Search PubMed⌕ Search

Biomedical subjects

H Kannan

Publications and source records attributed to H Kannan.

At least 37 records · Page 2Linked to original sources

Effects of anesthetics on norepinephrine release in the hypothalamic paraventricular nucleus region of awake rats.

The effects of pentobarbital sodium, chloralose and urethane on norepinephrine (NE) release in the hypothalamic paraventricular nucleus (PVN) region were examined in awake rats. An in vivo microdialysis method was used. Extracellular NE concentrations in the PVN region were measured by high performance liquid chromatography with electrochemical detection. Pentobarbital sodium (30 mg/kg, intravenously [i.v.]) and chloralose (50 mg/kg, i.v.) caused a 30-40% decrease in NE release while urethane (800 mg/kg, i.v.) caused a 50% increase. Plasma NE concentration was not altered after pentobarbital sodium and chloralose administrations, except for its increase in chloralose at 5 h, while the concentration increased significantly (P < 0.01) after urethane. These results suggest that, in the rat, these anesthetic agents have different effects on noradrenergic activity in the PVN region as well as on plasma NE.

Anesthetics↗

Neurons in the posterior insular cortex are responsive to gustatory stimulation of the pharyngolarynx, baroreceptor and chemoreceptor stimulation, and tail pinch in rats.

Extracellular unit responses to gustatory stimulation of the pharyngolaryngeal region, baroreceptor and chemoreceptor stimulation, and tail pinch were recorded from the insular cortex of anesthetized and paralyzed rats. Of the 32 neurons identified, 28 responded to at least one of the nine stimuli used in the present study. Of the 32 neurons, 11 showed an excitatory response to tail pinch, 13 showed an inhibitory response, and the remaining eight had no response. Of the 32 neurons, eight responded to baroreceptor stimulation by an intravenous (i.v.) injection of methoxamine hydrochloride (Mex), four were excitatory and four were inhibitory. Thirteen neurons were excited and six neurons were inhibited by an arterial chemoreceptor stimulation by an i.v. injection of sodium cyanide (NaCN). Twenty-two neurons were responsive to at least one of the gustatory stimuli (deionized water, 1.0 M NaCl, 30 mM HCl, 30 mM quinine HCl, and 1.0 M sucrose); five to 11 excitatory neurons and three to seven inhibitory neurons for each stimulus. A large number of the neurons (25/32) received converging inputs from more than one stimulus among the nine stimuli used in the present study. Most neurons (23/32) received converging inputs from different modalities (gustatory, visceral, and tail pinch). The neurons responded were located in the insular cortex between 2.0 mm anterior and 0.2 mm posterior to the anterior edge of the joining of the anterior commissure (AC); the mean location was 1.2 mm (n=28) anterior to the AC. This indicates that most of the neurons identified in the present study seem to be located in the region posterior to the taste area and anterior to the visceral area in the insular cortex. These results indicate that the insular cortex neurons distributing between the taste area and the visceral area receive convergent inputs from gustatory, baroreceptor, chemoreceptor, and nociceptive organs.

Animals↗

Difference in water intake but not in renal sympathetic nerve activity in response to central salt-loading or angiotensin II in awake Dahl salt-sensitive and -resistant rats.

Experiments were conducted to examine whether renal sympathetic nerve activity (RSNA) and water intake in response to central salt-loading or angiotensin II (A II) differ between freely-moving Dahl salt-sensitive (DS) and -resistant (DR) rats maintained on a low-salt diet. Intracerebroventricular (i.c.v.) administration of hypertonic saline (0.3 M, 1 microl/min, 20 min) or A II (100 ng/1 microl) evoked water intake, pressor response and suppression of RSNA in both strains. The cumulative water intake in DS rats over a 60-min period after i.c.v. infusion of hypertonic saline or A II was significantly attenuated compared with that in DR rats. The RSNA response did not show a significant difference between the strains. These results demonstrate that water intake, but not RSNA response to acute central salt-loading or A II differ between awake DR and DS rats.

Angiotensin II↗

Central actions of adrenomedullin on cardiovascular parameters and sympathetic outflow in conscious rats.

Adrenomedullin (ADM) is reported to be a peripherally acting hypotensive peptide, but its central actions are unclear. We investigated the effects of centrally administered ADM on blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) in conscious rats and sinoaortic-denervated (SAD) rats. We also investigated the receptors interacting with ADM using two putative antagonists. Intracerebroventricular administration of ADM in doses of 0.1 and 0.5 nmol/kg caused tachycardia and early inhibition of RSNA. Central ADM (1.0 nmol/kg) induced hypertension, tachycardia, and a decrease followed by an increase in RSNA. In SAD rats, increases in BP, HR, and RSNA at the late phase were enhanced by central ADM (1.0 nmol/kg), whereas the early decrease in RSNA remained. Thus the inhibition of RSNA via central ADM may be unrelated to the arterial baroreceptor reflex. Pretreatment with antagonists human calcitonin gene-related peptide-(8-37) and human ADM-(22-52) significantly suppressed the central actions of ADM. The findings suggest that ADM is involved as a neuropeptide in the receptor-mediated central regulation of the cardiovascular system and RSNA.

Adrenomedullin↗

Responses of neurons in the insular cortex to gustatory, visceral, and nociceptive stimuli in rats.

Extracellular unit responses to baroreceptor and chemoreceptor stimulation, gustatory stimulation of the posterior tongue, electrical stimulation of the superior laryngeal (SL) nerve, and tail pinch were recorded from the insular cortex of anesthetized and paralyzed rats. Forty-three neurons identified responded to stimulation by at least one of the stimuli used in the present study. Of the 43 neurons, 33 responded to tail pinch, and the remaining 10 had no response; 18 showed an excitatory response, and 15 showed an inhibitory response. Of the 43 neurons, 35 responded to electrical stimulation of the SL nerve; 27 showed an excitatory response, and 8 showed an inhibitory response. Of the 20 neurons that responded to baroreceptor stimulation by an intravenous injection of methoxamine hydrochloride (Mex), 11 were excitatory and 9 were inhibitory. Twenty-seven neurons were responsive to an intravenous injection of sodium nitroprusside (SNP); 10 were excitatory and 17 were inhibitory. Ten neurons were excited and 16 neurons were inhibited by arterial chemoreceptor stimulation by an intravenous injection of sodium cyanide (NaCN). Twenty-six neurons were responsive to at least one of the gustatory stimuli (1.0 M NaCl, 30 mM HCl, 30 mM quinine HCl, and 1.0 M sucrose): four to six excitatory neurons and three to nine inhibitory neurons for each stimulus. A large number of the neurons (42/43) received convergent inputs from more than one stimulus among the nine stimuli used in the present study. Most neurons (38/43) were responsive to two or more stimulus groups when the natural stimuli used in the present study are grouped into three, gustatory, visceral, and nociceptive stimuli. The neurons recorded were located in the insular cortex between 2.8 mm anterior and 1.1 mm posterior to the anterior edge of the joining of the anterior commissure (AC); the mean location was 1.0 mm (n = 43) anterior to the AC. This indicates that most of the neurons identified in the present study were located in the region posterior to the taste area and anterior to the visceral area in the insular cortex. These results indicate that the insular cortex neurons distributing between the taste area and the visceral area receive convergent inputs from baroreceptor, chemoreceptor, gustatory, and nociceptive organs and may have roles in taste aversion or in regulation of visceral responses.

Afferent Pathways↗

Centrally administered parathyroid hormone (PTH)-related protein(1-34) but not PTH(1-34) stimulates arginine-vasopressin secretion and its messenger ribonucleic acid expression in supraoptic nucleus of the conscious rats.

It has been suggested that PTH-related protein (PTHrP) is an endogenous modulator of cardiovascular systems. We have reported that PTHrP(1-34), but not PTH(1-34), causes the release of arginine-vasopressin (AVP) from the supraoptic nucleus (SON) of the hypothalamus in vitro through a novel receptor distinct from the PTH/PTHrP receptors (type I or type II) described previously. In this study, we have investigated the in vivo effects of PTHrP(1-34) on AVP secretion and its, messenger RNA (mRNA) expression in the SON in conscious rats. Intracerebroventricular (i.c.v.) administration of PTHrP(1-34) resulted in an increase in plasma AVP concentration in a dose-dependent manner (0-400 pmol/rat). The maximal effect was obtained at 15 min after i.c.v. administration of PTHrP(1-34). Neither PTHrP(7-34) nor PTH(1-34) had any effect on plasma AVP levels. PTHrP(1-34)-induced AVP secretion was antagonized by pretreatment with PTHrP(7-34) but not by that with PTH(1-34). In addition, in situ hybridization study revealed that AVP mRNA expression in the SON and paraventricular nucleus was significantly increased 30 min after i.c.v. administration of PTHrP(1-34) and reached a maximum at 180 min. Furthermore, in Northern blot analyses, AVP mRNA expression in the SON was increased to approximately a 2-fold of basal level by PTHrP(1-34). On the other hand, neither PTHrP(7-34) or PTH(1-34) had any effect on the mRNA expression. The PTHrP(1-34)-stimulated AVP mRNA expression was eliminated by pretreatment with PTHrP(7-34) but not with PTH(1-34). These results suggest that, in the central nervous system, PTHrP(1-34) is involved in AVP secretion through a novel receptor distinct from the PTH/PTHrP receptors reported previously, playing a role in the body water and electrolyte homeostasis.

Animals↗

Convergence of afferent inputs from the chorda tympani, lingual-tonsillar and pharyngeal branches of the glossopharyngeal nerve, and superior laryngeal nerve on the neurons in the insular cortex in rats.

The responses of single neurons in the insular cortex to electrical stimulation of the chorda tympani (CT), lingual-tonsillar branch of the glossopharyngeal (LT-IXth) nerve, pharyngeal branch of the glossopharyngeal (PH-IXth) nerve, and superior laryngeal (SL) nerve were recorded in anaesthetized and paralyzed rats. Ninety-four neurons responding to stimulation of at least one of the four nerves were identified from the insular cortex. Most of the neurons were located in the posterior portion of the insular cortex; the mean location was 0.8 mm anterior to the anterior edge of the joining of the anterior commissure (AC) and was 1.4 mm dorsal to the rhinal fissure (RF). Of the 94 neurons, 84 (89%) received convergent inputs from two or more nerves, and the remaining 10 (11%) received inputs from one nerve. The neurons responding to the CT stimulation were distributed more anteriorly than those responding to other three nerves in the anterior-posterior dimension. Our results indicate that the neurons recorded mainly from the posterior portion of the insular cortex receive convergent inputs from the oropharyngolaryngeal regions.

Animals↗

Effects of area postrema lesion and abdominal vagotomy on interleukin-1 beta-induced norepinephrine release in the hypothalamic paraventricular nucleus region in the rat.

Peripherally administered interleukin-1 beta (IL-1 beta) has been shown to increase extracellular norepinephrine (NE) concentration in the paraventricular nucleus (PVN) of the hypothalamus. The present study was carried out using an in vivo microdialysis technique in conscious rats in order to examine the possible involvement of the area postrema (AP) and the abdominal vagal afferent nerves in this effect. Extracellular NE concentrations in the PVN region were measured by high performance liquid chromatography with electrochemical detection. In AP-lesioned or abdominal-vagotomized rats, the NE increase was significantly attenuated compared to that in sham-operated rats; this reduction was greater in abdominal-vagotomized rats than in AP-lesioned rats. The results suggest that the AP as well as the abdominal vagal afferent nerves is involved in intraperitoneal (i.p.) administered IL-1 beta-induced NE release in the PVN region.

Abdomen↗

Effects of systemic interleukin-1beta administration on daily drinking and renal excretory function in conscious rats.

To elucidate the roles of interleukin-1beta (IL-1beta), a cytokine with several diverse actions, in the control of body fluid balance, its effects on daily drinking behavior and renal excretory function were examined in conscious rats. Administration of IL-1beta (4 microg/kg, I.P.) resulted in the suppression of both daily drinking and food intake and a decrease in daily urinary sodium and potassium excretion, but had no effect on urine volume. The IL-1beta-induced decrease in sodium excretion was abolished in renal-denervated rats. Kainic acid was then injected into the anteroventral third ventricle region, including the organum vasculosum of the lamina terminalis, to examine whether neurons in this region are involved in the IL-1beta-induced responses; the effects on daily drinking and urinary sodium and potassium excretion were abolished, whereas the effects on food intake, although attenuated, were still present. In contrast, electrical lesion of the subfomical organ did not affect the IL-1beta-induced responses. Thus, IL-1beta seems exert its effects on body fluid balance at several distinct sites in the central nervous system.

Animals↗

Convergence of oropharyngolaryngeal, baroreceptor and chemoreceptor afferents onto insular cortex neurons in rats.

Forty-two neurons that responded to electrical stimulation of at least one of four nerves, the chorda tympani (CT), the lingual-tonsillar branch of the glossopharyngeal (LT-IXth) nerve, the pharyngeal branch of the glossopharyngeal (PH-IXth) nerve and the superior laryngeal (SL) nerve, were identified from the insular cortex by using glass microelectrodes in paralysed and anesthetized rats. Four, 42, 41 and 40 neurons responded to the CT, LT-IXth, PH-IXth and SL nerve stimulation respectively. Of these 42 neurons, most (37/42, 88.1%) responded to three nerves (the LT-IXth, PH-IXth and SL), two (4.8%) responded to two nerves and the remaining three (7.1%) responded to all four nerves. No neurons responded to one specific stimulus. The responsiveness of these 42 neurons to baroreceptor and chemoreceptor stimulation by an i.v. injection of three drugs was investigated. For baroreceptor stimulation, methoxamine hydrochloride (Mex) and sodium nitroprusside (SNP) were used; for chemoreceptor stimulation, sodium cyanide (NaCN) was used. Of the 42 neurons, 31 (73.8%) showed an excitatory or inhibitory response to baroreceptor and chemoreceptor stimulation with at least one of the three drugs, and the remaining 11 (26.2%) showed no response. Of these 31 baroreceptor and chemoreceptor-sensitive neurons, 19 (61.3%) responded to two or all three drugs, and the rest (12; 38.7%) responded to one. Most neurons recorded were distributed in the posterior insular cortex. These results indicate that the neurons in the posterior insular cortex receive convergent inputs from the oropharyngolaryngeal region, the baroreceptors and the chemoreceptors, suggesting that the posterior insular cortex may integrate various sensory information.

Animals↗

Fiber types of the lingual branch of the trigeminal nerve, chorda tympani, lingual-tonsillar and pharyngeal branches of the glossopharyngeal nerve, and superior laryngeal nerve and their relation to the cardiovascular responses in rats.

The effect of repetitive electrical stimulation at 50 Hz for 20 s of the lingual branch of the trigeminal nerve (LN), chorda tympani (CT), lingual-tonsillar (LT-IXth) and pharyngeal (PH-IXth) branches of the glossopharyngeal nerve, and superior laryngeal nerve (SLN) on the changes in arterial blood pressure (BP) and heart rate (HR) were investigated in anesthetized and paralyzed rats. The compound action potentials in these nerves were simultaneously recorded to know the relationships between the fiber types and the cardiovascular responses. In all nerves except the CT, repetitive electrical stimulation of the nerve elicited a tachycardia and an increase in BP. These cardiovascular responses were mainly related to the component-2 in the compound action potentials in respective nerves. The conduction velocities of the component-2 in the five nerves examined in the present experiment were between 9.5 and 17.0 m/s (mean, n = 4-7). Other components which have faster (component-1) or slower conduction velocities (component-3 and -4) than the component-2 were not likely to elicit the cardiovascular responses. These results suggest that nociceptive and taste fibers of A-delta fibers innervating the oral cavity and pharyngolaryngeal region largely contribute to the cardiovascular responses.

Animals↗

Biphasic changes in behavioral, endocrine, and sympathetic systems in adjuvant arthritis in Lewis rats.

Adjuvant arthritis (AA) is an experimental model for rheumatoid arthritis, and is induced most easily in inbred Lewis rats by an intradermal injection of heat-killed Mycobacterium tuberculosis (MT) in incomplete Freund's adjuvant. Susceptivity to the arthritis in Lewis rats is thought to be related to a defect in their responses of the hypothalamo-pituitary-adrenal (HPA) axis to the disease. Because the use of an inbred strain is necessary for our immunological studies, we examined in Lewis rats changes in behavior, the HPA axis, and sympathetic nerve activities during development of the adjuvant arthritis. Following intradermal injections of heat-killed MT in adjuvant, the arthritis began to develop on day 12, reaching its maximum severity on day 21, and remained at the level for over a month. The body temperature rose from day 0 to 5 (the primary phase--before the onset of the arthritis). It then fell to normal temperature, and again rose from day 10 to 21 (the secondary phase--with fully developed arthritis). The behavioral (physical activity, food, and water intake) and hormonal parameters [plasma adrenocorticotropic hormone (ACTH) and corticosterone levels] also changed in two phases, similar to those observed in the temperature responses. No change in plasma vasopressin level was observed. Sympathetic nerve activities, assessed by changes in plasma noradrenalin levels, increased more in the primary than in the secondary phase. The possible causes for the biphasic changes associated with development of arthritis are discussed.

Animals↗

Activation of sympathetic outflow by recombinant human interleukin-1 beta in conscious rats.

The present study was undertaken to determine the effects of interleukin-1 beta (IL-1 beta) on renal sympathetic nerve activity (RSNA), arterial blood pressure (AP), heart rate (HR), and body temperature in conscious rats. Either intravenous or intracerebroventricular administration of IL-1 beta elicited increases in AP, HR, and RSNA accompanied by a rise in body temperature. The maximum changes in AP, HR, and RSNA occurred 10-15 min after intravenous injection of IL-1 beta (100 ng) and 20-25 min after intracerebroventricular injection (5 ng). The responses induced by the intravenous and intracerebroventricular injections lasted for approximately 15-30 min and did not appear when the animals were pretreated with the cyclooxygenase inhibitor indomethacin (10 mg/kg iv). Moreover, intracerebroventricular injection of prostaglandin E2 (1 microgram) produced responses similar to those induced by IL-1 but with shorter latency. Plasma norepinephrine and adrenocorticotropic hormone concentrations were increased after IL-1 beta injection. The results suggested that IL-1 beta augments cardiovascular and sympathetic outflow through the central action of prostaglandin E2 in conscious rats.

Adrenocorticotropic Hormone↗

Does recurrent inhibition exist in the paraventricular magnocellular neurosecretory cells in the male rat?

Extracellular recordings were performed from the paraventricular (PVN) neurosecretory cells in the anesthetized male rats. After sub- and suprathreshold stimulations to the neural stalk, two of 38 neurons showed inhibitory phases and eleven of the remaining 36 neurons showed inhibitory responses after suprathreshold stimulations. These results indicate that the recurrent inhibitory system exists in the PVN.

Action Potentials↗

Inhibition of nitric oxide synthase attenuates osmotic thirst in the rat.

Changes in water intake after intraperitoneal injection of a nitric oxide synthase (NOS) inhibitor was studied in the rat. Administration of NW-nitro-L arginine methyl ester (L-NAME) at a dose of 50 mg/kg attenuated osmotic thirst induced by intraperitoneal injection of hypertonic saline, but did not affect spontaneous intake of water and thirst induced by subcutaneous injection of angiotension II. Pretreatment with L-arginine significantly attenuated the inhibition of osmotic thirst evoked with subsequent L-NAME. Administration of NW-nitro-D-arginine methyl ester (D-NAME) altered neither the spontaneous nor the osmotic drinking behavior. These findings suggest that NO may affect the osmotically induced drinking.

Angiotensin II↗

Effects of centrally administered endothelin-3 on renal sympathetic nerve activity and renal blood flow in conscious rats.

Effects of intracerebroventricular (i.c.v.) administration of endothelin-3 (ET-3) on renal sympathetic nerve activity (RSNA) and renal blood flow (RBF), arterial blood pressure and heart rate were examined in conscious rats. Administration of ET-3 (1-50 pmol) through a chronically implanted cannula evoked an increase in arterial blood pressure and decreases in heart rate and RSNA, whereas RBF measured by Doppler flow probes did not change. Maximum changes in these responses occurred 10-15 min after i.c.v. administration of ET-3 and the responses returned to the control level after approximately 60 min. In sinoaortic denervated (SAD) rats, the decrease in RSNA induced by i.c.v. ET-3 was attenuated but still significantly persistent. During the experiments, we found that the injection of ET-3 (50-100 pmol) induced a barrel rotation, with an onset latency of 10-15 min. In those cases, prominent increases in arterial blood pressure and RSNA were observed, and these lasted for more than 60 min. The result shows that ET-3 can have centrally mediated effects on autonomic nerve activity as well as on cardiovascular function.

Animals↗