Cardiorespiratory effects of DL-homocysteic acid in caudal ventrolateral medulla

Bonham, Ann C.; Jeske, I

doi:10.1152/ajpheart.1989.256.3.h688

Cited by 45 publications

(30 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…18 It has been shown that intracerebroventricular injection of Ang II produces an increase in norepinephrine turnover in the Al area, 19 which raises the possibility that the depressor effects of Ang II could be mediated by an increase in the activity of Al cells. On the other hand, a recent study in the rat 20 indicated that excitation of Al cells does not produce a depressor response. Thus, despite the evidence that there is an interaction between central Ang II and brain catecholamine systems, 19 -21 the depressor effect produced by Ang II in the caudal VLM may be due to an action on non-Al cells.…”

Section: Discussionmentioning

confidence: 90%

Tonic cardiovascular effects of angiotensin II in the ventrolateral medulla.

1990

View full text Add to dashboard Cite

The rostral and caudal parts of the ventrolateral medulla play a major role in the control of blood pressure. Both regions contain a high density of receptor binding sites for angiotensin II, and it has been shown previously that microinjection of angiotensin II into the rostral ventrolateral medulla causes a rise in blood pressure. The aims of this study were to determine the cardiovascular effects of microinjection of angiotensin II and its specific antagonist T here is considerable evidence that angiotensin II (Ang II) in the brain may play a role in hypertension. For example, it is well established that Ang II can influence fluid and electrolyte balance and arterial blood pressure via an action on circumventricular organs and the nucleus tractus solitarius (for review, see Reference 1). Recently, it has also been demonstrated that microinjection of Ang II into sites within the rostral part of the ventrolateral medulla (VLM) or application of the peptide to the nearby ventral surface results in an increase of blood pressure. -3 Furthermore, the sites at which Ang II microinjection produces the largest pressor responses correspond very closely to the location of Ang II receptor binding sites.2 These sites are confined to a highly localized region referred to as the subretrofacial nucleus, which contains sym-

show abstract

Section: Discussionmentioning

confidence: 90%

Tonic cardiovascular effects of angiotensin II in the ventrolateral medulla.

1990

View full text Add to dashboard Cite

show abstract

“…The vast majority of morphological and electrophysiological lines of evidence suggest that cVRG expiratory neurons probably are not involved in the respiratory rhythmogenesis since they do not have axon collaterals and therefore connections with other medullary respiratory neurons (Merrill 1979;Von Euler 1986;Huang and St John 1988;Bianchi et al, 1995;Iscoe 1998). However, activation of cVRG neurons through microinjections of EAA receptor agonists caused transient inhibition of inspiratory activity in cats (Bongianni et al, 1994), rats (Bonham and Jeske 1989;Chitravanshi and Sapru 1999) and rabbits (Bongianni et al, 2005). Actually, microinjections of the broad-spectrum EAA receptor agonist D,Lhomocysteic acid (DLH) into the cVRG of the cat provoked the activation of expiratory motoneurons and a corresponding silent period in phrenic nerve activity (Bongianni et al, 1994).…”

Section: Caudal Ventral Respiratory Group (Nucleus Retroambigualis)mentioning

confidence: 99%

Brainstem mechanisms underlying the cough reflex and its regulation

Mutolo

2017

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

A B S T R A C TCough is a very important airway protective reflex. Cough-related inputs are conveyed to the caudal nucleus tractus solitarii (cNTS) that projects to the brainstem respiratory network. The latter is reconfigured to generate the cough motor pattern. A high degree of modulation is exerted on second-order neurons and the brainstem respiratory network by sensory inputs and higher brain areas. Two medullary structures proved to have key functions in cough production and to be strategic sites of action for centrally active drugs: the cNTS and the caudal ventral respiratory group (cVRG). Drugs microinjected into these medullary structures caused downregulation or upregulation of the cough reflex. The results suggest that inhibition and disinhibition are prominent regulatory mechanisms of this reflex and that both the cNTS and the cVRG are essential in the generation of the entire cough motor pattern. Studies on the basic neural mechanisms subserving the cough reflex may provide hints for novel therapeutic approaches. Different proposals for further investigations are advanced.

show abstract

“…Effect of CVLM microinjection of ANG- (1)(2)(3)(4)(5)(6)(7) and ANG II on baroreflex sensitivity. Unilateral microinjection of ANG-(1-7) into the CVLM produced a significant decrease in MAP (baseline MAP ϭ 110 Ϯ 6 mmHg, ⌬MAP ϭ Ϫ11 Ϯ 1.5 mmHg, n ϭ 10) that was similar to the decrease produced by ANG II (baseline MAP ϭ 99 Ϯ 5 mmHg, ⌬MAP ϭ Ϫ11 Ϯ 1.9 mmHg, n ϭ 13).…”

Section: Effect Of Rvlm Microinjection Of Ang-(1-7)mentioning

confidence: 99%

“…Peripheral mechanism involved in the baroreflex modulatory effects induced by microinjection of ANG- (1)(2)(3)(4)(5)(6)(7) or ANG II into the CVLM. We next evaluated the contribution of the parasympathetic tonus to the modulatory effect of the ANG peptides at the CVLM on the baroreflex control of HR.…”

Section: Effect Of Rvlm Microinjection Of Ang-(1-7)mentioning

confidence: 99%

Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla

Alzamora¹,

Santos²,

Campagnole‐Santos³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

-We determined the effect of microinjection of ANG-(1-7) and ANG II into two key regions of the medulla that control the circulation [rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively)] on baroreflex control of heart rate (HR) in anesthetized rats. Reflex bradycardia and tachycardia were induced by increases and decreases in mean arterial pressure produced by intravenous phenylephrine and sodium nitroprusside, respectively. The pressor effects of ANG-(1-7) and ANG II (25 pmol) after RVLM microinjection (11 Ϯ 0.8 and 10 Ϯ 2 mmHg, respectively) were not accompanied by consistent changes in HR. In addition, RVLM microinjection of these angiotensin peptides did not alter the bradycardic or tachycardic component of the baroreflex. CVLM microinjections of ANG-(1-7) and ANG II produced hypotension (Ϫ11 Ϯ 1.5 and Ϫ11 Ϯ 1.9 mmHg, respectively) that was similarly not accompanied by significant changes in HR. However, CVLM microinjections of angiotensins induced differential changes in the baroreflex control of HR. ANG-(1-7) attenuated the baroreflex bradycardia (0.26 Ϯ 0.06 ms/mmHg vs. 0.42 Ϯ 0.08 ms/mmHg before treatment) and facilitated the baroreflex tachycardia (0.86 Ϯ 0.19 ms/mmHg vs. 0.42 Ϯ 0.10 ms/mmHg before treatment); ANG II produced the opposite effect, attenuating baroreflex tachycardia (0.09 Ϯ 0.06 ms/mmHg vs. 0.31 Ϯ 0.07 ms/mmHg before treatment) and facilitating the baroreflex bradycardia (0.67 Ϯ 0.16 ms/mmHg vs. 0.41 Ϯ 0.05 ms/mmHg before treatment). The modulatory effect of ANG II and ANG-(1-7) on baroreflex sensitivity was completely abolished by peripheral administration of methylatropine. These results suggest that ANG II and ANG-(1-7) at the CVLM produce a differential modulation of the baroreflex control of HR, probably through distinct effects on the parasympathetic drive to the heart. baroreflex control of heart rate; renin-angiotensin system; arterial pressure THE BARORECEPTOR AFFERENTS terminate primarily in the intermediate portion of the nucleus of the solitary tract (NTS) subjacent to the area postrema in the dorsal medulla (15, 32). Although many brain stem and forebrain regions participate in the modulation of the sympathetic and parasympathetic outflows, regions inside the ventrolateral medulla (VLM) are essential for the effectiveness of the baroreceptor reflex (32). The caudal VLM (CVLM) has been functionally defined as a tonically active sympathoinhibitory vasodepressor region (15,32,44) that contains a synaptic relay within the baroreflex circuit, connecting the NTS to a site on the sympathoexcitatory reticulospinal neurons, the rostral VLM (RVLM). The RVLM is known to play an essential role in the tonic and reflex control of sympathetic vasomotor tone (15, 32). Two groups of cardiovascular neurons have been functionally defined in the CVLM: neurons that relay baroreflex inputs from the NTS to the RVLM and neurons that are insensitive to the baroreflex input (14, 44). In addition, the CVLM depressor response, in part, is associated with vagally mediated decrease in h...

show abstract

Cardiorespiratory effects of DL-homocysteic acid in caudal ventrolateral medulla

Cited by 45 publications

References 0 publications

Tonic cardiovascular effects of angiotensin II in the ventrolateral medulla.

Tonic cardiovascular effects of angiotensin II in the ventrolateral medulla.

Brainstem mechanisms underlying the cough reflex and its regulation

Baroreflex modulation by angiotensins at the rat rostral and caudal ventrolateral medulla

Contact Info

Product

Resources

About