Spinal vasopressin mechanisms of cardiovascular regulation

1986 ◽  
Vol 251 (3) ◽  
pp. R510-R517 ◽  
Author(s):  
J. P. Porter ◽  
M. J. Brody
Keyword(s):  
Spinal Cord ◽  
Arterial Pressure ◽  
Neural Control ◽  
Intrathecal Injection ◽  
Cardiovascular Regulation ◽  
Spinal Subarachnoid Space ◽  
Vascular Beds ◽  
Vasopressinergic Neurons ◽  
Stimulation Of ◽  
Related Increase

Extrahypothalamic vasopressin-containing neurons have been implicated in the central neural control of the cardiovascular system. In the present study we investigated the possibility that vasopressinergic neurons arising from the paraventricular nucleus (PVN) and terminating in the spinal cord are involved in the regulation of vasomotor functions. Vasopressin (1-17 pmol) was injected into the spinal subarachnoid space of conscious rats instrumented with Doppler flow probes and indwelling intrathecal catheters. The peptide produced a dose-related increase in arterial pressure accompanied by vasoconstriction in the mesenteric, renal, and hindquarter vascular beds. Pretreatment, intrathecally, with 0.5 nmol of the vasopressin antagonist d(CH2)5Me(Tyr)AVP completely prevented the increase in arterial pressure expected after subsequent intrathecal injection of vasopressin. However, the changes in arterial pressure and vascular resistances produced by stimulation of the PVN were not affected by the intrathecal antagonist. Stimulation of the PVN in Brattleboro rats, which lack hypothalamic and spinal vasopressin, produced hemodynamic responses similar to those produced in Long-Evans control rats. Taken together, these data suggest that spinal vasopressin can act within the spinal cord to alter vasomotor functions; however, the hemodynamic effects evoked by stimulation of the PVN do not appear to depend on spinal vasopressinergic mechanisms.

Effects of WAY100635, a selective 5-HT1A-receptor antagonist on the micturition-reflex pathway in the rat

2001 ◽  
Vol 280 (5) ◽  
pp. R1407-R1413 ◽  
Author(s):  
Hidehiro Kakizaki ◽  
Mitsuharu Yoshiyama ◽  
Tomohiko Koyanagi ◽  
William C. De Groat
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Receptor Antagonist ◽  
Intrathecal Injection ◽  
Cervical Cord ◽  
Dependent Manner ◽  
Reflex Pathway ◽  
Micturition Reflex ◽  
Female Wistar Rats ◽  
Stimulation Of

5-Hydroxytryptamine (5-HT) receptors in the central nervous system have been implicated in the control of micturition. The present study was undertaken to evaluate the effects of a selective 5-HT1A-receptor antagonist { N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]- N-(2-pyridinyl)cyclohexanecarboxamide trihydrochloride (WAY100635)} on the micturition-reflex pathway in urethane-anesthetized female Wistar rats. Rhythmic isovolumetric bladder contractions evoked by bladder distension were abolished by 0.3- to 3-mg/kg iv or 30- to 100-μg intrathecal (it) administration of WAY100635 in a dose-dependent manner for periods of 3–15 min. Intrathecal injection of WAY100635 was effective only if injected at the L6-S1 spinal cord level, but not at the thoracic or cervical cord levels. WAY100635 (30–100 μg it) significantly reduced the amplitude of bladder contractions evoked by electrical stimulation of the pontine micturition center. However, the field potentials in the rostral pons evoked by electrical stimulation of pelvic nerve were not affected by intrathecal or intravenous injection of WAY100635. These results suggest that 5-HT1A receptors at the L6-S1 level of the spinal cord have an important role in the tonic control of the descending limb of the micturition-reflex pathway in the rat.

Spinal cord regulation of sympathetic activity in intact and spinal rats

1994 ◽  
Vol 266 (4) ◽  
pp. H1485-H1493 ◽  
Author(s):  
Y. Hong ◽  
D. F. Cechetto ◽  
L. C. Weaver
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Excitatory Amino Acid ◽  
Intrathecal Injection ◽  
Cardiovascular Responses ◽  
Homocysteic Acid ◽  
Arterial Blood ◽  
Cord Injury

Excitatory amino acid (EAA) and cholinergic neurotransmission in the spinal cord of urethan-anesthetized rats was investigated to assess mechanisms regulating sympathetic activity after spinal cord injury. Blockade of EAA transmission by intrathecal injection of kynurenic acid decreased arterial blood pressure by 24 +/- 4 mmHg, heart rate by 15 +/- 10 beats/min, and renal sympathetic nerve activity (RSNA) by 85 +/- 4% in intact rats. In rats with cervical spinal transections, this blockade decreased RSNA by 51 +/- 5% and had no effect on arterial pressure and heart rate. Muscarinic blockade by intrathecal atropine decreased RSNA by 12 +/- 3 and 32 +/- 6% in intact and spinal rats, respectively, and caused no cardiovascular responses in either group. Combined blockade of EAA and muscarinic receptors in spinal rats decreased RSNA by 77 +/- 1%. Intrathecal injections of the EAA agonist D,L-homocysteic acid in spinal rats caused initial increases (335 +/- 28%) in RSNA lasting approximately 3 min and later sustained increases (157 +/- 19%) lasting 36 +/- 8 min. Only the early excitation increased arterial pressure by 17 +/- 3 mmHg, and then pressure returned to baseline values. The EAA agonist kainic acid increased RSNA by 402 +/- 90% in spinal rats, an effect lasting 70 +/- 5 min, and increased arterial pressure by only 8 +/- 2 mmHg for 12 +/- 5 min. These findings suggest that tonic activity of spinal neurons with EAA and cholinergic receptors maintains tonic RSNA after spinal cord transection. However, this activity does not play a major role in maintaining arterial pressure, even if it is increased substantially by EAA receptor stimulation.

scholarly journals Dissociation by Chloralose of the Cardiovascular and Cerebrovascular Responses Evoked from the Cerebellar Fastigial Nucleus

1990 ◽  
Vol 10 (3) ◽  
pp. 375-382 ◽  
Author(s):  
Costantino Iadecola ◽  
Mary E. Springston ◽  
Donald J. Reis
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Initial Dose ◽  
Cardiovascular Responses ◽  
Fastigial Nucleus ◽  
Neural Pathways ◽  
Cerebrovascular Autoregulation ◽  
Brain And Spinal Cord ◽  
Stimulation Of

We studied the effects of chloralose anesthesia on the elevation in arterial pressure (AP), heart rate (HR), and regional CBF (rCBF) elicited by stimulation of the cerebellar fastigial nucleus (FN). Rats were anesthetized with an initial dose of chloralose (40 mg/kg s.c), paralyzed, and artificially ventilated. The FN was stimulated (50–100 μA, 50 Hz, 1 s on/1 s off) with microelectrodes stereotaxically implanted. During the stimulation AP was carefully maintained within cerebrovascular autoregulation. CBF was measured by the [14C]iodoantipyrine technique with regional dissection. In rats that received only the initial dose of chloralose, FN stimulation elevated rCBF in brain and spinal cord, up to 209 ± 13% of control in frontal cortex (n = 5; p < 0.01, analysis of variance). Administration of additional chloralose (10 mg/kg i.v., 30 min prior to measurement of CBF) did not affect resting rCBF (n = 5), the EEG, or the elevation in AP and HR elicited by FN stimulation (n = 4). However, the additional chloralose abolished the elevations in rCBF (n = 5; p > 0.05). Thus, the cerebrovasodilation elicited from the FN is more susceptible to the effects of additional anesthesia than the elevation in AP and HR. These results indicate that the cerebrovascular and cardiovascular responses elicited from the FN are functionally distinct and provide additional evidence for the notion that these responses are mediated by different neural pathways and transmitters.

N-Methyl-D-Aspartate Antagonist Inhibits NR-1 Subunit Phosphorylation of the Spinal N-Methyl-D-Aspartate Receptor Induced by Low Frequency Electroacupuncture

2007 ◽  
Vol 35 (06) ◽  
pp. 987-993 ◽  
Author(s):  
Byeol-Rim Kang ◽  
Chang-Beohm Ahn ◽  
Byung-Tae Choi
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Peripheral Nerves ◽  
Intrathecal Injection ◽  
Low Frequency ◽  
Serine Phosphorylation ◽  
Lumbar Spinal Cord ◽  
Aspartate Receptor ◽  
Lumbar Spinal ◽  
Stimulation Of

We investigated whether the 2 Hz electroacupuncture (EA) analgesia is associated with phosphorylation of N-methyl-D-aspartate receptor (NMDAR) NR-1 subunits and NMDAR antagonism in the lumbar spinal cord of rats. EA stimulation produced an increase of serine phosphorylation of NMDAR NR-1 subunits in the spinal cord as compared with normal conditions. However, the intrathecal injection of NMDAR antagonist D-2-amino-5-phosphonopentanoic acid significantly prevented serine phosphorylation of NMDAR NR-1 subunits induced by EA stimulation in the dorsal horn of spinal cord. These results indicate that EA analgesia by stimulation of peripheral nerves may be involved in an increase of NR-1 serine phosphorylation in the dorsal horn of the spinal cord.

Fastigial stimulation releases vasopressin in amounts that elevate arterial pressure

1983 ◽  
Vol 244 (5) ◽  
pp. H687-H694 ◽  
Author(s):  
A. Del Bo ◽  
A. F. Sved ◽  
D. J. Reis
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Stimulus Train ◽  
Specific Antagonist ◽  
6 Hydroxydopamine ◽  
Stimulation Of ◽  
Intact Rats

Electrical stimulation of the cerebellar fastigial nucleus (FN) in anesthetized, paralyzed, and artificially ventilated rat with a 10-s stimulus train (50 Hz) resulted in a stimulus-locked elevation in arterial pressure (AP) and heart rate, the fastigial pressor response (FPR). Blockade of autonomic effectors by chemosympathectomy (produced by treatment with 6-hydroxydopamine) combined with adrenalectomy, or by spinal cord transection at C1, abolished the FPR but unmasked an elevation of AP with longer latency (10-12 s) and duration (2-4 min), termed the residual FPR. The residual FPR was 1) abolished by midbrain transection, 2) blocked by administration of a specific antagonist of the vasopressor response to arginine vasopressin (AVP) [1,d(CH2)5Tyr(Me)AVP], and 3) was absent in homozygous and attenuated in heterozygous rats of the Brattleboro strain. FN stimulation elevated AVP threefold (from 13 +/- 1 to 38 +/- 8 pg/ml, P less than 0.02; n = 6) in intact rats and sevenfold in rats with combined chemosympathectomy and adrenalectomy (from 14 +/- 1 to 96 +/- 11 pg/ml, P less than 0.001; n = 9). Stimulation of the cerebellar FN can release AVP. In the absence of sympathoadrenal effectors, the amount so released is enhanced and capable of elevating AP.

Attenuating effects of intrathecal clonidine on the exercise pressor reflex

1991 ◽  
Vol 70 (2) ◽  
pp. 516-522 ◽  
Author(s):  
J. M. Hill ◽  
M. P. Kaufman
Keyword(s):  
Arterial Pressure ◽  
Intrathecal Injection ◽  
Muscular Contraction ◽  
Muscle Afferents ◽  
Ventilatory Responses ◽  
Exercise Pressor Reflex ◽  
Adrenergic Antagonist ◽  
Anesthetic Action ◽  
Intrathecal Clonidine ◽  
Stimulation Of

We tested the hypothesis that intrathecal injection of clonidine, an alpha 2-adrenergic agonist, attenuated the reflex cardiovascular and ventilatory responses to static muscular contraction in cats. Before clonidine (1 microgram in 0.2 ml), contraction-induced reflex increases (n = 10) in mean arterial pressure and ventilation averaged 25 +/- 3 mmHg and 359 +/- 105 ml/min, respectively, whereas after clonidine these increases averaged 8 +/- 4 mmHg and 200 +/- 114 ml/min, respectively (P less than 0.05). Clonidine had no effect on the heart rate response to contraction. Intrathecal injection of yohimbine (10 micrograms; n = 5), an alpha 2-adrenergic antagonist, but not prazosin (10 micrograms; n = 3), an alpha 1-adrenergic antagonist, prevented the attenuating effects of clonidine on the reflex pressor and ventilatory responses to contraction. Our findings were not due to the spread of clonidine to the medulla, because the reflex pressor and ventilatory responses to contraction were not attenuated by injection of clonidine (1 microgram) onto the medulla (n = 3). In addition, our findings were not due to a clonidine-induced withdrawal of sympathetic outflow, because intrathecal injection of clonidine (1 microgram) did not attenuate increases in arterial pressure and ventilation evoked by high-intensity electrical stimulation of the cut central end of the sciatic nerve (n = 5). Furthermore, our findings were not due to a local anesthetic action of clonidine, because application of this agent to the dorsal roots had no effect on the discharge of group IV muscle afferents. We conclude that stimulation of alpha 2-adrenergic receptors in the spinal cord attenuates the reflex pressor and ventilatory responses to static contraction.

Aortic baroreceptors play a predominant role in the regulation of hindlimb vascular resistance in rats

1994 ◽  
Vol 267 (2) ◽  
pp. R476-R480 ◽  
Author(s):  
B. H. Machado ◽  
L. G. Bonagamba ◽  
J. A. Castania ◽  
J. V. Menani
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Carotid Baroreceptor ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Freely Moving ◽  
Vascular Beds ◽  
Aortic Baroreceptors ◽  
Stimulation Of

In previous studies using bilateral carotid occlusion in conscious freely moving rats we suggested that aortic baroreceptors may play a more important role in the regulation of hindlimb than in renal and mesenteric vascular resistances. In the present study we performed electrical stimulation of the aortic baroreceptor nerve and analyzed the changes in mean arterial pressure and in hindlimb, renal, and mesenteric vascular resistances. All the experiments were performed under urethan anesthesia. Unilateral electrical stimulation (3 V, 2 ms, 50 Hz) of the aortic baroreceptor nerve produced a fall in arterial pressure (-27 +/- 3 mmHg) and an important reduction in hindlimb vascular resistance (-43 +/- 5%), with an increase in renal (+3 +/- 14%) and mesenteric (+48 +/- 12%) vascular resistances. Similar changes in arterial pressure as well as in the resistance of the three vascular beds studied were also observed during electrical stimulation of the aortic baroreceptor nerve in rats with bilateral carotid baroreceptor denervation or in rats treated with methylatropine. The data obtained with electrical stimulation indicated that aortic baroreceptors play a more important role in the regulation of blood flow in hindlimb than in renal and mesenteric vascular beds.

Inhibition of baroreflex vagal bradycardia by nasal stimulation in rats

1999 ◽  
Vol 276 (1) ◽  
pp. H176-H184 ◽  
Author(s):  
Masayoshi Kobayashi ◽  
Zhi Bin Cheng ◽  
Shoichiro Nosaka
Keyword(s):  
Spinal Cord ◽  
Adrenergic Receptor ◽  
Acetylcholine Release ◽  
Cardiovascular Regulation ◽  
Ringer Solution ◽  
Distilled Water ◽  
Nasal Application ◽  
Vagal Bradycardia ◽  
Prejunctional Inhibition ◽  
Stimulation Of

Nasal stimulation provokes hypertension and bradycardia. We report here that such stimulation inhibits baroreflex vagal bradycardia (BVB). In chloralose- and urethan-anesthetized, β-adrenergic receptor-blocked rats, the aortic depressor nerves were cut and electrically stimulated to induce BVB. Nasal application of smoke, warm distilled water, or cold or hot Ringer solution suppressed BVB, but application of warm Ringer solution did not. Smoke-induced inhibition was abolished by trigeminal but not olfactory denervation. Neither suprapontine decerebration nor C3 spinal cord transection affected the inhibition. Bradycardia induced by electrical stimulation of the peripheral cut end of the cervical vagus nerve (VIB) was suppressed by long-lasting smoke application. Intravenous prazosin, a proposed blocker of prejunctional inhibition of acetylcholine release from the vagus terminals, abolished VIB inhibition but attenuated BVB inhibition only slightly. Thus nasal stimulation inhibits BVB, and this inhibition is mediated exclusively by the trigeminal nerve and occurs principally at the pontomedullary level, although the potential exists for contribution of the prejunctional mechanism. The inhibition of BVB might contribute to cardiovascular regulation associated with protection from atmospheric hazards.

Microinjection of vasopressin into the locus coeruleus of conscious rats

1984 ◽  
Vol 247 (4) ◽  
pp. H675-H681 ◽  
Author(s):  
K. H. Berecek ◽  
H. R. Olpe ◽  
R. S. Jones ◽  
K. G. Hofbauer
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Locus Coeruleus ◽  
Neural Control ◽  
Cardiovascular Responses ◽  
Adrenergic Blockade ◽  
Central Action ◽  
Dose Injection ◽  
Stimulation Of

To determine whether vasopressin plays a role in central neural control of cardiovascular function by acting on the locus coeruleus we monitored arterial pressure and heart rate responses to graded injections of vasopressin (1-30 ng, 0.1-0.3 microliter) in the locus coeruleus of conscious, restrained rats. Cannulas were stereotaxically implanted in the locus coeruleus 2-5 days prior to experiment. Injections of vasopressin into the locus coeruleus produced dose-related increases in mean arterial pressure (12 +/- 2 to 57 +/- 6 mmHg) and heart rate (27 +/- 6 to 123 +/- 16 beats/min), which lasted over 1 h at the highest dose. Injection of the antipressor vasopressin antagonist d(CH2)5Tyr(Me) arginine vasopressin (10 ng) into the locus coeruleus blocked the cardiovascular responses to vasopressin. Administration of vasopressin into an area lateral to the locus coeruleus had no effect on mean arterial pressure but produced an increase in heart rate. Equivalent doses of saline, angiotensin II, and norepinephrine (NE) had minimal or opposite (NE) effects on arterial pressure and heart rate. Peripheral alpha-adrenergic blockade with phentolamine and beta-adrenergic blockade with propranolol blocked the cardiovascular responses to injection of vasopressin in the locus coeruleus. These results suggest that vasopressin may act in the region of the locus coeruleus to exert a central action on the cardiovascular system that is mediated by a stimulation of sympathetic outflow.

Sign in / Sign up

Export Citation Format

Share Document