5, 10, and 20 ng.kg-1.min-1 increased mean arterial pressure from 108 +/- 5 to 126 +/- 5 mmHg, from 101 +/- 4 to 130 +/- 4 mmHg, and from 99 +/- 3 to 138 +/- 4 mmHg, respectively (P less than 0.001). Plasma cortisol concentration increased from 19 +/- 4 to 27 +/- 4 ng/ml, from 19 +/- 4 to 43 +/- 4 ng/ml, and from 19 +/- 4 to 71 +/- 6 ng/ml (P less than 0.01), and plasma vasopressin concentration increased from 2.2 +/- 0.3 to 3.1 +/- 0.3 pg/ml, from 2.3 +/- 0.3 to 3.5 +/- 0.4 pg/ml, and from 2.2 +/- 0.4 to 5.0 +/- 0.5 pg/ml (P less than 0.01). In five to six baroreceptor-denervated dogs, angiotensin II infusion produced increases in mean arterial pressure, plasma vasopressin concentration, and plasma cortisol concentration that were not consistently different from those in the intact dogs. These results demonstrate that baroreceptor denervation does not enhance the vasopressin or cortisol responses to angiotensin II infusion in conscious dogs.

Angiotensin II↗

PubMed1989

Potentiation of hormonal responses to hemorrhage and fasting, but not hypoglycemia in conscious adrenalectomized rats.

Bilateral adrenalectomy (ADRX) in rats removes the source of two major stress-responsive hormones, corticosterone and epinephrine. To test how ADRX rats withstand stress, we performed the following experiments in adult male rats provided with indwelling femoral arterial and venous cannulae and either ADRX or sham-adrenalectomized (Sham) 3 days later and given 0.5% NaCl to drink. Five to 6 days after adrenal surgery the rats were studied after either a 15 ml/kg.5 min hemorrhage or after an overnight fast followed by insulin-induced hypoglycemia. In fed unstressed ADRX rats, basal mean arterial blood pressure was slightly decreased; heart rate was increased; blood volume, vasopressin, and oxytocin concentrations were not different from sham values; and renin and norepinephrine were significantly elevated. The recovery of arterial pressure after hemorrhage in the ADRX rats was similar to that in the sham group over a 5-h period; however, the responses of vasopressin and oxytocin were significantly greater, and those of renin and norepinephrine were markedly potentiated in the ADRX group. Heart rate recovered faster in the ADRX group and was elevated, compared to the sham value, for most of the 5-h period. Restitution of blood volume was attenuated in the ADRX group, although the restitution of plasma protein was not different between the groups. A significant difference in the change in plasma osmolality between groups after hemorrhage may account for the attenuated restitution of blood volume. After an overnight fast, which reduced blood volume in both groups of rats, the plasma renin concentration rose still further in ADRX rats; the differences in other measured variables observed between fed ADRX and sham groups remained the same. The insulin-induced 50% decrease in glucose caused minor effects on arterial blood pressure and heart rate and occasioned responses in renin and norepinephrine of similar magnitudes in the two groups. We conclude that in the absence of the adrenals, rats restore arterial pressure after hemorrhage remarkably well through potentiation of the responses of other vasoactive neural and hormonal systems. In these studies the marked potentiation of the renin response suggests that the renin-angiotensin system may be important in the maintenance of arterial blood pressure after reductions in blood volume.

Adrenalectomy↗

PubMed1988

Long-term recording of cerebrospinal fluid pressure in freely behaving rats.

Literature values for 'normal', 'control', 'resting' or 'baseline' cerebrospinal fluid pressure (CSF-p) of rats reveal a large variability. Anesthesia, restraint, brief recordings at variable times from various sites and simultaneous infusions into the recording cannula may partly explain the variability. Here, we report values of continuous, day/night CSF-p recordings from a lateral ventricle in conscious, relatively unrestrained and freely behaving rats. The mean (+/- S.E.M.) daytime/nighttime values were 11.4 +/- 2.0 and 14.9 +/- 2.3 cm H2O, respectively (P less than 0.05). Minimum, but not maximum CSF-p's during the day were lower (P less than 0.05) than at night. The results provide a normative data base for studies designed to evaluate experimental or pathological phenomena affecting CSF-p.

Animals↗

PubMed1988

Effect of vasopressin blockade on blood pressure during water deprivation in intact and baroreceptor-denervated conscious dogs.

Previous studies have provided evidence that vasopressin plays an important role in blood pressure regulation during water deprivation. However, these investigations have been complicated by reflex compensatory increases in cardiac output and renin secretion. The aim of the present study was to investigate the effect of blockade of the vasoconstrictor action of vasopressin in conscious water-deprived dogs in which the low- and/or high-pressure baroreceptors were denervated to minimize reflex responses. Vasopressin blockade in sham-operated dogs (n = 7) did not change arterial pressure. Heart rate rose from 78 +/- 9 to 119 +/- 13 beats/min (P less than 0.01), and plasma renin activity increased from 10.9 +/- 2.1 to 21.6 +/- 4.6 ng.ml-1.3 h-1 (P less than 0.01). In carotid sinus-denervated dogs (n = 6), vasopressin blockade again failed to decrease arterial pressure. Heart rate increased from 105 +/- 10 to 132 +/- 10 beats/min (P less than 0.01), and plasma renin activity rose from 6.8 +/- 1.7 to 15.5 +/- 2.4 ng.ml-1.3 h-1 (P less than 0.01). The antagonist also failed to change blood pressure in cardiac-denervated dogs (n = 5). Heart rate increased from 111 +/- 9 to 119 +/- 1 beats/min (P less than 0.01), but plasma renin activity did not increase significantly. In marked contrast, vasopressin blockade in sinoaortic/cardiac-denervated dogs (n = 7) promptly decreased arterial pressure from 115 +/- 8 to 94 +/- 7 mmHg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Effects of CRF and ANG II on ACTH and vasopressin release in conscious dogs.

The aim of the present study was to examine the effects of corticotropin-releasing factor (CRF) in conscious dogs and to determine whether the stimulation of adrenocorticotropic hormone (ACTH) release by angiotensin II (ANG II) results from potentiation of the action of CRF. In addition, the possible role of CRF in the stimulation of vasopressin released by ANG II was investigated. The following experiments were performed: 1) intravenous saline infusion; 2) ANG II (10 ng.kg-1.min-1) alone; 3) vasopressin (1 ng.kg-1.min-1) alone; 4) CRF (0.001, 0.01, or 0.1 microgram/kg iv) bolus; 5) vasopressin (1 ng.kg-1.min-1) and CRF (0.1 microgram/kg) together; 6) CRF (0.001, 0.01, or 0.1 microgram/kg) and ANG II (10 ng.kg-1.min-1) together; 7) ANG II (10 ng.kg-1.min-1) followed 15 min later with CRF (0.001, 0.01, or 0.1 microgram/kg). Each dose of CRF was tested on a different day. Infusion of ANG II alone stimulated the release of ACTH, cortisol, and vasopressin. Administration of CRF produced dose-dependent increases in plasma ACTH and cortisol concentrations, and the highest dose of CRF increased plasma vasopressin concentration. CRF given together with ANG II did not potentiate the stimulation of ACTH release by CRF. Vasopressin at the dose tested did not stimulate ACTH release but potentiated the ACTH response to CRF. ANG II stimulated vasopressin release but did not potentiate the AVP response to CRF. These results show that, in conscious dogs, ANG II and CRF each increase plasma ACTH concentration and that the ACTH response to CRF is potentiated by vasopressin but not by ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1988

Intravenous vasopressin infusion decreases plasma ACTH concentration in conscious dogs.

Vasopressin infusion increases arterial and atrial pressures, which could stimulate arterial and cardiac baroreceptors to inhibit adrenocorticotropin (ACTH) secretion. Therefore, the current experiments were performed to test the hypothesis that vasopressin infusion decreases plasma ACTH concentration in conscious dogs. Vasopressin was infused for 90 min in three doses (0.5, 1.0, and 2.0 ng.kg-1.min-1) that produced increases in plasma levels within the physiological range. Only the highest dose of vasopressin increased mean arterial pressure, but left atrial pressure increased with all doses, and right atrial pressure increased with the two highest doses. A bradycardia was produced with all doses of vasopressin. Plasma ACTH concentration decreased from 44 +/- 12 to 25 +/- 7 (P less than 0.01), from 50 +/- 11 to 26 +/- 9 (P less than 0.001), and from 70 +/- 15 to 28 +/- 4 pg/ml (P less than 0.001) with infusion of 0.5, 1.0, and 2.0 ng.kg-1.min-1 vasopressin, respectively. In contrast, plasma cortisol concentration first increased (P less than 0.05) with each vasopressin dose, but after 15-30 min it decreased back to control levels. These results demonstrate that intravenous infusion of vasopressin decreases plasma ACTH concentration. Because the inhibition is associated with increases in atrial pressure and decreases in heart rate, it may be mediated via activation of the baroreceptor reflex.

Adrenocorticotropic Hormone↗

PubMed1988

Regional cerebral glucose utilization during vasopressin-induced barrel rotations or bicuculline-induced seizures in rats.

Regional cerebral metabolic rates of glucose (rCMRglu) were measured in conscious rats grouped according to three treatments: control, bicuculline (5.5 mg/kg s.c.), and intracerebroventricular arginine vasopressin (0.5 micrograms/5 microliter). Rats in the latter group were pre-exposed to the peptide 48 h earlier to render them 100% susceptible to a motor output termed barrel rotation (BR). Marked increases in rCMRglu occurred in all brain areas investigated after bicuculline. Increases after intracerebroventricular arginine vasopressin were smaller and occurred in fewer brain areas. Opposite to bicuculline, arginine vasopressin reduced rCMRglu in hippocampus and auditory cortex. The data confirm marked stimulation of rCMRglu during bicuculline-induced seizures and provide initial data for an endogenous peptide that causes BR. Generalized seizures and BR may share some neural substrates, but they produce distinct changes in rCMRglu. The rCMRglu changes are compatible with the interpretation that BR is initiated by brainstem/cerebellar areas that process visual-vestibular information, with subsequent involvement of higher brain structures.

Animals↗

PubMed1988

Functional response of healthy and diseased glomeruli to a large, protein-rich meal.

Differential solute clearances and hormone assays were used to characterize the effect of a large, protein-rich meal (1.5 g/kg) on glomerular function in 12 healthy volunteers (group I) and 12 patients with chronic glomerular disease (group II). Changes from baseline during 3 h after the meal included an elevation of plasma osmolality, progressive urinary concentration, and increasingly positive fluid balance. Plasma renin activity and arginine vasopressin levels (measured in group II only) increased significantly. Nevertheless, the rate of peak postmeal renal plasma flow became elevated by 13 and 33% in groups I and II, respectively. Corresponding peak increases in postmeal glomerular filtration rate exceeded baseline by 10 and 16%. In the proteinuric subjects of group II the fractional clearances of albumin, IgG and uncharged dextrans in the radius interval 36-54 A, declined significantly after the meal. A similar depression of the fractional dextran-clearance profile was observed also in group I. Applying the fractional clearances of relatively permeant dextrans (radii less than or equal to 44 A) to a model of hindered solute transport through an isoporous membrane, we estimate that transmembrane hydraulic pressure difference increased by 12% in group I and by between 0 to 12% in group II after protein ingestion. We conclude (i) that oral protein ingestion increases glomerular ultrafiltration pressure and rate in both normal and diseased glomeruli, (ii) that this hemodynamic response may be mediated in part by the glomerulopressor hormones angiotensin II and arginine vasopressin, and (iii) that the foregoing hemodynamic changes exert no acute adverse effect on glomerular barrier size-selectivity.

Adult↗

PubMed1988

Effect of baroreceptor denervation on the inhibition of renin release by vasopressin.

Previous studies have suggested that the inhibition of renin secretion by acute administration of vasopressin in conscious dogs results from a reflex reduction in renal nerve activity. In the present investigation, this hypothesis was tested by studying the effect of total baroreceptor denervation or selective low pressure baroreceptor denervation on the suppression of PRA by vasopressin in conscious, chronically prepared dogs. In eight sham-operated dogs, a 45-min infusion of vasopressin (2.0 ng/kg.min, iv) decreased PRA from 10.5 +/- 1.9 to 5.9 +/- 1.0 ng/ml.3 h (P less than 0.01). Mean arterial pressure did not change (110 +/- 10 to 107 +/- 7 mm Hg), but heart rate decreased from 84 +/- 9 to 69 +/- 8 beats/min (P less than 0.05). In contrast, vasopressin infusion failed to significantly decrease PRA in seven sinoaortic/cardiac denervated dogs (9.5 +/- 1.7 to 7.4 +/- 2.0 ng/ml.3 h), although decreases did occur in three of the dogs. Mean arterial pressure increased from 104 +/- 5 to 125 +/- 6 mm Hg (P less than 0.01), but heart rate did not change (112 +/- 4 to 107 +/- 5 beats/min). When renal perfusion pressure was maintained at the preinfusion level in three sinoaortic/cardiac denervated dogs, vasopressin infusion failed to decrease PRA (2.3 +/- 0.6 to 2.4 +/- 0.6 ng/ml.3 h). In six cardiac denervated dogs, vasopressin infusion decreased PRA from 5.3 to 0.9 to 3.1 +/- 0.7 ng/ml.3 h (P less than 0.01). Results obtained with two lower doses of vasopressin (0.5 and 1.0 ng/kg.min) were generally similar to the responses observed during infusion at 2.0 ng/kg.min. Angiotensin II (5.0 ng/kg.min) suppressed PRA in all groups of dogs. These experiments demonstrate that the inhibition of renin secretion by acute administration of vasopressin in conscious dogs is prevented by total baroreceptor denervation, but not by denervation of the low pressure baroreceptors alone. These results suggest that the suppression of renin release by vasopressin is a reflex response resulting from activation of the high pressure baroreceptors.

Angiotensin II↗

PubMed1988

Effect of longitudinal physical training and water immersion on orthostatic tolerance in men.

To test the hypothesis that moderately intense physical training has no effect on orthostasis, orthostatic and fluid-electrolyte-endocrine responses to 60 degrees head-up tilt were compared before and after 6 h of water immersion (34.5 +/- 0.1 degrees C) up to the neck following 6 months of exercise training. During the tilt test the five male subjects (27-42 years) each wore a lower-body positive-pressure suit (MAST-111A antishock trousers). The tilt procedure consisted of a 40-min supine control period (suit deflated), followed by a maximum 90-min tilt period (suit inflated to 50 +/- 5 mm Hg for 30 min, then deflated for 60 min or until presyncope). The mean +/- S.E. pretraining cycle ergometer peak VO2 was 3.20 +/- 0.14 L.min-1 (39 +/- 2 ml.min-1.kg-1), 3.36 +/- 0.27 L.min-1 (42 +/- 4 ml.min-1.kg-1) after 3 months (N.S.), and increased by 18% to 3.78 +/- 0.36 L.min-1 (48 +/- 5 ml.min-1.kg-1, +22%, p less than 0.05) posttraining. During pretraining, water immersion tilt tolerance decreased from 74 +/- 16 min before to 34 +/- 9 min (delta = 40 min, p less than 0.05) after immersion. During posttraining, water immersion tilt tolerance decreased similarly from 74 +/- 16 min preimmersion to 44 +/- 13 min (delta = 30 min, p less than 0.05) postimmersion (74 vs. 74 min, N.S.; 34 vs. 44 min, N.S.).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Site-dependent central effects of aldosterone in rats.

A relationship between the subcommissural organ (SCO) and the adrenal glands has long been suspected. This report provides further information about the effects of a continuous D-aldosterone infusion into the SCO area of conscious, adult male Sprague-Dawley rats. A 6-day aldosterone infusion (5 ng/h) increased urinary sodium excretion, decreased adrenal medullary cross-sectional area, elevated adrenal corticosterone content and terminal plasma epinephrine concentration. Mineralocorticoid infusions directly into a lateral cerebral ventricle did not affect these parameters but, unlike SCO area infusions, decreased consummatory behavior. Infusions of tritiated aldosterone into the SCO area revealed that radioactivity was mainly confined to dorsomedial portions of the brain near the SCO, whereas the pineal body contained only background radioactivity. The data support the concept that the SCO area interacts with physiological systems related to both the adrenal cortex and medulla.

Adrenal Glands↗

PubMed1987

Increased synthesis and release of atrial peptide during DOCA escape in conscious dogs.

The escape from the sodium-retaining effects of prolonged mineralocorticoid treatment in animals and humans was first noted over 40 yr ago, but despite intense study the mechanisms responsible for the escape phenomenon have not been identified. Putative "natriuretic hormones" have been proposed to account for the escape phenomenon. To determine whether atrial natriuretic peptides (ANP) could participate in the escape phenomenon, the mineralocorticoid deoxycorticosterone acetate (DOCA) was administered to conscious dogs for 14 days. Escape was accompanied by a doubling of plasma ANP concentration and four- to sevenfold increases in cardiac ANP messenger RNA. There were also significant increases in mean arterial blood pressure during the last 8 days of DOCA treatment. Thus increases in the synthesis and secretion of ANP and increases in atrial pressure may represent mechanisms that contribute to the escape from mineralocorticoid-induced sodium retention.

Animals↗

PubMed1987

Regulation of drinking and vasopressin secretion: role of organum vasculosum laminae terminalis.

We have proposed that the organum vasculosum laminae terminalis (OVLT) contains osmoreceptors involved in the regulation of drinking and secretion of arginine vasopressin (AVP) in the dog. By use of the technique of electrolytic ablation, conscious dogs were evaluated for their responses to acute peripheral challenges of hypertonic NaCl and angiotensin II (ANG II) and hemorrhage (20 ml/kg) before and after destruction of the OVLT (n = 7) or adjacent tissue (n = 9) as a control. Lesions confined to the tip of the optic recess and destroying greater than 90% of the OVLT caused a dramatic increase in the threshold to drink and increase plasma AVP levels and a significant (P less than 0.01) reduction in the magnitude of these responses to an osmotic stimulus. Drinking and secretion of AVP in response to ANG II, but not the rise in peripheral corticosteroids, were also blocked (P less than 0.01) by ablation of the OVLT. In contrast responses to hemorrhage were not affected by the lesion. These results support the hypothesis that the OVLT contains osmoreceptors involved in physiological responses to cellular dehydration and suggest involvement in drinking and secretion of AVP in response to ANG II. The results also indicate that forebrain mechanisms which depend on the OVLT are independent of mechanisms responding to hemorrhage in conscious dogs.

Animals↗

PubMed1987

Drinking, oropharyngeal signals, and inhibition of vasopressin secretion in dogs.

Ingestion of water leads to a rapid fall in plasma levels of vasopressin in 24-h water-deprived dogs. The rapid inhibition of vasopressin secretion is not due to absorption of water and dilution of plasma nor is it due to gastric distension. Blood pressure rises sharply during drinking, and this may provide the afferent signal leading to inhibition of vasopressin secretion. Other possibilities include a generalized increase in oropharyngeal motor activity or simply the sight of water. To test these hypotheses, 24-h water-deprived dogs were given either phenylephrine, to mimic the rise in blood pressure observed during drinking, offered canned meat, to induce oropharyngeal motor activity and swallowing, or presented with a bowl of water that was placed just out of reach. Administration of phenylephrine, ingestion of food, and the presence of water all caused increases in blood pressure, which were similar to the rise in blood pressure during drinking. However, none of these paradigms caused a fall in plasma vasopressin. In contrast, ingestion of water consistently led to a significant fall in plasma vasopressin, which was detectable within 3 min of drinking and well before changes in plasma osmolality. Therefore we conclude that the mechanism by which ingestion of water causes rapid inhibition of vasopressin secretion in dehydrated dogs cannot be dependent on a rise in blood pressure, a nonspecific increase in oropharyngeal motor activity, or the presence of water.

Animals↗

PubMed1987

Effects of fentanyl on vasopressin secretion in human subjects.

To test the influence of an opioid on vasopressin (AVP) secretion, plasma AVP concentration was measured in five semirecumbent unmedicated volunteers before and during two continuous i.v. infusions of fentanyl. Infusion rates were adjusted to produce steady-state plasma fentanyl concentrations of 2.0 +/- 0.4 and 4.1 +/- 0.6 ng/ml; mild to moderate hypercarbia was induced during the control and infusion periods. Fentanyl increased plasma AVP concentration in a dose-dependent manner to 559 +/- 215 and 929 +/- 199% of the basal level of 1.9 +/- 0.7 pg/ml. Neither mild hypercarbia (PCO2 = 50 +/- 1 mm Hg) in the absence of fentanyl nor moderate hypercarbia (PCO2 = 66 +/- 3 mm Hg) in the presence of fentanyl changed plasma AVP concentration. Neither fentanyl nor hypercarbia, nor the combination of the two, altered plasma renin activity.

Adult↗

PubMed1987

Vasopressin and motion sickness in cats.

Levels of arginine vasopressin (AVP) in blood plasma and cerebrospinal fluid (CSF) were measured in cats under several motion-sickness-inducing conditions. Plasma AVP increased significantly in both susceptible and resistant animals exposed to motion. When vomiting occurred, levels of plasma AVP were dramatically elevated (up to 27 times resting levels). There was no difference in resting levels of AVP of susceptible and resistant cats. Levels of CSF-AVP were not elevated immediately after vomiting, but the resting levels of CSF-AVP were lower in animals that vomited during motion than in those animals which did not vomit during motion. The results of these experiments show that changes in systemic AVP are directly related to vomiting induced by motion, however, CSF-AVP apparently does not change in association with vomiting. CSF-AVP does appear to be lower in animals that reach frank vomiting during motion stimulation than in animals which do not vomit.

Acceleration↗