Central interleukin-1β antibody increases renal and splenic sympathetic nerve discharge

2003 ◽  
Vol 284 (5) ◽  
pp. H1536-H1541 ◽  
Author(s):  
Ning Lu ◽  
Yan Wang ◽  
Frank Blecha ◽  
Richard J. Fels ◽  
Heather P. Hoch ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Pressor Response ◽  
Interleukin 1Β ◽  
Intracerebroventricular Administration ◽  
Intracerebroventricular Infusion ◽  
Arterial Blood ◽  
Nerve Discharge ◽  
Intact Rats

We tested the hypothesis that intracerebroventricular (lateral ventricle) administration of interleukin-1β (IL-1β) antibody increases the level of sympathetic nerve discharge (SND) in α-chloralose-anesthetized rats. Mean arterial pressure (MAP), heart rate (HR), and SND (splenic and renal) were recorded before (Preinfusion), during (25 min), and for 45 min after infusion of IL-1β antibody (15 μg, 50 μl icv) in baroreceptor-intact (intact) and sinoaortic-denervated (SAD) rats. The following observations were made. First, intracerebroventricular infusion of IL-1β antibody (but not saline and IgG) significantly increased MAP and the pressor response was higher in SAD compared with intact rats. Second, renal and splenic SND were significantly increased during and after intracerebroventricular IL-1β antibody infusion and sympathoexcitatory responses were higher in SAD compared with intact rats. Third, intracerebroventricular administration of a single dose of IL-1β antibody (15 μg, 5 μl for 2 min) significantly increased splenic and renal SND in intact rats. These results suggest that under the conditions of the present experiments central neural IL-1β plays a role in the tonic regulation of SND and arterial blood pressure.

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

2002 ◽  
Vol 282 (4) ◽  
pp. R1174-R1184 ◽  
Author(s):  
Daniela M. Sartor ◽  
Anthony J. M. Verberne
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Gastrointestinal Tract ◽  
Sympathetic Nerve ◽  
Vagal Afferents ◽  
Ventrolateral Medulla ◽  
Vasomotor Function ◽  
Arterial Blood ◽  
Potential Mediator ◽  
Nerve Discharge

Cholecystokinin (CCK) is a potential mediator of gastrointestinal vasodilatation during digestion. To determine whether CCK influences sympathetic vasomotor function, we examined the effect of systemic CCK administration on mean arterial blood pressure (MAP), heart rate (HR), lumbar sympathetic nerve discharge (LSND), splanchnic sympathetic nerve discharge (SSND), and the discharge of presympathetic neurons of the rostral ventrolateral medulla (RVLM) in α-chloralose-anesthetized rats. CCK (1–8 μg/kg iv) reduced MAP, HR, and SSND and transiently increased LSND. Vagotomy abolished the effects of CCK on MAP and SSND as did the CCK-A receptor antagonist devazepide (0.5 mg/kg iv). The bradycardic effect of CCK was unaltered by vagotomy but abolished by devazepide. CCK increased superior mesenteric arterial conductance but did not alter iliac conductance. CCK inhibited a subpopulation (∼49%) of RVLM presympathetic neurons whereas ∼28% of neurons tested were activated by CCK. The effects of CCK on RVLM neuronal discharge were blocked by devazepide. RVLM neurons inhibited by exogenous CCK acting via CCK-A receptors on vagal afferents may control sympathetic vasomotor outflow to the gastrointestinal tract vasculature.

Effect of nitric oxide within the paraventricular nucleus on renal sympathetic nerve discharge: role of GABA

1998 ◽  
Vol 275 (3) ◽  
pp. R728-R734 ◽  
Author(s):  
Kun Zhang ◽  
Kaushik P. Patel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Gaba System ◽  
Renal Sympathetic ◽  
Nerve Discharge

Both nitric oxide (NO) and GABA are known to provide inhibitory inputs to the paraventricular nucleus (PVN) of the hypothalamus and are involved in the control of sympathetic outflow. The purpose of the present study was to examine the interaction of NO and GABA in the regulation of renal sympathetic nerve activity in rats. The responses of renal nerve activity, blood pressure, and heart rate to microinjection of sodium nitroprusside (SNP), an NO donor, into the PVN were measured in the presence and absence of blockade of the GABA system (bicuculline; 2 nmol). Microinjection of SNP (50, 100, and 200 nmol) into the PVN elicited significant decreases in renal nerve discharge, arterial blood pressure, and heart rate, reaching −36.4 ± 9.7%, −11 ± 5 mmHg, and −34 ± 14 beats/min, respectively, at the highest dose. These responses were eliminated by blockade of the GABA system. Conversely, microinjection of N ω-nitro-l-arginine methyl ester (l-NAME; 50, 100, and 200 nmol) elicited significant increases in the renal sympathetic nerve discharge, arterial blood pressure, and heart rate, reaching 88.9 ± 16.6%, 9 ± 1 mmHg, and 29 ± 9 beats/min, respectively, at the highest dose. These sympathoexcitatory responses were masked by prior blockade of the GABA system with bicuculline. The sympathoexcitatory effect of l-NAME was also eliminated by activation of the GABA system with muscimol. In conclusion, our data indicate that the inhibitory effect of endogenous NO within the PVN on the renal sympathetic nerve activity is mediated by GABA.

Blood pressure during routine activity, stress, and feeding in black racer snakes (Coluber constrictor)

1993 ◽  
Vol 264 (1) ◽  
pp. R79-R84 ◽  
Author(s):  
J. N. Stinner ◽  
D. L. Ely
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Acute Stress ◽  
Pressor Response ◽  
Routine Activity ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Coluber Constrictor ◽  
S Peak ◽  
Hematological Changes

The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.

Baroreflex modulation of sympathetic nerve activity to muscle in heat-stressed humans

2002 ◽  
Vol 282 (1) ◽  
pp. R252-R258 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Whole Body ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Arterial Blood ◽  
The Relationship

To identify whether whole body heating alters arterial baroreflex control of muscle sympathetic nerve activity (MSNA), MSNA and beat-by-beat arterial blood pressure were recorded in seven healthy subjects during acute hypotensive and hypertensive stimuli in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature ( P < 0.01), MSNA ( P < 0.01), heart rate ( P< 0.01), and skin blood flow ( P < 0.001), whereas mean arterial blood pressure did not change significantly ( P > 0.05). During both normothermic and heat stress conditions, MSNA increased and then decreased significantly when blood pressure was lowered and then raised via intravenous bolus infusions of sodium nitroprusside and phenylephrine HCl, respectively. The slope of the relationship between MSNA and diastolic blood pressure during heat stress (−128.3 ± 13.9 U · beats−1 · mmHg−1) was similar ( P = 0.31) with normothermia (−140.6 ± 21.1 U · beats−1 · mmHg−1). Moreover, no significant change in the slope of the relationship between heart rate and systolic blood pressure was observed. These data suggest that arterial baroreflex modulation of MSNA and heart rate are not altered by whole body heating, with the exception of an upward shift of these baroreflex curves to accommodate changes in these variables that occur with whole body heating.

Comparative study of pressor and heart rate responses to angiotensin II and noradrenaline in pregnant and non-pregnant women

1992 ◽  
Vol 82 (2) ◽  
pp. 157-162 ◽  
Author(s):  
Margaret Ramsay ◽  
Fiona Broughton Pipkin ◽  
Peter Rubin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Pregnant Women ◽  
Arterial Blood Pressure ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Arterial Blood ◽  
Diastolic Arterial Blood Pressure ◽  
In Pregnancy

1. Twenty-eight healthy non-pregnant women and 28 women in the first or second trimester of pregnancy were studied. They were given an incremental intravenous infusion of either noradrenaline or angiotensin II. Pressor and heart rate responses were documented. 2. Dose-pressor response curves were constructed for the two agents in pregnant and non-pregnant women (n=14 in each group). The regression parameters of slope and intercept were calculated, and were used to derive the variables of dose required to elicit a 10 mmHg rise in systolic or diastolic blood pressure. 3. The pressor response to angiotensin II was diminished in pregnancy, with approximately twice the dose being required to raise the systolic or diastolic arterial blood pressure as in non-pregnant subjects. 4. The systolic pressor response to noradrenaline was slightly diminished in pregnancy, but the diastolic pressor response was unchanged. There were no significant differences between the doses of noradrenaline required to elicit a 10 mmHg rise in systolic or diastolic arterial blood pressure in pregnant or non-pregnant subjects. 5. There was a diminution in the bradycardia evoked in response to both hormones in pregnancy. 6. We conclude that the well-documented pressor insensitivity to angiotensin II during pregnancy is a specific phenomenon, not a manifestation of a generalized reduction in vascular reactivity.

The Brain as a Possible Site for the Cardiovascular Effects of β-Adrenoceptor Blocking Agents in Cats

1974 ◽  
Vol 48 (s2) ◽  
pp. 269s-272s
Author(s):  
M. D. Day ◽  
A. G. Roach
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Effects ◽  
Intracerebroventricular Administration ◽  
Blocking Agents ◽  
Intracerebroventricular Infusion ◽  
Pressor Responses ◽  
Maximum Inhibition ◽  
The Brain

1. dl-Propranolol, l-propranolol, dl-alprenolol, pindolol (LB46), practolol, ICI 66082, sotalol and oxprenolol all produced prolonged falls in blood pressure and heart rate after intracerebroventricular administration in conscious normotensive cats. 2. Transient initial pressor responses and tachycardias were observed after intracerebroventricular infusions of all the β-adrenoceptor antagonists used, except ICI 66082. 3. d-Propranolol, d-alprenolol, procaine and lignocaine all produced initial increases in blood pressure and heart rate but did not subsequently cause any reduction in either blood pressure or heart rate. 4. The time of maximum hypotension and bradycardia after intracerebroventricular infusion of β-adrenoceptor antagonists coincided with the maximum inhibition of the centrally mediated tachycardia observed after intracerebroventricular isoprenaline.

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