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W T Talman

Publications and source records attributed to W T Talman.

72 records · Page 4Linked to original sources
PubMed1984

Modulation of cardiovascular and electrocortical activity through serotonergic mechanisms in the nucleus tractus solitarius of the rat.

The nucleus tractus solitarius (NTS) is an integral part of the baroreceptor reflex arc. Thus, stimulation of the NTS elicits changes in arterial pressure and heart rate as well as in numerous other physiologic parameters including electrocortical activity. Serotonin (5-HT), which has been implicated in cardiovascular and electrocortical control, is present in nerve terminals within the NTS. Therefore, this study was designed to determine whether 5-HT may effect that control within the NTS. Serotonin injected into the NTS of anesthetized rats produced marked changes in the EEG, arterial pressure, and heart rate. EEG activity changed from irregular 1-5 Hz, 350-500 microV waves with an overlying 13-15 Hz, low voltage rhythm to a regular, 5 Hz, 250-300 microV rhythm. The dose-dependent cardiovascular changes were maximal at a dose of 400 pmol which produced a fall of mean arterial pressure of 48 +/- 2 mm Hg from a baseline of 96 +/- 4 mm Hg and of heart rate of 90 +/- 9 bpm from a baseline of 400 +/- 18 bpm (n = 6; P less than 0.001). Both the cardiovascular and EEG effects of 5-HT injected into the NTS were blocked by the prior injection of the 5-HT antagonist metergoline at the same site. However, the bilateral microinjection of metergoline into the NTS did not affect the baroreceptor reflex. Thus, although serotonergic mechanisms in the NTS may be involved in the modulation of electrocortical and cardiovascular activity, they are not integral to the baroreceptor reflex arc.

Animals↗
PubMed1984

Glutamatergic mechanisms in the nucleus tractus solitarius in blood pressure control.

The nucleus tractus solitarius (NTS), the site of termination of visceral afferents of the ninth and tenth cranial nerves, mediates and integrates the reflex cardiovascular and noncardiovascular responses to stimulation of cardiopulmonary and other visceral afferents. On injection into the NTS, the amino acid L-glutamate (L-Glu) and its excitatory analogs produce dose-dependent hypotension and bradycardia, a baroreceptor reflex-like response. The L-Glu antagonist glutamate diethyl ester blocks the response both to L-Glu and to baroreceptor reflex activation. Electrical stimulation of vagal c-fibers selectively releases 3H into a push-pull cannula after preloading of the NTS with L-[3H]Glu or D-[3H]aspartate. The NTS contains a high-affinity uptake system for inactivation of L-Glu. Like L-Glu, acetylcholine and serotonin, which are also found in the NTS, both elicit a baroreceptor reflex-like response when microinjected into the NTS. However, cholinergic and serotonergic antagonists do not block the baroreceptor reflex. A glutamatergic neuron (or neurons) projecting into NTS appears to be an integral part of the baroreceptor reflex arc.

Acetylcholine↗
PubMed1983

Ricin transport distinguishes between central and peripheral neurons.

Ricin conjugated to horseradish peroxidase was retrogradely transported by peripheral neurons of the nodose ganglion after microinjection into the nucleus tractus solitarius but was not transported by central neurons projecting to the nucleus tractus solitarius. Similarly, ricin was not transported by central neurons projecting to the caudate nucleus. Differences in labeling of central and peripheral neurons with ricin may reflect differences in surface glycoconjugates on processes of these neurons.

Animals↗
PubMed1983

Cholinergic mechanisms in the nucleus tractus solitarii and cardiovascular regulation in the rat.

To determine the role played by cholinergic neurons in cardiovascular regulation by the nucleus tractus solitarii (NTS), microinjections (0.1 microliter) of acetylcholine (ACh) or carbachol (C) were made into the NTS of rats, and the changes in arterial pressure and heart rate were recorded. The dose-dependent hypotension and bradycardia which resulted were mediated by the activation of muscarinic, but not nicotinic, receptors confined to the NTS. Blockade of muscarinic receptors bilaterally in the NTS resulted in mild hypertension and attenuated, but did not abolish, the baroreceptor reflex. Eserine, injected into the NTS, augmented and prolonged the action of acetylcholine and slightly increased the maximal baroreceptor reflex response. Thus, cholinergic mechanisms in the NTS tend tonically to lower arterial pressure and may modulate the baroreceptor reflex, without being an integral part of the reflex arc.

Acetylcholine↗
PubMed1981

Baroreflex actions of substance P microinjected into the nucleus tractus solitarii in rat: a consequence of local distortion.

Biologically active substance P (SP) (1000 ng in 0.1 microliter saline) microinjected into the nucleus tractus solitarii (NTS) of 25 rats did not affect arterial pressure, heart rate, or the baroreceptor reflex. However, microinjection of saline alone in volumes greater than 0.3 microliter consistently elicited hypotension and bradycardia followed occasionally by transient hypertension. These data suggest that previously reported cardiovascular effects of SP microinjected into the NTS resulted from local distortion.

Afferent Pathways↗
PubMed1981

Antagonism of the baroreceptor reflex by glutamate diethyl ester, an antagonist to L-glutamate.

Recent reports have suggested that the excitatory amino acid L-glutamate is a neurotransmitter released by baroreceptor afferent nerves at their termination in the nucleus tractus solitarii (NTS). In this study we have examined the effect on arterial pressure, heart rate and baroreflex activity of the glutamate antagonist glutamate diethyl ester (GDEE) microinjected into the NTS of 50 rats anesthetized with Chloralose. Bilateral injections of GDEE produced dose dependent transient hypertension. The threshold dose was 2.5 micrograms/NTS and at a dose of 15 micrograms/NTS a maximal rise in arterial pressure and heart rate (from 95 +/- 8.7 mm Hg to 153 +/- 6.4 mm Hg and from 322 +/- 14.7 beats/min to 364 +/- 16.2 beats/min respectively, P less than 0.001, n = 6) occurred. A dose of 15 micrograms/NTS also completely blocked the baroreflex when injections were made bilaterally and it totally antagonized the cardiovascular effects of L-glutamate when injected immediately prior to L-glutamate. The hypertension, the antagonism of L-glutamate, and the blockade of the baroreflex persisted for 20-30 min. In that L-glutamate mediates a baroreflex-like response upon injection into NTS and in that GDEE blocks that response while at the same time blocking the naturally occurring baroreflex, the data are consistent with L-glutamate being a neurotransmitter of baroreflex afferents.

Afferent Pathways↗
PubMed1981

Evidence that glutamic acid is the neurotransmitter of baroreceptor afferent terminating in the nucleus tractus solitarius (NTS).

The possibility that L-glutamic acid (L-Glu) might be the neurotransmitter of baroreceptor afferents terminating in the nucleus tractus solitarius (NTS) and affecting activity of the autonomic nervous system was tested using a variety of techniques. Effects on blood pressure and heart rate of microinjections of L-Glu and antagonists into the NTS supported this contention. Use of blocking agents was confirmatory. Biochemical studies provided evidence that the agent (glutamic acid) is synthesized, stored and reaccumulated in these nerve endings. Furthermore, it was shown that L-Glu is released from the NTS in vivo. Degeneration of afferent terminals due to removal of the nodose ganglia reduced L-Glu levels in the NTS. After discussion of this and additional evidence that L-Glu is the transmitter and a consideration of reasons for eliminating other possibilities (substance P, etc.) it was concluded that L-glutamic acid is the neurotransmitter of baroreceptor afferents.

Afferent Pathways↗
PubMed1981

Acute hypertension after the local injection of kainic acid into the nucleus tractus solitarii of rats.

Kainic acid (KA), an analogue of L-glutamate, was microinjected in 0.1 microliter of saline into the nucleus tractus solitarii (NTS) of adult rats. In rats anesthetized with halothane or alpha-chloralose, KA injected unilaterally elicited hypotension, bradycardia, and apnea. The threshold dose was 0.1-0.2 ng (10(-13) mol). Doses greater than 0.2 ng blocked responses to subsequent injections for at least 30 minutes. Doses of KA greater than 15 ng reduced the reflex bradycardia elicited by raising the arterial pressure with phenylephrine and produced arterial hypertension in rats anesthetized with alpha-chloralose or in other rats within 15 minutes of terminating halothane anesthesia. Bilateral injection of KA in doses greater than 15 ng completely blocked baroreflexes and resulted in a dose-dependent elevation of arterial pressure (167 +/- 9.4; P less than 0.001) both in alpha-chloralose-anesthetized rats and in awake rats after the termination of halothane anesthesia. The hypertension rapidly led to pulmonary edema and death. Procaine microinjected also elicited fulminating hypertension; vehicle did not. Doses of KA producing hypertension caused no histological or biochemical evidence of neuronal death. The cardiovascular responses to KA were restricted to sites in the intermediate one-third of NTS and could not be elicited by injection into adjacent sites in brainstem. The results indicate that, in low doses, KA injected into NTS stimulates neurons which mediate the baroreflex, whereas, in higher doses, it produces baroreflex blockade and neurogenic hypertension. The results suggest that fulminating hypertension can be produced by nondestructive perturbations of neurochemical transmission in brain. Since the cardiovascular responses of KA are similar to those produced by microinjection into NTS of the amino acid neurotransmitter glutamic acid, the study adds further support to the hypothesis that L-glutamate is the neurotransmitter released by baroreceptor afferent nerves.

Acute Disease↗
PubMed1980

Evidence for L-glutamate as the neurotransmitter of baroreceptor afferent nerve fibers.

Microinjection of L-glutamate into the intermediate nucleus tractus solitarii in anesthetized rats elicits hypotension, bradycardia, and apnea, simulating baroreceptor reflexes. Ablation of the nodose ganglion results in selective reduction of high-affinity uptake of L-glutanate in the nucleus tractus solitarii. L-Glutamate may be the neurotransmitter of afferent nerve fibers from arterial baroreceptors.

Afferent Pathways↗
PubMed1980

A hierarchical organization of blood pressure during natural behaviour in rat and the effects of central catecholamine neurons thereon.

1. Changes in arterial pressure associated with a repertoire of natural behaviour patterns in the rat were examined. 2. A hierarchy of such changes was found. Eating and drinking were associated with higher pressures than grooming and exploration, which in turn were associated with higher pressures than resting. 3. Desynchronized sleep was associated with higher pressures than slow-wave sleep. 4. Lesions of the catecholamine neurons of the A2 region of the medulla did not disrupt the normal hierarchy but resulted in an exaggerated pressor response.

Animals↗
PubMed1980

Chronic lability of arterial pressure in the rat does not evolve into hypertension.

1. In rats, electrolytic lesions of the A2 group of catecholamine neurons result in lability of arterial pressure without hypertension. 2. To establish whether labile arterial pressure, when chronic, will lead to fixed hypertension, we placed lesions in the A2 area of adult male Sprague-Dawley rats and measured mean arterial pressure, heart rate and their variability (expressed as the standard deviation) 11 months later. Controls were age-matched, unoperated or sham-operated rats. 3. In rats with A2 lesions: (a) the mean arterial pressure was lower (103 +/- 7.5 mmHg; n = 6; P < 0.05) than in sham-operated (123 +/- 4.7 mmHg; n = 4) or unoperated (120 +/- 3.1 mmHg; n = 9) controls; (b) the standard deviation of mean arterial pressure was higher (16 +/- 1.8 mmHg; P < 0.001) than in sham-operated (5 +/- 0.7 mmHg) or unoperated controls (7 +/- 0.6 mmHg); (c) the mean and standard deviation of heart rate did not differ between groups. No histopathological changes were detected in the A2 group. 4. Chronic lability of arterial pressure does not evolve into sustained hypertension nor does it induce systemic lesions.

Animals↗
PubMedDate not supplied

Centrally administered bombesin modulates gastric motility.

Intracerebroventricular bombesin alters arterial pressure and gastrointestinal transit in rats. In order to evaluate the influence of bombesin on arterial and gastric intraluminal pressure in a specific site in the central nervous system, we microinjected bombesin into the medial subnucleus of the nucleus tractus solitarius (mNTS) in 28 rats anesthetized with choralose. Bombesin (78 pmole in 25 nl), but not vehicle, caused an increase of tonic gastric intraluminal pressure (2.6 +/- 0.5 cm H2O) and of phasic gastric intraluminal pressures but did not acutely alter arterial pressure. The effect on tonic and phasic gastric intraluminal pressure was dose-dependent. The threshold dose was 7.8 pmole. Intravenous bombesin caused a similar dose-dependent rise in tonic gastric intraluminal pressure but did not significantly change the mean amplitude of phasic gastric intraluminal pressures. Transection of the cervical spinal cord and both cervical vagus nerves blocked the effect of centrally but not peripherally administered bombesin. We conclude that bombesin microinjected into the mNTS does not influence arterial pressure but does raise tonic and phasic gastric intraluminal pressures. Bombesin may act in the NTS as a central modulator of gastric motility.

Animals↗
PubMedDate not supplied

Vasopressin contributes to hypertension caused by nucleus tractus solitarius lesions.

Lesions of the nucleus tractus solitarius (NTS) were studied to determine whether they elevate plasma vasopressin levels and, if so, whether these elevated levels of vasopressin contribute to the hypertension caused by NTS lesions. Bilateral electrolytic lesions of the NTS caused acute, severe hypertension in rats anesthetized with chloralose and in conscious, freely moving rats. After placement of the NTS lesions there was a greater than tenfold elevation in plasma vasopressin levels. Administration of an antagonist of the vasoconstrictor action of vasopressin markedly diminished the hypertension in both conscious and anesthetized rats. Following ganglionic blockade with chlorisondamine, NTS lesions still elicited hypertension, and the magnitude of the hypertension was not different from that observed in rats not treated with chlorisondamine. The hypertension produced by lesions of the NTS in ganglionic-blocked rats was completely abolished by administration of a vasopressin antagonist. These results indicate that (1) NTS lesions elevate plasma vasopressin levels and (2) elevated plasma vasopressin contributes to the hypertension produced by such lesions.

Animals↗
PubMedDate not supplied

Transient ischemic attacks associated with hypotension in hypertensive patients with carotid artery stenosis.

In a group of 132 patients with transient ischemic attacks ((TIAs) 7 patients (4 men, 3 women, ages 64 to 81) had TIAs preceded by hypotension. The average fall of mean blood pressure during an attack was 26.4 +/- 5.5 mm Hg (SD). Only one of these patients had a TIA which was not preceded by hypotension. This episode occurred during a paroxysm of coughing. All 7 of these patients had hypertension, and cerebral arteriography performed in 4 of the 7 revealed hemodynamically significant carotid artery stenosis. Each of the 4 patients developed hypotension and a TIA after the procedure. Twenty of the other patients had hypotensive episodes but did not develop focal neurological deficits. None of these patients had carotid artery stenosis. This study suggests that hypertensive patients with carotid artery stenosis may be at risk to develop focal cerebral ischemia during acute hypotensive episodes.

Aged↗