Biomedical subjects

L C Keil

Publications and source records attributed to L C Keil.

At least 55 records · Page 3Linked to original sources

PubMed1991

Mechanism of drinking-induced inhibition of vasopressin secretion in dehydrated dogs.

Ingestion of water stimulates a powerful inhibitory input to secretion of arginine vasopressin (AVP) in many species. A previous study in dogs has suggested that the stimulus arises from activation of oropharyngeal receptors, but the nature of the stimulus is unknown. The objectives of this study were to determine if the taste, osmolality, or temperature of the solution ingested constituted an important element in the inhibitory mechanism and if these same attributes affected the volume ingested in response to 24 h of water deprivation in conscious dogs. Experiments consisted of a control period, a 6-min period of access to fluid, and a 60-min period after drinking, with blood samples taken frequently to assess changes in plasma AVP. Dogs were placed in a sling that allowed them to stand or lie supported with easy access to a bowl. The solutions were water at 20 and 38 degrees C; 0.9% NaCl at 20 and 38 degrees C; 1.8 and 2.7% NaCl at 20 degrees C; 5% glucose and mannitol and 10% mannitol at 20 degrees C; and liquified food at 20 degrees C. In the time-control experiment dogs were allowed to see but not drink water for 6 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effect of head-up tilt on vasopressin secretion and arterial pressure in anesthetized rats.

The effect of 45 or 60 degrees head-up tilt on plasma arginine vasopressin (AVP) concentration, mean arterial pressure, and heart rate was studied in inactin-anesthetized rats. In all rats, there was a fall in blood pressure that was maximal within about 20-40 s and then returned toward normal. After 45 degrees head-up tilt for 30 min, AVP was increased from 7.0 +/- 1.7 to 21.0 +/- 5.9 pg/ml. Sixty-degree head-up tilt increased AVP at 5, 15, and 30 min, respectively, from 10.6 +/- 2.9 to 22.1 +/- 4.8 pg/ml, from 10.6 +/- 2.5 to 28.5 +/- 5.3, and from 16.1 +/- 4.7 to 62.6 +/- 10.3 pg/ml. After bilateral cervical vagotomy, 60 degrees head-up tilt for 30 min increased AVP, but the change was significantly reduced compared to intact animals. Bilateral sinoaortic denervation increased basal values of AVP, and there was no further increase during tilt. Bilateral electrolytic lesions of the hypothalamic paraventricular nuclei caused only a moderate reduction in the AVP response to tilt. When the effect of endogenous angiotensin II was antagonized by saralasin or its production was blocked by enalapril, the AVP response to tilt was reduced. The mean arterial pressure fell during the 1st min, but recovered rapidly when rats treated with a V1 vasopressin receptor antagonist were tilted. The data indicate that head-up tilt increases AVP secretion in anesthetized rats, that the response is mediated by the vagus and particularly by the arterial baroreceptors, and that circulating angiotensin II contributes to the response. However, the increased circulating AVP is not necessary for the maintenance of arterial pressure.

Anesthesia↗

PubMed1991

Cerebrospinal fluid pressure of conscious rats after venous constriction at the right atrium.

Thoracic shifts of blood stimulate diuresis and natriuresis during spaceflight. The available literature is not conclusive as to whether thoracic afferent neurons are essential for this response. Possibly, an acute elevation in cerebrospinal fluid pressure (CSF-p) activates central compensatory mechanisms. This is because central venous pressure is elevated by thoracic blood shifts and may reduce the pressure gradient for drainage of CSF into the venous sinuses. We tested whether rats with constriction of the venous return at the level of the heart (0.4 mm maximum diameter) had CSF-p different from sham-operated controls. CSF-p in the immediate postoperative period, as well as 1 and 10 days after surgery, were within normal limits and did not differ (p greater than 0.05). Blood collected at the end of the experiment showed no group differences (p greater than 0.05) in the hematocrit, or concentrations of sodium, potassium or vasopressin. Thus, changes in CSF-p, per se, appear to be insufficient to explain the cardiovascular or salt/water balance readjustments observed in spaceflight. It is likely that compensatory systems are highly redundant.

Animals↗

PubMed1991

Role of endogenous angiotensin II in the control of vasopressin secretion during hypovolemia and hypotension in conscious rabbits.

In order to investigate the physiological role of angiotensin II (ANG II) in the control of vasopressin (VP) secretion, the VP responses to hypotension induced by hemorrhage (20 ml/kg, n = 10) or nitroprusside infusion (1-10 micrograms/kg.min, n = 9) were studied with or without blockade of ANG II formation by the converting enzyme inhibitor captopril in conscious rabbits. Administration of captopril (5 mg/kg, iv) caused a small decrease in mean arterial pressure but did not enhance the hypotensive response to subsequent hemorrhage or nitroprusside infusion. The renin response to both stimuli was enhanced by captopril, whereas the increase in plasma ANG II concentration was attenuated. Plasma VP (PAVP) concentration increased during hemorrhage (2.0 +/- 0.2-113.6 +/- 47.7 pg/ml, P less than 0.01) and nitroprusside infusion (2.1 +/- 0.3-5.1 +/- 1.0 pg/ml, P less than 0.01). Captopril did not change basal plasma PAVP, nor did it attenuate the VP responses to hemorrhage or nitroprusside. Indeed, captopril tended to enhance the VP responses to hemorrhage (2.3 +/- 0.3-147.1 +/- 65.9 pg/ml) and nitroprusside infusion (1.9 +/- 0.2-15.4 +/- 6.0 pg/ml). The relationship between log PAVP and mean arterial pressure during hemorrhage and nitroprusside infusion in the presence of captopril was not different than in the absence of captopril. These results indicate that in conscious rabbits, the renin-angiotensin system does not contribute to the increase in VP secretion during hypotension induced by hemorrhage or nitroprusside infusion.

Angiotensin II↗

PubMed1991

Cerebrospinal fluid pressure in conscious head-down tilted rats.

Cerebrospinal fluid pressure (PCSF) was continuously measured in conscious male Sprague-Dawley rats gently restrained by a cotton towel. PCSF, evaluated in 15-min time blocks over a 3-h experiment, increased slightly (p less than 0.05) during the first 30 min of a control hour at 0 degree. There was a transient increase for about 5 min immediately after tilt (-45 degrees) that may have been due to head movement after the position change. However, PCSF was statistically unchanged (p greater than 0.05) during the 2nd (-45 degrees) hour and the 3rd (0 degree) recovery hour. The data show that the dynamics of intracranial pressure regulation can accommodate the acute cephalad fluid shift after tilting.

Animals↗

PubMed1991

Role of afferent renal nerves in the control of vasopressin secretion.

Several lines of evidence indicate that the kidneys can influence the secretion of vasopressin. We have reported that electrical stimulation of the renal nerves increases plasma vasopressin concentration in dogs and rabbits, and other investigators have reported that selective stimulation of afferent renal nerves in cats and rats increases plasma vasopressin concentration or the activity of neurosecretory neurons in the supraoptic nucleus. Intrarenal infusion of bradykinin, which is known to excite afferent renal nerves, has also been reported to increase the activity of putative vasopressin neurons in the supraoptic nucleus of rats. Recently, we observed that intrarenal infusion of bradykinin in rabbits increases plasma vasopressin concentration, and that this response is markedly reduced by renal denervation. We have also reported that activation of renal mechanoreceptors by elevating intrarenal pressure increases plasma vasopressin concentration in rabbits, and that this response is blocked by renal denervation. In order to determine if the kidneys participate in the physiological regulation of vasopressin release, we investigated the effect of renal denervation on the osmotic and non-osmotic control of vasopressin secretion in conscious, chronically-prepared rabbits. We found that renal denervation did not significantly reduce the vasopressin responses to hypertonic saline infusion, 24-hour water deprivation, hemorrhage or nitroprusside infusion. In summary, these observations indicate that the kidneys can influence the secretion of vasopressin via the afferent renal nerves. However, the physiological significance of the observations remains to be determined.

Animals↗

PubMed1990

Haemodynamic and ADH responses to central blood volume shifts in cardiac-denervated humans.

Haemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in 10 cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6 degrees head-down tilt (HDT) followed by 30 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15 and 30 min of HDT, and 5, 15 and 30 min of seated recovery. Blood samples were analysed for haematocrit, plasma osmolality, plasma renin activity (PRA) and ADH. Resting plasma volume (PV) was measured by Evans blue dye and per cent changes in PV during posture changes were calculated from changes in haematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. In the cardiac transplant subjects, mean HR decreased (BP less than 0.05) from 102 b.p.m. pre-HDT to 94 b.p.m. during HDT and returned to 101 b.p.m. in seated recovery while BP was slightly elevated (P less than 0.05). PV was increased by 6.3% (P less than 0.05) by the end of 30 min of HDT but returned to pre-HDT levels following seated recovery. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P less than 0.05) from 90 +/- 5 ml pre-HDT to 105 +/- 4 ml during HDT and returned to 88 +/- 5 ml in seated recovery. Plasma ADH was reduced by 28% (P less than 0.05) by the end of HDT and returned to pre-HDT levels with seated recovery. PRA was also reduced by 28% (P less than 0.05) with HDT. These responses were similar to those of six normal cardiac-innervated control subjects and one heart-lung recipient. Therefore, cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man.

Adult↗

PubMed1990

Intracranial hypertension after cerebroventricular infusions in conscious rats.

Cerebrospinal fluid (CSF) pressure (PCSF) was recorded in conscious, relatively unrestrained, and freely behaving rats during a 24-h infusion of artificial CSF (25% synthesis rate) into one lateral ventricle or divided equally into both lateral ventricles. Fourier analysis of PCSF of uninfused rats showed a circadian rhythm; nighttime PCSF was higher (P less than 0.01) than daytime. Unilateral and bilateral infusions did not affect PCSF during the first 2 h, but it then increased in an exponential manner, doubling (P less than 0.01) in both groups by 4 h. The induced intracranial hypertension stabilized at 4 h in unilaterally infused rats, but the PCSF increased further in the bilateral group, so that the overall pressure for 24 h was higher (P less than 0.01. No symptoms emerged in uninfused or unilateral infused rats after 24 h, however, 5 of 13 bilaterally infused rats displayed neurological symptoms (P = 2.4%). These low-volume, long-term infusions may be a model of intracranial hypertension. One explanation for the PCSF increase is that artificial CSF diluted neurochemical control systems beyond autoregulatory capacity. This hypothesis accommodates the exacerbated PCSF rise in bilaterally infused rats, since the same volume bathed a larger ependymal-choroidal surface area.

Animals↗

PubMed1990

Effects of baroreceptor denervation on endocrine and drinking responses to caval constriction in dogs.

Plasma arginine vasopressin (AVP), plasma renin activity (PRA), and water intake (H2OIN) are increased by thoracic inferior vena caval constriction (TIVCC). To assess the role of the cardiac and sinoaortic baroreceptors in these responses, 9 sham-, 10 cardiac-(CD), 6 sinoaortic-(SAD), and 4 combined cardiac and sinoaortic-(CD + SAD) denervated conscious dogs were studied. All animals were studied while normally hydrated 1) with no access to water (H2O-) and 2) while drinking was permitted (H2O+). TIVCC caused similar reductions (P less than 0.001) of mean arterial (-32 +/- 4 mmHg), left atrial pressure (-6.5 +/- 1.1 cmH2O), and right atrial pressure (-4.2 +/- 0.8 cmH2O) in all groups. After TIVCC in sham dogs with H2O-, AVP increased from 3.6 +/- 0.7 to 72.8 +/- 12.6 pg/ml (P less than 0.001). AVP was similar with SAD (57.1 +/- 6.9) but was reduced with CD (30.9 +/- 3.0) and CD + SAD (17.7 +/- 4.0). In all groups, PRA increased from 4.5 +/- 0.7 to 23.8 +/- 3.0 ng.ml-1 x 3 h-1 and plasma angiotensin II (ANG II) increased from 14.0 +/- 2.8 to 59.5 +/- 13.0 pg/ml (P less than 0.001). Plasma adrenocorticotropic hormone (ACTH) increased similarly in all groups (55 +/- 5 to 128 +/- 25 pg/ml). Plasma norepinephrine (NE) levels increased similarly in all groups (298 +/- 61 to 654 +/- 88 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1990

Role of renal nerves in regulation of vasopressin secretion and blood pressure in conscious rabbits.

The observation that electrical stimulation of the renal nerves increases vasopressin secretion raises the possibility that the renal nerves may participate in the control of vasopressin secretion. In the present investigation, the effects of renal denervation on the vasopressin response to two reflex stimuli (nitroprusside infusion and hemorrhage) and two osmotic stimuli (hypertonic saline infusion and water deprivation) were studied in conscious, chronically prepared rabbits. Nitroprusside infusion in 13 intact and 14 denervated rabbits caused similar decreases in mean arterial pressure (MAP) and the increase in plasma arginine vasopressin concentration (PAVP) in intact (2.6 +/- 0.3 to 5.8 +/- 0.9 pg/ml, P less than 0.01) and denervated (2.8 +/- 0.3 to 5.7 +/- 1.3 pg/ml, P less than 0.01) rabbits was not significantly different. Hemorrhage (20 ml/kg) in 15 intact and 14 denervated rabbits caused similar decreases in MAP. Again, the increase in PAVP from 2.7 +/- 0.3 to 159.0 +/- 37.1 pg/ml (P less than 0.01) in intact and from 5.0 +/- 1.7 to 115.4 +/- 45.6 pg/ml (P less than 0.01) in denervated rabbits was not significantly different, nor was the relationship between PAVP and MAP in the two groups. In seven intact rabbits, hypertonic saline infusion increased PAVP from 4.0 +/- 0.9 to 10.9 +/- 2.8 pg/ml (P less than 0.05). The change in six denervated rabbits was not significantly different, nor was the relationship between PAVP and plasma osmolality. During water deprivation (24 h) in six intact rabbits, PAVP increased from 4.0 +/- 0.7 to 6.9 +/- 0.6 pg/ml (P less than 0.05). Again, the increase in PAVP in six denervated rabbits was not significantly different from that in the intact rabbits. The change in MAP during water deprivation in the two groups was also not significantly different. Renal cortical norepinephrine concentration in denervated kidneys was less than 10 ng/g wet wt. These results indicate that, in conscious rabbits, renal denervation does not impair the osmotic or reflex regulation of vasopressin secretion, nor does it interfere with blood pressure regulation during hypovolemia or hypotension.

Animals↗

PubMed1990

Intrapericardial denervation: radial artery blood flow and heart rate responses to LBNP.

Eight rhesus monkeys were used to study responses of radial artery blood flow velocity (RABFV) and heart rate (HR) to low (0 to -20 mmHg) and high (0 to -60 mmHg) ramp exposures during supine lower body negative pressure (LBNP). These levels were chosen to separate peripheral vascular responses associated with stimulation of low- and high-pressure baroreceptors. Four monkeys had efferent and afferent cardiac denervation by use of the Randall procedure with pharmacological (phenylephrine and atropine) verification. Animals were studied 3 wk after surgery to avoid reinnervation. Findings were compared with those of four identically treated intact animals. Denervated animals showed no change in RABFV or HR during low-level LBNP; however, HR increased significantly (P less than 0.05) when LBNP reached -50 mmHg and blood flow velocity also fell (P less than 0.05) starting at -30 mmHg pressure. In contrast, intact animals showed steady decreases in RABFV during both high- and low-pressure protocols, with HR showing a 6-beat/min increase (P less than 0.05) starting at -20 mmHg pressure. As with denervated animals, intact animals showed a more pronounced increase in HR after reaching a level of -60 mmHg suction. Cardiac output (electromagnetic flowmeter, ascending aorta) fell significantly in both groups starting at -30 mmHg pressure. Left ventricular pressure (Konigsberg pressure cell) in three intact animals showed a progressive fall in systolic pressure starting at -10 mmHg suction, which became significant at -55 mmHg pressure. These results demonstrate that cardiac denervation by use of the Randall technique significantly affects RABFV and HR responses to LBNP in rhesus monkeys. The lack of RABFV change during LBNP in denervated animals suggests that these changes coupled with HR response can be used as an effective method to verify the completeness of denervation of low-pressure baroreceptors in animals that have undergone intrapericardial denervation.

Animals↗

PubMed1990

Corticosterone, but not glucose, treatment enables fasted adrenalectomized rats to survive moderate hemorrhage.

Fed adrenalectomized rats survive the stress of hemorrhage and hypovolemia, whereas fasted adrenalectomized rats become hypotensive and hypoglycemic after the first 90 min and die within 4 h. We have studied the effects of glucose and corticosterone (B) infusions after hemorrhage as well as treatment with B at the time of adrenalectomy on the capacity of chronically prepared, conscious, fasted, adrenalectomized rats to survive hemorrhage. We have also measured the magnitudes of vasoactive hormone responses to hemorrhage. Maintenance of plasma glucose concentrations did not sustain life; however, treatment of rats at the time of adrenalectomy with B allowed 100% survival, and acute treatment of adrenalectomized rats at the time of hemorrhage allowed about 50% survival during the 5-h posthemorrhage observation period. Rats in the acute B infusion group that died exhibited significantly increased plasma B and significantly decreased plasma glucose concentrations by 2 h compared to the rats that lived. Plasma vasopressin, renin, and norepinephrine responses to hemorrhage were markedly augmented in the adrenalectomized rats not treated with B, and plasma vasopressin concentrations were significantly elevated at 1 and 2 h in all of the rats that subsequently died compared to values in those that lived. We conclude that: 1) death after hemorrhage in fasted adrenalectomized rats is not a result of lack of glucose; 2) chronic and, to an extent, acute treatment of fasted adrenalectomized rats with B enables survival; 3) fasted adrenalectomized rats exhibit strong evidence of hepatic insufficiency which is not apparent in either fed adrenalectomized rats or B-treated fasted adrenalectomized rats; 4) death after hemorrhage in fasted adrenalectomized rats may result from hepatic failure as a consequence of marked splanchnic vasoconstriction mediated by the actions of extraordinarily high levels of vasoactive hormones after hemorrhage; and 5) B appears to act to decrease the magnitude of response of vasoactive hormones after hemorrhage in fasted adrenalectomized rats.

Adrenalectomy↗

PubMed1990

Effects of carotid occlusion and angiotensin II on vasopressin secretion in intact and vagotomized conscious rabbits.

Experiments were performed in conscious rabbits with sectioned aortic depressor nerves to determine whether there is an interaction between angiotensin II (Ang II) and the baroreceptor reflexes in the control of arginine vasopressin (AVP) secretion. Baroreceptor reflexes were activated by a 5- or 10-min period of bilateral carotid occlusion with or without background infusion of Ang II at 10 or 20 ng/kg.min. Carotid occlusion increased mean arterial pressure, right atrial pressure, and heart rate, but did not change plasma AVP (PAVP) concentration. Infusion of Ang II at 10 ng/kg.min increased PAVP from 4.0 +/- 0.9 to 6.3 +/- 1.8 pg/ml (P less than 0.05). Carotid occlusion during Ang II infusion produced the same cardiovascular changes as before Ang II, but still failed to increase PAVP. Because increased atrial pressure can inhibit AVP secretion, the experiments were repeated in acutely vagotomized rabbits. Vagotomy increased heart rate but did not change mean arterial pressure or PAVP. Carotid occlusion after vagotomy increased PAVP from 2.2 +/- 0.2 to 3.3 +/- 0.5 pg/ml (P less than 0.05). Ang II infusion again increased PAVP but did not enhance the AVP response to carotid occlusion (2.9 +/- 0.4 to 3.9 +/- 0.7 pg/ml). These results provide further evidence for a role of the carotid sinus baroreceptors and vagal afferents in the control of AVP secretion and demonstrate that Ang II stimulates AVP secretion in rabbits. However, they do not reveal any interaction between Ang II and the baroreceptor reflexes in the control of AVP secretion.

Angiotensin II↗

PubMed1989

Immunoreactive atrial natriuretic peptide in the retina of rats and rabbits.

Immunoreactive atrial natriuretic peptide (ANP) has been detected in retinal tissue by radioimmunoassay, although it is unclear whether it was in retinal cells or represented residual peptide from blood and/or ocular fluids. We report here, using the immunoperoxidase method and a highly specific anti-rat ANP, that the peptide was localized consistently in the outer and inner plexiform layers of retinas of rats and rabbits. This information raises important issues: what are the implications for retinal function and, since blood-borne radioligands do not reveal retinal 'receptors', what is the endogenous target of retinal ANP?

Animals↗

PubMed1989

Physiological responses to low dose infusions of atrial peptide in conscious dogs.

Mongrel dogs prepared with chronic catheters in their femoral artery and vein and urinary bladder received 60 minute infusions of atrial peptide ranging from 5 to 100 ng/kg/min. Infusion of atrial peptides caused dose dependent increases in plasma atrial peptide concentration with doses of 25 ng/kg/min or less increasing plasma concentrations to levels observed in normal animals during stimulation of endogenous atrial peptide secretion. Atrial peptide infusion at doses of 10 ng/kg/min and above caused significant decreases in mean arterial pressure which were not accompanied by statistically significant changes in heart rate. Atrial peptide infusion at doses of 25 ng/kg/min and above increased urinary sodium excretion and urine flow rate. Atrial peptide infusion was without effect on plasma vasopressin, ACTH and corticosterone concentrations. However, atrial peptide infusion resulted in dose dependent decreases in plasma aldosterone concentration and plasma renin activity, but the decreases were only significant with the high physiologic (25 ng/kg/min) and pharmacologic doses (50 & 100 ng/kg/min). These data show that atrial peptide infusions in conscious dogs have minimal effects when infused in small doses that mimic endogenous atrial peptide release. At higher doses, significant effects on the cardiovascular, renal and endocrine systems can be observed but their physiological significance is unclear.

Aldosterone↗

PubMed1989

Responses to acute hypoxemia in fetal sheep at 0.6-0.7 gestation.

A majority of previous studies of fetal responses to acute hypoxemia has focused on the response of the sheep fetus greater than 120 days of gestation when many regulatory systems have been established. To assess the response of younger, less well-developed fetuses, we exposed two groups of fetal sheep (I, 84-91 days; II, 97-99 days gestational age) to acute hypoxemia by giving the ewe a gas mixture containing 9% O2 to breathe. We decreased descending aortic PO2 in both groups of fetuses [I, 24 +/- 6 to 14 +/- 3 (SD) Torr; II, 23 +/- 3 to 12 +/- 4 Torr] by a degree similar to that achieved in previous studies of fetuses greater than 120 days of gestation. Mean arterial blood pressure (I, 31 +/- 6; II, 40 +/- 3 Torr) did not change significantly from control values, and heart rate (I, 224 +/- 27; II, 203 +/- 16 beats/min) increased significantly in group II fetuses with hypoxemia. In group I and II fetuses, as in older fetuses, cerebral, myocardial, and adrenal blood flows, measured by the microsphere technique, increased, and pulmonary blood flow decreased. These responses mature early and are likely local vascular responses to decreases in oxygen content. Combined ventricular output and umbilical-placental blood flow decreased significantly in both groups. Unlike the response of the fetus greater than 120 days, acute hypoxemia did not decrease blood flow to the musculoskeletal and cutaneous circulations (group I only), gastrointestinal, or renal circulations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Vascular responsiveness in adrenalectomized rats with corticosterone replacement.

To determine under resting, unstressed conditions the circulating glucocorticoid concentrations that best maintain sensitivity of the vascular smooth muscle and baroreceptor responses to vasoactive agents, rats with vascular cannulas were sham-adrenalectomized (sham) or adrenalectomized (ADRX) and provided with four levels of corticosterone replacement (approximately 100 mg fused pellets of corticosterone: cholesterol 0, 20, 40, and 80% implanted subcutaneously at the time of adrenal surgery). Changes in vascular and baroreflex responses were determined after intravenous injection of varying doses of phenylephrine and nitroglycerin with measurement of arterial blood pressure and heart rate in the conscious, chronically cannulated rats. Vascular sensitivity was decreased, and resting arterial blood pressure tended to be decreased in the adrenalectomized rats; both were restored to normal with levels of corticosterone (40%), which also maintained body weight gain, thymus weight, and plasma corticosteroid binding globulin concentrations at normal values. The baroreflex curve generated from the sham group was different from the curves generated from the ADRX+0, 20, and 40% groups, but not different from that of the ADRX+80% group, suggesting that the baroreflex is maintained by higher levels of corticosterone than are necessary for the maintenance of the other variables. These data demonstrate that physiological levels of corticosterone (40% pellet) restore vascular responsiveness, body weight, thymus weight, and transcortin levels to normal in ADRX rats, whereas higher levels (80% pellet) are necessary for restoration of the baroreflex.

Adrenalectomy↗

PubMed1989

Paraventricular stimulation with glutamate elicits bradycardia and pituitary responses.

The excitatory neurotransmitter, L-glutamate (0.5 M, pH 7.4), or the organic acid, acetate (0.5 M, pH 7.4), was microinjected (50 nl over 2 min) directly into the paraventricular nuclei (PVN) of pentobarbital sodium-anesthetized rats while arterial blood pressure and heart rate and plasma adrenocorticotropic hormone (ACTH), vasopressin, and oxytocin were measured. Activation of PVN neurons with L-glutamate led to increases in plasma ACTH, vasopressin, and oxytocin and a profound bradycardia (approximately 80 beats/min) with little change in arterial blood pressure. Microinjection of acetate had no effect on the above variables. The decrease in heart rate was shown to be dependent on the concentration of glutamate injected and the volume of injectate. The bradycardia was mediated through the autonomic nervous system because ganglionic blockade (pentolinium tartrate) eliminated the response; atropine and propranolol severely attenuated the bradycardia. The bradycardia was greatest when L-glutamate was microinjected into the caudal PVN. Injections into the rostral PVN or into nuclei surrounding the PVN led to small or nonsignificant decreases in heart rate. Focal electric stimulation (2-50 microA) of the PVN also led to decreases in heart rate and arterial blood pressure. These data suggest that activation of PVN neurons leads to the release of ACTH, vasopressin, and oxytocin from the pituitary and a bradycardia that is mediated by the autonomic nervous system.

Adrenocorticotropic Hormone↗