Microinjection of substance P and ACh into rat intermediolateral nucleus elicits cardiovascular responses.
ABSTRACT The effects of substance P (SP) or acetylcholine (ACh) microinjected into the intermediolateral nucleus of the spinal cord (IMLn) on arterial pressure (AP) and heart rate (HR) were investigated in 22 male Wistar rats under urethan and artificial ventilation. L-Glutamate (Glu) was microinjected into the IMLn between C7 and T4 to locate cardiovascular sites. Micropipettes containing Glu were stereotaxically positioned in 82 histologically verified sites in the IMLn between C7 and T4 on both the right and left sides. Microinjection of 4-10 nl of 0.18 M Glu in 30 of 39 explored sites at the T2 level elicited significant increases in HR (+24.2 +/- 3.1 beats/min). These changes were accompanied by significant increases in mean AP (+11.4 +/- 1.2 mmHg) at the T2 level (32/47 sites). Microinjection of 4-10 nl of SP (3 X 10(-7) to 3 X 10(-4) M) or ACh (0.005-0.5 M) in the right IMLn at the T2 level elicited increases in HR but did not affect AP. The duration of the responses to SP or ACh was significantly longer than the duration of the responses to Glu. The responses to ACh could be blocked by prior microinjection of 5 X 10(-2) M atropine. No responses were ever obtained in the left IMLn by microinjection of Glu, SP, or ACh. These results support the hypothesis that Glu, ACh, and SP mediate sympathoexcitation in the IMLn of the rat and that these excitatory responses have different temporal patterns.
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ABSTRACT: The aim of this study was to determine which of the muscarinic receptor subtypes are involved in the modulation of the urethrogenital reflex (UGR) in male, spinal cord-transected rats. The electromyographic (EMG) responses of the bulbospongiosus muscle (BS) to the topical spinal application of muscarine and the combination of muscarine and the selective muscarine receptor antagonists methoctramine (M2), AFDX (M2), 4DAMP (M3) and tropicamide (M4) were determined before and after the elicitation of UGR by way of the mechanical stimulation of the urethra. When 50- and 100-mug doses of muscarine were applied without urethral stimulation, a rhythmic activity of the BS was observed, similar to the one found when UGR was evoked. The M3 and M4 - but not the M2 - antagonists prevented BS response to muscarine when urethral stimulation was not performed. When UGR was elicited following urethral stimulation muscarine produced an increase in burst duration and a decrease in burst frequency. The M2 antagonist reverted the effects of muscarine on the UGR, while the M3 and M4 antagonists produced a significant increase in the frequency and in the bursts number, when compared to the control muscarine response. The differences observed in BS responses to muscarine and muscarine antagonists before and after UGR elicitation were probably linked to the intrinsic effects of the endogenous acethylcholine (Ach) released after urethral stimulation. The present results suggest a cholinergic modulation of UGR in spinal cord-transected rats mediated by the M2, M3 and M4 muscarinic receptor subtypes.Pharmacology Biochemistry and Behavior 06/2005; 81(1):100-13. DOI:10.1016/j.pbb.2005.02.011 · 2.82 Impact Factor
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ABSTRACT: Sympathetic preganglionic neurons (SPNs), located in the intermediolateral cell column (IML) of the thoracolumbar spinal cord, contribute to the maintenance of arterial pressure (AP) and heart rate (HR) within normal limits under different physiological conditions. The purpose of this study was to examine the effects of microinjecting the putative inhibitory transmitters glycine (GLY) or gamma-amino-butyric acid (GABA) into functionally identified cardioacceleratory and vasoconstrictor IML sites at T1-T3. Rats were anesthetized (1.4 g/kg urethane i.p.), paralysed with decamethonium bromide (3.3 mg/kg i.v.) and artificially ventilated. Glutamate (GLU) microinjection (10-20 nl, pH = 7.4, 0.15 M in phosphate-buffered saline (PBS)) was used to identify 29 vasoconstrictor sites, of which 23 were also cardioacceleratory, in the right side of the T2 segment. GLY microinjection (10-20 nl, pH = 7.4, 0.5 M in PBS) into these sites resulted in significant decreases in both AP (n = 18) and HR (n = 14). The AP and HR responses to GLY were brief in duration and were attenuated by the specific GLY antagonist strychnine (STR). Microinjection of GABA (10-20 nl, pH = 7.4, 0.15-0.84 M in PBS, n = 6) and its agonist muscimol (10-20 nl, pH = 7.4, 0.9 mM in PBS, n = 6) into GLU-identified sites in the IML caused no changes in AP or HR. However, after the application of either GABA or muscimol, the changes in AP or HR elicited by GLU were eliminated, suggesting that GABA and muscimol decrease the excitability of SPNs.(ABSTRACT TRUNCATED AT 250 WORDS)Brain Research 02/1994; 634(1):13-9. DOI:10.1016/0006-8993(94)90253-4 · 2.83 Impact Factor
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ABSTRACT: Afferent renal nerves (ARN) have been implicated in the development of one-kidney renal wrap (1K-WRAP) hypertension. The role of renal nerves in desoxycorticosterone acetate-salt (DOCA) hypertension, a low-renin model of hypertension, is controversial. The present study was designed to determine if spinal substance P (SP) and/or calcitonin gene-related peptide (CGRP) in ARN affects the development of 1K-WRAP or DOCA hypertension in adult rats. Selective long-term partial depletion of spinal SP and CGRP within small primary afferent nerve fibers including unmyelinated ARN was achieved by intrathecal administration of capsaicin. After capsaicin treatment, 1K-WRAP hypertension was induced by removing the right kidney and wrapping the left kidney with a figure-8 ligature. In a second group of rats, DOCA hypertension was induced by subcutaneous application of desoxycorticosterone pellets after unilateral nephrectomy. Systolic arterial pressure was monitored for 8 weeks by tail cuff plethysmography after which direct blood pressure measurement was performed followed by immunohistochemistry. Intrathecal capsaicin administration had no significant effect on SP-ir and CGRP-ir of ARN soma located within thoracic dorsal root ganglia whereas immunoreactivity against these peptides was reduced by one third to one half in the dorsal horn, indicating effective long-term spinal depletion of these neuropeptides. Intrathecal capsaicin enhanced the development of 1K-WRAP hypertension, since arterial pressure was greater in the treated group. In contrast, DOCA hypertension was unaffected by capsaicin pretreatment. Considering the neurotoxic action of capsaicin for SP-ir and CGRP-ir unmyelinated primary afferent neurons, we hypothesize that spinal SP, CGRP and/or related peptides existing in ARN and other capsaicin-sensitive unmyelinated primary afferent neurons in the lower thoracic spinal cord may ameliorate 1K-WRAP hypertension, but not DOCA hypertension.Journal of the Autonomic Nervous System 01/1995; 50(2):189-99. DOI:10.1016/0165-1838(94)90009-4