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Catecholamines administered intracerebroventricularly (i.c.v.) have cardiovascular effects mediated by the CNS. Although hypotension constitutes the more prominent response, an increase in blood pressure has also been reported after the intracerebroventricular injection of these amines. Anaesthesia interferes with pressor responses mediated by the CNS to a larger extent than with depressor mechanisms and constitutes one of the major factors influencing the pattern of response to the amines. The depressor response observed after the intracerebroventricular administration of noradrenaline is reversed into increases in blood pressure in awake animals. In the present experiment, the action of intracerebroventricularly injected noradrenaline was compared in anaesthetized and conscious rats. The results indicated that the pressor response in awake rats was not mediated by the sympathetic nervous system and involved the release of a pituitary humoral-factor, most probably vasopressin, whereas the depressor response observed in anaesthetized animals was not dependent on pituitary mediation. The involvement of histaminergic mechanisms in the CNS in the control of the pressor response to intracerebroventricularly administered noradrenaline in the rat is proposed.
Peristaltic reflex activity in the guinea-pig isolated ileum was elicited by slow intraluminal infusion of Tyrode solution. The reflex was abolished by the ganglionic blocking drug hexamethonium. However, in more than half of the preparations, the peristaltic reflex was restored by the opioid antagonist naloxone. Hexamethonium-resistant peristaltic waves were blocked by tetrodotoxin or atropine. These data suggest that ganglionic transmission through nicotinic acetylcholine receptors may not be essential for the peristaltic reflex provided that the inhibitory action of endogenous opioids has been eliminated.
The influence of nicotinic transmission in the interpeduncular nucleus of the ventral midbrain on recovery from general anesthesia (3% halothane in oxygen) was assessed in rats. Immediately upon withdrawal of the anesthetic, nicotine (2 microliters, 10(-5) to 10(-1) M) was injected into the interpeduncular nucleus. Larger doses of nicotine (10(-2) and 10(-1) M) significantly (P < 0.05) prolonged the recovery of righting reflexes (to 371 +/- 55 and 362 +/- 67 sec, respectively, mean +/- SE), compared with injection of saline (187 +/- 19 sec). Prior intramuscular administration of the nicotinic antagonist, mecamylamine (2 mg/kg) significantly reduced the effect of 10(-2) M nicotine (to 211 +/- 43 sec). Injection of the nicotinic antagonist, hexamethonium (10(-1) M) led to a low mean recovery time (181 +/- 21 sec), not significantly different from control. Prolongation of recovery by 10(-2) M nicotine was not found to be significant when sites more dorsal to the interpeduncular nucleus were injected. An observed tendency for injection of nicotine to slow the post-anesthesia rate of breathing was not statistically significant and not correlated anatomically with the injection site in the midbrain. Increased release of acetylcholine has been shown previously to occur in the interpeduncular nucleus during anesthesia. The present results suggest that nicotinic activation of the interpeduncular nucleus facilitates or sums with the mechanisms in the brain that produce anesthesia under halothane.
Injections of acetylcholine (ACh) into the lateral septal area (LSA) caused blood pressure increases in unanesthetized freely moving rats. ACh was injected in the dose range of 0.1-54 nmol/500 nl using regular metal needles (200 microns o.d.). In the LSA, injections of carbachol or ACh (2.5 nmol/500 nl) were equipotent (+22 +/- 2 and +19 +/- 3 mmHg, respectively) suggesting the existence of an ACh-sensitive pressor site in the LSA. Maximum responses to ACh injected either intracerebroventricularly (i.c.v.) or into the LSA were not significantly different (+23 +/- 1 and +21 +/- 2 mmHg, respectively). However, the ED50 for the injection into the LSA (0.24 nmol) was significantly lower than that observed after i.c.v. injection (2.6 nmol), ruling out a possible leakage of ACh from the LSA and into the ventricular space. This idea is supported by data showing that the effect of the intraseptal injection of 30 nmol of ACh was blocked by pretreatment with 3 nmol of atropine either i.c.v. or into the LSA, whereas the effects of i.c.v. ACh were completely blocked by i.c.v. atropine, but only partially (42%) when atropine was injected into the LSA. The idea of the existence of an ACh-sensitive site in the LSA is further supported by the more direct observation that injections of 30 nmol/100 nl of ACh into the LSA using glass needles (50-70 microns o.d.) caused similar pressor responses. Neither the i.v. pretreatment with pentolinium or adrenalectomy affected the response to 30 nmol/500 nl of ACh injected into the LSA, ruling out the involvement of the sympathetic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)
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We studied the effects of prostaglandin E2 (PGE2) on the contractile responses of in vitro guinea pig tracheal preparations with intact vagal innervation. The preparation was stimulated either through the vagal nerves (NS) or with an electrical field (EFS) and trachealis response was assessed from the pressure change inside the tracheal tube. Ganglionic blockade by hexamethonium inhibited responses to NS but did not affect EFS while both responses to NS and EFS were abolished by atropine or tetrodotoxin. This indicates that responses to both stimulation modalities were mediated by cholinergic nerves but that NS involved a ganglionic relay whereas EFS did not. Within the frequency range of 0.1-20 Hz, there was a gradual increase in the pressure generated by the trachealis muscle with increasing frequency of stimulation. The frequency-response relationship was similar for NS and EFS. Thus, the ganglion does not appear to play an important filtering or amplifying role under those conditions. PGE2 (1-50 mM) produced a concentration-dependent inhibition of NS and EFS without affecting responses to exogenous acetylcholine (ACh). This suggests that the main action of PGE2 is to reduce ACh release from post-ganglionic nerve terminals. PGE2 inhibited EFS to a larger extent than NS; we postulate a possible excitatory effect of PGE2 on neurotransmission in the airway ganglia.
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