Search

It is well known that renal nerves directly affect renal vascular resistance, tubular sodium reabsorption, and renin secretion. Inhibition of renal sympathetic nerve activity (RSNA) decreases renal vascular resistance, tubular sodium reabsorption, and renin secretion, leading to an increase in sodium excretion. Although several studies show that inhibition of RSNA promotes sodium excretion during an acute blood volume expansion, there is limited research relating to the importance of RSNA inhibition that contributes to sodium homeostasis during a long-term increase in sodium intake. Therefore, to dissect the underlying mechanisms of sodium excretion, a mathematical model of a cardiovascular system consisting of two kidneys, each with an independent RSNA, was developed. Simulations were performed to determine the responses of RSNA and sodium excretion to an increased sodium intake. In these simulations, RSNA in the left kidney was fixed at its normal steadystate value, while RSNA in the contralateral kidney was allowed to change normally in response to the increased sodium intake. The results demonstrate that the fixed-RSNA kidney excretes less sodium than the intact-RSNA collateral kidney. Because each kidney is exposed to the same arterial pressure and circulatory hormones, the impaired sodium excretion in the absence of RSNA inhibition supports the hypothesis that RSNA inhibition contributes to natriuresis in response to a long-term increase in sodium intake. [ABSTRACT FROM AUTHOR]

Lesions of the lateral parabrachial nucleus (LPBN) impair blood pressure recovery after hypotensive blood loss (Am J Physiol Regul Integr Comp Physiol 280: R1141, 2001). This study tested the hypothesis that posthemorrhage blood pressure recovery is mediated by activation of neurons, located in the ventrolateral aspect of the LPBN (VL-LPBN), that initiates blood pressure recovery by restoring sympathetic vasomotor drive. Hemorrhage experiments (16 ml/kg over 22 min) were performed in unanesthetized male Sprague-Dawley rats prepared with bilateral ibotenate lesions or guide cannulas directed toward the external lateral subnucleus of the VL-LPBN. Hemorrhage initially decreased mean arterial pressure (MAP) from ∼100 mmHg control to 40-50 mmHg, and also decreased heart rate. In animals with sham lesions, MAP returned to 84 ± 4 mmHg by 40 min posthemorrhage, and subsequent autonomic blockade with hexamethonium reduced MAP to 53 ± 2 mmHg. In contrast, animals with VL-LPBN lesions remained hypotensive at 40 min posthemorrhage (58 ± 4 mmHg) and hexamethonium had no effect on MAP, implying a deficit in sympathetic tone. VL-LPBN lesions did not alter the renin response or the effect of vasopressin VI receptor blockade after hemorrhage. Posthemorrhage blood pressure recovery was also significantly delayed by VL-LPBN infusion of the ionotropic glutamate receptor antagonist kynurenic acid. Both VL-LPBN lesions and VL-LPBN kynurenate infusion caused posthemorrhage bradycardia to be significantly prolonged. Bradycardia was reversed by hexamethonium or atropine, but did not contribute to posthemorrhage hypotension. Taken together, these data support the hypothesis that stimulation of VL-LPBN glutamate receptors mediates spontaneous blood pressure recovery by initiating restoration of sympathetic vasomotor drive. [ABSTRACT FROM AUTHOR]

Previous studies have shown that the sympathetically mediated oscillations of arterial pressure (AP), the so-called Mayer waves, are shifted from 0.4 to 0.6 Hz after acute α-adrenoceptor blockade in conscious rats. This raises the possibility that, under physiological conditions, Mayer waves are mediated by the conjoint action of norepinephrine and other sympathetic cotransmitters. To evaluate the possible role of the cotransmitter ATP in determining the frequency of Mayer waves, AP and renal sympathetic nerve activity (RSNA) were simultaneously recorded in 10 conscious rats with cardiac autonomic blockade before and after acute blockade of P2 receptors with pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid. P2 receptor blockade did not alter the mean level and overall variability of AP and RSNA but shifted peak coherence between AP and RSNA from 0.43 ± 0.02 to 0.22 ± 0.01 Hz. A model of the sympathetic limb of the arterial baroreceptor reflex was designed to simulate Mayer waves at 0.2 and 0.6 Hz, with norepinephrine and ATP, respectively, acting as the sole sympathetic cotransmitter. When both cotransmitters acted in concert, a single oscillation was observed at 0.4 Hz when the gain ratio of the adrenergic to the purinergic components was set at 15. The model thus accounted for an important role for ATP in determining Mayer wave frequency, but not in sustaining the mean level of AP or controlling its overall variability. [ABSTRACT FROM AUTHOR]

Estradiol valerate (EV)-induced polycystic ovaries (PCO) in rats are associated with higher ovarian release and content of norepinephrine, decreased β2-adrenoceptors (ARs), and dysregulated expression of α1-AR subtypes, all preceded by an increase in the production of ovarian NGF. The aim of this study was to further elucidate the role of NGF in the ovaries by blocking the action of NGF during development of EV-induced PCO in rats. Control and EV-injected rats were treated with intraperitoneal injections of IgG (control and PCO groups) or with anti-NGF antibodies (anti-NGF and PCO anti-NGF groups) every third day for 5 wk starting from the day of PCO induction. Rat weight, estrous cyclicity, ovarian morphology, ovarian mRNA, and protein expression of α1-AR subtypes, β2-AR, the NGF receptor tyrosine kinase A (TrkA), p75 neurotrophin receptor (p75NTR), and tyrosine hydroxylase (TH) were analyzed. Ovaries in both PCO and PCO anti-NGF groups decreased in size as well as in number and size of corpora lutea. mRNA expression of α1a-AR and TrkA in the ovaries was lower, whereas expression of α1b- and α1d-AR and TH was higher, in the PCO group than in controls. Protein quantities of al-ARs, TrkA, p75NTR, and TH were higher in the PCO group compared with controls, whereas the protein content of β2-AR was lower. Anti-NGF treatment in the PCO group restored all changes in mRNA and protein content, except that of α1b-AR and TrkA mRNAs, to control levels. The results indicate that the NGF/NGF receptor system plays a role in the pathogenesis of EV-induced PCO in rats. [ABSTRACT FROM AUTHOR]

Numerous epidemiological studies suggest an inverse relationship between low birth weight (LBW) and hypertension, an observation now supported by numerous animal studies. The mechanisms linking LBW and hypertension appear to be multifactorial and involve alterations in the normal regulatory systems and renal functions involved in the long-term control of arterial pressure. Recent studies using animal models of fetal programming suggest that programming during fetal life occurs in response to an adverse fetal environment and results in permanent adaptive responses that lead to structural and physiological alterations and the subsequent development of hypertension. This review summarizes the adaptive responses observed in the different models used to induce a suboptimal fetal environment and discusses insights into the mechanisms mediating the fetal programming of hypertension. [ABSTRACT FROM AUTHOR]

We investigated the roles of the renin-angiotensin system and the significance of interactions between angiotensin II and nitric oxide, in responses of regional kidney perfusion to electrical renal nerve stimulation (RNS) in pentobarbital sodium-anesthetized rabbits. Under control conditions, RNS (0.5-8 Hz) reduced total renal blood flow (RBF; -89 ± 3% at 8 Hz) and cortical perfusion (CBF; -90 ± 2% at 8 Hz) more than medullary perfusion (MBF; -55 ± 5% at 8 Hz). Angiotensin I1 type 1 (AT1)-receptor antagonism (candesartan) blunted RNS-induced reductions in RBF (P = 0.03), CBF (P = 0.007), and MBF (P = 0.04), particularly at 4 and 8 Hz. Nitric oxide synthase inhibition with NG-nitro-L-arginine (L-NNA) enhanced RBF (P = 0.003), CBF (P = 0.001), and MBF (P = 0.03) responses to RNS, particularly at frequencies of 2 Hz and less. After candesartan pretreatment, L-NNA significantly enhanced RNS-induced reductions in RBF (P = 0.04) and CBF (P = 0.007) but not MBF (P = 0.66). Renal arterial infusion of angiotensin II (5 ng·kg-1·min-1) selectively enhanced responses of MBF to RNS in L-NNA-pretreated but not in vehicle-pretreated rabbits. In contrast, greater doses of angiotensin II (5–15 ng·kg-1·min-1) blunted responses of MBF to RNS in rabbits with intact nitric oxide synthase. These results suggest that endogenous angiotensin II enhances, whereas nitric oxide blunts, neurally mediated vasoconstriction in the renal cortical and medullary circulations. In the renal medulla, but not the cortex, angiotensin II also appears to be able to blunt neurally mediated vasoconstriction. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated that microinjection of the putative group III metabotropic glutamate receptor (mGluR) agonist, L(+)-2-amino-4-phosphonobutyric acid (L-AP4), into the nucleus tractus solitarius (NTS) produces depressor and sympathoinhibitory responses. These responses are significantly attenuated by a group III mGluR antagonist and may involve ionotropic glutamatergic transmission. Alternatively, a previous report in vitro suggests that preparations of L-AP4 may nonspecifically activate NMDA channels due to glycine contamination (Contractor A, Gereau RW, Green T, and Heinemann SF. Proc Natl Acad Sci USA 95: 8969–8974, 1998). Therefore, the present study tested whether responses to L-AP4 specifically require the N-methyl-D-aspartate (NMDA) receptor and whether they are due to actions at the glycine site on the NMDA channel. To test these possibilities in vivo, we performed unilateral microinjections of L-AP4, glycine, and selective antagonists into the NTS of urethane-anesthetized rats. L-AP4 (10 mM, 30 nl) produced sympathoinhibitory responses that were abolished by the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid (AP-5, 10 mM) but were unaffected by the non-NMDA antagonist 6-nitro-7-sulfamobenzoquinoxaline-2,3-dione (NBQX, 2 mM). Microinjection of glycine (0.02–20 mM) failed to mimic sympathoinhibitory responses to L-AP4, even in the presence of the inhibitory glycine antagonist, strychnine (3 mM). Strychnine blocked pressor and sympathoexcitatory actions of glycine (20 mM) but failed to reveal a sympathoinhibitory component due to presumed activation of NMDA receptors. The results of these experiments suggest that responses to L-AP4 require NMDA receptors and are independent of non-NMDA receptors. Furthermore, although it is possible that glycine contamination or other nonspecific actions are responsible for the sympathoinhibitory actions of L-AP4, our data and data in the literature argue against this possibility. Thus we conclude that responses to L-AP4 in the NTS are mediated by an interaction between group III mGluRs and NMDA receptors. Finally, we also caution that nonselective actions of L-AP4 should be considered in future studies. [ABSTRACT FROM AUTHOR]

After periods of microgravity or bed rest, individuals often exhibit reduced Vo2 max, hypovolemia, cardiac and vascular effects, and autonomic dysfunction. Recently, alterations in expression of vascular and central nervous system NO synthase (NOS) have been observed in hindlimb-unloaded (HU) rats, a model used to simulate physiological effects of microgravity or bed rest. We examined the effects of 14 days of hindlimb unloading on hemodynamic responses to systemic NOS inhibition in conscious control and HU rats. Because differences in NO and autonomic regulation might occur after hindlimb unloading, we also evaluated potential differences in resting autonomic tone and effects of NOS inhibition after autonomic blockade. Administration of nitro-L-arginine methyl ester (L-NAME; 20 mg/kg iv) increased mean arterial pressure (MAP) to similar levels in control and HU rats. However, the change in MAP in response to L-NAME was less in HU rats, that had an elevated baseline MAP. In separate experiments, atropine (1 mg/kg iv) increased heart rate (HR) in control but not HU rats. Subsequent administration of the ganglionic blocker hexamethonium (30 mg/kg iv) decreased MAP and HR to a greater extent in HU rats. Administration of L-NAME after autonomic blockade increased MAP in both groups to a greater extent compared with intact conditions. However, the pressor response to L-NAME was still reduced in HU rats. These data suggest that hindlimb unloading in rats reduces peripheral NO as well as cardiac parasympathetic tone. Along with elevations in sympathetic tone, these effects likely contribute to alterations in vascular control and changes in autonomic reflex function following spaceflight or bed rest. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that women have blunted sympathetic neural responses to orthostatic stress compared with men, which may be elicited under hypovolemic conditions. Muscle sympathetic nerve activity (MSNA) and hemodynamics were measured in eight healthy young women and seven men in supine position and during 6 min of 60° head-up tilt (HUT) under normovolemic and hypovolemic conditions (randomly), with ∼4-wk interval. Acute hypovolemia was produced by diuretic (furosemide) administration ∼2 h before testing. Orthostatic tolerance was determined by progressive lower body negative pressure to presyncope. We found that furosemide produced an ∼13% reduction in plasma volume, causing a similar increase in supine MSNA in men and women (mean ± SD of 5 ± 7 vs. 6 ± 5 bursts/min; P = 0.895). MSNA increased during HUT and was greater in the hypovolemic than in the normovolemic condition (32 ± 6 bursts/min in normovolemia vs. 44 ± 15 bursts/min in hypovolemia in men, P = 0.055; 35 ± 9 vs. 45 ± 8 bursts/min in women, P < 0.001); these responses were not different between the genders (gender effect: P = 0.832 and 0.814 in normovolemia and hypovolemia, respectively). Total peripheral resistance increased proportionately with increases in MSNA during HUT; these responses were similar between the genders. However, systolic blood pressure was lower, whereas diastolic blood pressure was similar in women compared with men during HUT, which was associated with a smaller stroke volume or stroke index. Orthostatic tolerance was lower in women, especially under hypovolemic conditions. These results indicate that men and women have comparable sympathetic neural responses during orthostatic stress under normovolemic and hypovolemic conditions. The lower orthostatic tolerance in women is predominantly because of a smaller stroke volume, presumably due to less cardiac filling during orthostasis, especially under hypovolemic conditions, which may overwhelm the vasomotor reserve available for vasoconstriction or precipitate neurally mediated sympathetic withdrawal and syncope. [ABSTRACT FROM AUTHOR]

Leptin increases sympathetic nervous system (SNS) activity in brown adipose tissue and renal nerves. Experiments described here tested whether SNS innervation is required for peripheral, physiological concentrations of leptin to reduce body fat. In experiment 1, one epididymal (EPI) fat pad was sympathectomized by local injection of 6-hydroxydopamine (6OHDA) in C57BL/6 mice that were then infused for 13 days with PBS or 10 μg leptin/day from an intraperitoneal miniosmotic pump. Surprisingly, EPI denervation increased total body fat of PBS-infused mice but leptin decreased the size of both injected and noninjected EPI pads in 6OHDA mice. Experiment 2 was identical except for the use of male Sprague-Dawley rats that were infused with 50 μg leptin/day. Leptin had little effect on EPI weight or norepinephrine (NE) content, but denervation of one EPI pad decreased the effect of leptin on intact EPI, inguinal and retroperitoneal (RP) fat and increased the size of the mesenteric fat pad. Experiment 3 included groups in which either one EPI or one RP pad was denervated. RP denervation reduced RP NE content but did not prevent a leptin-induced reduction in fat pad mass. Therefore, the SNS is not required for low doses of leptin to reduce body fat. EPI denervation significantly increased adipocyte number in contralateral EPI and RP fat pads and this was prevented by leptin. These changes in intact pads of rats with one denervated fat pad imply communication between fat depots and suggest that both leptin and the SNS regulate the size of individual depots. [ABSTRACT FROM AUTHOR]

Siberian hamsters (Phodopus sungorus) exhibit a naturally occurring, reversible seasonal obesity with body fat peaking in long ‘summerlike’ days (LDs) and reaching a nadir in short ‘winterlike’ days (SDs). These SD-induced decreases in adiposity are mediated largely via sympathetic nervous system (SNS) innervation of white adipose tissue (WAT), as indicated by increased WAT norepinephrine (NE) turnover. We examined whether SDs also increase sensitivity to NE-stimulated lipolysis. This was accomplished by measuring NE- and β3-adrenoceptor (β3-AR) agonist (BRL-37344)-induced lipolysis (glycerol release) as well as NE-induced cAMP accumulation by inguinal, epididymal, and retroperitoneal WAT (IWAT, EWAT, and RWAT) in isolated adipocytes of LD- and SD-housed hamsters. SDs increased potency/efficacy of NE-triggered lipolysis in a temporally and fat pad-specific manner. Thus when WAT pad mass decreased most rapidly (5 wk of SDs), potency (sensitivity/ECso) and efficacy (maximal response asymptote) of NE-stimulated lipolysis were increased for all WAT pads and also at 10 wk for IWAT compared with their LD counter-parts. SD enhancement of lipolysis was similar for NE and BRL-37344 in IWAT adipocytes. These results, coupled with our previous demonstration that SDs upregulate WAT β3-AR mRNA expression, suggest that increased β3-ARs mediated the SD-induced increased NE sensitivity. NE-stimulated adipocyte accumulation of cAMP was greater after 5 wk of SDs for IWAT and EWAT and after 10 wk of SDs for IWAT compared with LDs, with no photoperiod effect for RWAT. Therefore, the SD-induced increase in SNS drive to WAT and increased sensitivity to this drive may work together to increase lipolysis in SDs. [ABSTRACT FROM AUTHOR]

We used spectral analysis and event-triggered averaging to determine the effects of chemical inactivation of the medullary lateral tegmental field (LTF) on 1) the relationship of intratracheal pressure (ITP, an index of vagal lung inflation afferent activity) to sympathetic nerve discharge (SND) and phrenic nerve activity (PNA) and 2) central respiratory rate in paralyzed, artificially ventilated dial-urethane-anesthetized cats. ITP-SND coherence value at the frequency of artificial ventilation was significantly (P < 0.05; n = 18) reduced from 0.73 ± 0.04 (mean ± SE) to 0.24 ± 0.04 after bilateral microinjection of muscimol into the LTF. Central respiratory rate was unexpectedly increased in 12 of these experiments (0.28 ± 0.03 vs. 0.95 ± 0.25 Hz). The ITP-PNA coherence value was variably affected by chemical inactivation of the LTF. It was unchanged when central respiratory rate was also not altered, decreased when respiratory rate was increased above the rate of artificial ventilation, and increased when respiratory rate was raised from a value below the rate of artificial ventilation to the same frequency as the ventilator. Chemical inactivation of the LTF increased central respiratory rate in four of six vagotomized cats but did not significantly affect the PNA-SND coherence value. These data demonstrate that the LTF 1) plays a critical role in mediating the effects of vagal lung inflation afferents on SND but not PNA, 2) helps maintain central respiratory rate in the physiological range, but 3) is not involved in the coupling of central respiratory and sympathetic circuits. [ABSTRACT FROM AUTHOR]

This study quantified the effect of interrupting the descending input to the sympathetic preganglionic neurons on the dynamic behavior of arterial blood pressure (BP) in the unanesthetized rat. BP was recorded for ∼4-h intervals in six rats in the neurally intact state and in the same animals after complete spinal cord transection (SCT) between T4 and T5. In the intact state, power within the frequency range of 0.35-0.45 Hz was 1.53 ± 0.38 mmHg²/Hz (mean ± SD by fast Fourier transform). One week after SCT, power within this range decreased significantly (P < 0.05) to 0.43 ± 0.62 mmHg²/Hz. To test for self-similarity before and after SCT, we analyzed data using a wavelet (i.e., functionally, a digital bandpass filter) tuned to be maximally sensitive to fluctuations with periods of ∼2, 4, 8, 16, 32, or 64 s. in the control state, all fluctuations with periods of ∼4 s conformed to a "self-similar" (i.e., fractal) distribution. In marked contrast, the oscillations with a period of -2 s (i.e., -0.4 Hz) were significantly set apart from those at lower frequencies. One day and seven days after the complete SCT, however, the BP fluctuations at -0.4 Hz now also conformed to the same self-similar behavior characteristic of the lower frequencies. We conclude that 1) an intact sympathetic nervous system endows that portion of the power spectrum centered around ∼0.4 Hz with properties (e.g., a periodicity) that differ significantly from the self-similar behavior that characterizes the lower frequencies and 2) even within the relatively high frequency range at 0.4 Hz self-similarity is the "default" condition after sympathetic influences have been eliminated. [ABSTRACT FROM AUTHOR]

Characterizes the effects of intravenously administered cholecystokinin (CCK) on mean arterial blood pressure, heart rate, lumbar sympathetic nerve discharge, splanchnic SND and regional vascular conductance. Overview of CCK; Effects of CCK on sympathetic vasomotor outflow; Cardiac actions of CCK.

Presents a study that examined the impact of litter size alone on the regulation of sympathetic nervous system activity. Effect of litter size on tissue norepinephrine (NE) levels in rats; Effect of litter size on sucrose-induced stimulation of tissue [³H] turnover in rats; Effect of litter size on weight gain in rats.

Presents a study that tested the role of the sympathetic nervous system in the progressive increase in mean arterial pressure. Evidence for both an increase and a decrease in activity of the nitric oxide (NO) system in the diabetic state; Interrelationship between NO, the sympathetic nervous system and the renin-angiotensin system; Explanation for the increase in the blood pressure of rats.

Presents a study which tested the hypothesis that sympathetic nerve activity is attenuated in a hyperbaric environment. Evaluation of modulation of hemodynamic variables; Measurement of muscle sympathetic nerve activity; Comparison of hyperbaric measurements with those at normal atmosphere.

Presents a study that examined the role of serotonin, 5-hydroxytryptamine type 1A (5-HT[sub1A]) receptors in the rostral ventrolateral medulla in the mediation of the sympathoinhibitory and hypotensive responses to severe hemorrhage. Analysis of renal sympathetic nerve activity subjected to blockade of 5-HT[sub1A]; Examination of blood pressure response to 5-HT[sub1A]; Assessment of the role of baroreceptors/chemoreceptors.

Presents a study that examined the role of N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonist on the sympathetic nerve discharge (SND) of the lateral tegmented field (LTF) neurons. Examination of LTF with activity correlated to the cardiac-related rhythm in SND; Effect of microiontophoresis of non-NMDA receptor antagonist on LTF neuronal activity; Impact of microiontophoresis of NMDA receptor antagonist on LTF neuronal activity.

Presents a study which tested the hypothesis that central hyperosmotic stimulation increases renal sympathetic nerve activity by a mechanism involving ANG II type 1-receptor activation in the hypothalamic paraventricular nucleus. Methods; Results; Discussion.

Presents a study which evaluated the hypothesis that orexins, acting on sympathetic preganglionic neurons in the rat spinal cord, increase sympathetic outflow. Methods; Results; Discussion.

Presents a study which examined the roles of sympathetic and vagal cardiac afferents in electromyographic responses to pericardial algogenic chemicals. Materials and methods; Results; Discussion.

Presents a study which examined the effects of clonidine injected unilaterally into the rostral ventrolateral medulla of conscious, unrestrained rats. Methods; Results; Discussion.

Presents a study which investigated the effects of chronic hypoxia on sympathetic nerve function in fetal and adult middle cerebral and facial arteries of sheep. Methods; Results; Discussion.

Presents a study which tested the hypothesis that application of lower body positive pressure during orthostasis would reduce the baroreflex-mediated enhancement in sympathetic activity in humans. Methods; Results; Discussion.

Describes the dynamics of neural control over renal blood flow (RBF) and develops a mathematical model with associated parameters. Decrease in RBF after stimulation of the renal nerves with the pseudo-random binary sequence; Magnitude response between the stimulus and RBF; Difficulty in assessing the impact of endogenous sympathetic nerve activity on the renal vasculature.

Presents information on a study which examined the effects of glucocorticoids on arterial baroreceptor reflex control of renal sympathetic nerve activity. Factors which contribute to the effects of glucocorticoids; Methodology; Results of the study.

Focuses on a study which assessed whether physiological activation of the sympathetic nervous system induced by exercise changes adipose tissue responsiveness to catecholamines in humans. Materials and methods of the study; Results; Discussion of the results.

Presents information on a study which examined the effect of norepinephrine reuptake blockade with desipramine on the spontaneous variability of arterial pressure and renal sympathetic nerve activity in conscious rats. Methods used in the study; Results and discussion.

Presents information on a study which discussed the differential neural control of intrarenal blood flow. Information on the role of renal sympathetic nerve activity in the regulation of renal hemodynamics and excretory functions; Methodology; Effects of varying amplitude of renal sympathetic nerve stimulation; Effects of varying frequency of renal sympathetic nerve stimulation.

Presents information on a study on the effect of electrical stimulation of the caudal medullary raphe to changes in cardiac and vertebral sympathetic nerves and renal sympathetic nerve discharges in cats. Methodology of the study; Results and discussion; Conclusion.

Provides information on a study which examined how long-lasting microgravity simulation by six degrees of head-down bed rest induces changes in the baroreflex control of muscle sympathetic nerve activity (MSNA) and changes in responses of MSNA to orthostasis. Methods used in the experiment; Results; Discussion.

Presents information on a study which investigated the changes in muscle sympathetic nerve activity from the tibial nerve during brief periods of microgravity produced by parabolic flight. Methods; Results; Discussion.

Presents information on a study which investigated the frequency response characteristics of sympathetic transmission to skin blood vessels in rats. Methods; Results; Discussion.

Discusses a study which tested the hypothesis that hypertonicity can produce sustained excitation of nonrenal sympathetic nerves. How the study was conducted; Effects of water deprivation on baseline parameters; Effects of 5DW infusion in water-deplete and -replete rats; Effects of saline infusion in water-deprived rats.

Presents a study on the ability of different frequencies in sympathetic nerve activity (SNA) to induce oscillations in the renal blood flow (RBF). Methodology of the study; Results and discussion; Conclusion.

Discusses a study which examined the effects of development and chronic high-altitude hypoxia on sympathetic nerve function in sheep arteries. Effect of nitric oxide synthase inhibition; Effect of capsaicin treatment; Effects of treatments on basal norepinephrine release in middle cerebral and facial arteries.

Examines the effect of activation of a unique population of renal sympathetic nerve fibers on renal blood flow (RBF) dynamics using anesthetized rats with a renal sympathetic nerve activity (RSNA) recording electrode. Demographics of rats with intact renal innervation; Physiological responses of rats with renal denervation; Comparison of rats with intact renal innervation and rats with renal denervation.

Presents information on a study which suggested that acute physiological elevations in plasma insulin decrease cardiac vagal tone and modulation and that insulin produces nonuniform increases in muscle and cardiac sympathetic activity in humans. Methods of the study; Presentation of hyperinsulinemic/euglycemic clamp; Mediation of insulin sympathoexcitatory effects; Conclusions.

Presents information on a study documenting a rostral ventrolateral medulla (RVLM) catechol activation on systemic hydrogen load. Significant changes in mean arterial pressure among saline, intact and deafferented groups; Methodology used in the study; What the results indicate.

Presents information on a study that tests the hypothesis that the area postrema is necessary for endogenous angiotensin II (ANG II) to chronically maintain lumbar sympathetic nerve activity (LSNA) and heart rate in conscious sodium-deprived rats. Effect of the NAG II type 1-receptor antagonist, losartan on LSNA; What the results suggest.

Examines the role of renal sympathetic nerves in renal blood flow (RBF) response to hemorrhage of conscious rabbits. Methodology used in the study; Changes that occured during hemorrhage; Comparison of interaction between RBF and arterial blood pressure in intact and denervated rabbits; Effects of interaction between arterial pressure and and RBF and renal nerves during hemorrhage.

Examines how the lateral parabrachial nucleus (LPBN) neurons influenced the baroreflex control of arterial pressure and sympathetic nerve activity. Physiologic action of parabrachial nucleus (PBN); Methodology used; Baroreflex control of blood pressure and renal sympathetic nerve activity (RNSA) during electrical, chemical activation of the LPBN; Baroreflex control of blood pressure and RSNA during chemical inactivation of LPBN).

Evaluates the significance of sympathetic nervous system (SNS) effects on the venous system in intact, unanesthetized trout. Effects of epinephrine on trout veins in vivo; Function of SNS in trout; Implications of the study results.

Studies the role of nitric oxide within the paraventricular nucleus (PVN) of the hypothalamus in the regulation of renal sympathetic nerve (RSN) activity. Measurement of basan RSN discharge, arterial blood pressure and heart rate; Responses to microinjections of different drugs into PVN.

Examines whether prostaglandins mediate the lipopolysaccharide (LPS)-induced increase in splenic sympathetic nerve activity. Determination of the possible site of action of both LPS and prostaglandins.

Presents a study on the role of endogenous interleukin-1 and sympathetic innervation on vasoconstriction in the spleen. Low doses of lipopolysaccharide (LPS) increase the splenic blood flow; Vasoconstriction induced by stimulation of the splenic nerve; Ganglionic blockade.

Determines the contribution of endogenous brain stem angiotensin to renal sympathetic reflexes in conscious rabbits. Effect of hypoxia on baroreflex curves; Effects of Losartan or Ringer on the baroreflex curves; Effect of Losartan or Ringer on baroreflex curves during hypoxia. Effect of Losartan or Ringer on baroreflex curves during hypoxia plus carbon dioxide.

Examines the role of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate receptors within the caudal ventrolateral medulla in mediating the sympathetic baroreceptor reflex in anesthetized and paralyzed rats. Elimination of the aortic nerve stimulation-evoked hypotension and inhibition of splanchnic sympathetic nerve activity; Bilateral injections.

Explores the renal sympathetic responses to infusion of hypertonic solutions into lateral cerebral ventricles in conscious sheep. Reduction of renal sympathetic nerve activity through intracerebroventricular infusion of artificial cerebrospinal fluid; Decrease in plasma renin concentration; Increase in arterial pressure.