A depressant area in the lateral nodulus-uvula of the cerebellum for renal sympathetic nerve activity and systemic blood pressure in the rabbit

Physiological responses at birth include increases in heart rate (HR), blood pressure, sympathetic nerve activity, and circulating vasoactive peptides. The factors mediating these responses are not known. To test the hypothesis that afferent input from peripheral mechanoreceptors (arterial and cardiopulmonary baroreceptors) and chemoreceptors contribute to the sympathoexcitatory and hormonal responses at birth, we studied the effects of sinoaortic denervation (SAD) and SAD with vagotomy (Vx) on changes in HR, mean arterial blood pressure (MABP), renal sympathetic nerve activity (RSNA), and catecholamine, arginine vasopressin (AVP), and ANG II levels at birth in term sheep. One hour after delivery by cesarean section, RSNA increased by 168 ± 49 and 192 ± 32% (relative to fetal values) in SAD and SAD-Vx animals, respectively. Significant increases in HR (18 ± 5 and 20 ± 6%) and MABP (24 ± 4 and 20 ± 5%) were also observed 1 h after delivery in SAD and SAD-Vx lambs, respectively. These responses are similar to those seen in intact sheep delivered at the same gestational age. AVP levels markedly increased after birth (19.8 ± 6.7 to 136.1 ± 75.9 pg/ml) in SAD-Vx lambs, whereas SAD animals displayed no change in AVP concentrations. Plasma ANG II also did not change after birth in either group, although levels were consistently higher ( P < 0.01) in SAD compared with SAD-Vx animals. In the presence of SAD, Vx resulted in significantly greater plasma levels of norepinephrine, although levels did not change after birth in either group. The epinephrine responses at birth were similar in both groups of animals. The present data suggest that afferent input from peripheral chemoreceptors and mechanoreceptors contributes little to the hemodynamic and sympathetic responses after delivery by cesarean section. On the other hand, these peripheral mechanisms appear to be involved in modulating endocrine responses at birth.

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Intracerebroventricular leptin increases lumbar and renal sympathetic nerve activity and blood pressure in normal rats

Diabetes ◽

10.2337/diabetes.46.12.2040 ◽

1997 ◽

Vol 46 (12) ◽

pp. 2040-2043 ◽

Cited By ~ 76

Author(s):

J. C. Dunbar ◽

Y. Hu ◽

H. Lu

Keyword(s):

Blood Pressure ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Renal Sympathetic

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Intracerebroventricular Leptin Increases Lumbar and Renal Sympathetic Nerve Activity and Blood Pressure in Normal Rats

Diabetes ◽

10.2337/diab.46.12.2040 ◽

1997 ◽

Vol 46 (12) ◽

pp. 2040-2043 ◽

Cited By ~ 230

Author(s):

Joseph C Dunbar ◽

Yuange Hu ◽

Huiqing Lu

Keyword(s):

Blood Pressure ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Renal Sympathetic

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Renal sympathoinhibition mediated by 5-HT1Areceptors in the RVLM during severe hemorrhage in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2002.282.1.r122 ◽

2002 ◽

Vol 282 (1) ◽

pp. R122-R130 ◽

Cited By ~ 22

Author(s):

C. Dean ◽

M. Bago

Keyword(s):

Blood Pressure ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Ventrolateral Medulla ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Arterial Blood ◽

Severe Hemorrhage ◽

Renal Sympathetic

The role of 5-hydroxytryptamine type 1A (5-HT1A) receptors in the rostral ventrolateral medulla (RVLM) in the mediation of the sympathoinhibitory and hypotensive responses to severe hemorrhage was examined in pentobarbital sodium-anesthetized rats. The control response to hemorrhage (1 ml/min to 50 mmHg) consisted of a fall in arterial blood pressure and an initial baroreflex increase in renal sympathetic nerve activity followed after 2 min by a rapid decline in blood pressure accompanied by a decrease in renal sympathetic nerve activity. In response to hemorrhage in animals in which the specific 5-HT1A receptor antagonist WAY-100635 was microinjected into the pressor area of the RVLM, the fall in blood pressure was delayed and attenuated while renal sympathetic nerve activity was increased and maintained above baseline. In barodenervated animals with blockade of RVLM 5-HT1A receptors, there was no change in renal sympathetic nerve activity in response to hemorrhage. These data suggest that renal sympathoinhibition elicited in response to severe hemorrhage is mediated by 5-HT1A receptors in the RVLM.

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Sympathoinhibition from ventrolateral periaqueductal gray mediated by the caudal midline medulla

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00326.2005 ◽

2005 ◽

Vol 289 (5) ◽

pp. R1477-R1481 ◽

Cited By ~ 9

Author(s):

C. Dean

Keyword(s):

Blood Pressure ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Periaqueductal Gray ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Depressor Response ◽

Arterial Blood ◽

Renal Sympathetic

Activation of neurons in the ventrolateral region of the periaqueductal gray (vlPAG) can elicit a decrease in renal sympathetic nerve activity and blood pressure. The present study investigated whether the vlPAG-evoked sympathoinhibitory response depends on neurons in the caudal midline medulla (CMM). In pentobarbital-anesthetized rats, activation of neurons in the vlPAG evoked a decrease in renal sympathetic nerve activity to 29.4 ± 4.8% below baseline levels and arterial blood pressure fell 8.9 ± 1.6 mmHg ( n = 20). Microinjection of the GABA agonist muscimol into sympathoinhibitory regions of the CMM significantly attenuated the vlPAG-evoked sympathoinhibition to 17.9 ± 4.1% below baseline and the depressor response to 4.3 ± 1.2 mmHg. At 65% (13/20) of the sites examined, the vlPAG-evoked sympathoinhibition was responsive to CMM muscimol microinjection and attenuated from 34.2% to 11.5%, with the depressor response reduced from 14.8 to 3 mmHg. Microinjection of muscimol at the remaining 35% of the CMM sympathoinhibitory sites was ineffective on the vlPAG-evoked sympathoinhibition and depressor response. These data indicate that sympathoinhibitory and hypotensive responses elicited by activation of neurons in the vlPAG can be mediated by neurons in the sympathoinhibitory region of the CMM. The finding that the vlPAG-evoked response is not affected by muscimol at all CMM sympathoinhibitory sites also suggests that sympathoinhibitory sites in the CMM are not homogeneous and can mediate functionally different responses.

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