Identification of carotid vascular receptors that control adrenal catecholamine secretion in dogs

1992 ◽  
Vol 262 (5) ◽  
pp. R872-R878
Author(s):  
W. C. Engeland ◽  
C. D. Zippe ◽  
D. S. Gann
Keyword(s):  
Carotid Sinus ◽  
Carotid Occlusion ◽  
Catecholamine Secretion ◽  
Adrenal Vein ◽  
Carotid Baroreceptors ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Reflex Control ◽  
Adrenal Secretion

The role of carotid sinus and thyrocarotid mechanoreceptors in the reflex control of adrenal medullary function was assessed in anesthetized dogs with adrenal vein catheters. Dogs underwent carotid sinus, thyrocarotid junction, combined carotid sinus and thyrocarotid junction, or sham denervation. On the day after surgery, catecholamine secretion was measured after carotid occlusion proximal to the thyrocarotid junction, cervical vagotomy, and repeat carotid occlusion, each separated by 90 min. After combined carotid denervation, baseline norepinephrine secretion was increased, resulting in a decreased epinephrine-to-norepinephrine ratio. Carotid occlusion before vagotomy did not change the secretion of catecholamines or the epinephrine-to-norepinephrine ratio. After sham carotid denervation, acute vagotomy did not affect catecholamine secretion. However, after denervation of the carotid sinus or thyrocarotid junction, vagotomy resulted in small increases in catecholamine secretion without changing the epinephrine-to-norepinephrine ratio; the magnitude of the response was augmented after combined denervation. At 90 min after vagotomy in dogs with intact carotid baroreceptors, carotid occlusion increased adrenal secretion of catecholamines and decreased the epinephrine-to-norepinephrine ratio. After denervation of carotid sinus or thyrocarotid junction receptors, carotid occlusion increased secretion of catecholamines without changing the epinephrine-to-norepinephrine ratio; the response was abolished by combined denervation. These results show that both carotid sinus and thyrocarotid receptors contribute to the adrenomedullary response to carotid occlusion and to acute vagotomy. Also, reduction in the activity of carotid sinus and thyrocarotid junction receptors chronically (by denervation) or acutely (by carotid occlusion) results in preferential secretion of norepinephrine over epinephrine.

Mechanical role of expiratory muscles during breathing in upright dogs

1988 ◽  
Vol 64 (3) ◽  
pp. 1060-1067 ◽  
Author(s):  
G. A. Farkas ◽  
R. E. Baer ◽  
M. Estenne ◽  
A. De Troyer
Keyword(s):  
Tidal Volume ◽  
Progressive Increase ◽  
Substantial Contribution ◽  
Postural Changes ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Expiratory Muscles ◽  
Spontaneously Breathing

To examine the mechanical effects of the abdominal and triangularis sterni expiratory recruitment that occurs when anesthetized dogs are tilted head up, we measured both before and after cervical vagotomy the end-expiratory length of the costal and crural diaphragmatic segments and the end-expiratory lung volume (FRC) in eight spontaneously breathing animals during postural changes from supine (0 degree) to 80 degrees head up. Tilting the animals from 0 degree to 80 degrees head up in both conditions was associated with a gradual decrease in end-expiratory costal and crural diaphragmatic length and with a progressive increase in FRC. All these changes, however, were considerably larger (P less than 0.005 or less) postvagotomy when the expiratory muscles were no longer recruited with tilting. Alterations in the elastic properties of the lung could not account for the effects of vagotomy on the postural changes. We conclude therefore that 1) by contracting during expiration, the canine expiratory muscles minimize the shortening of the diaphragm and the increase in FRC that the action of gravity would otherwise introduce, and 2) the end-expiratory diaphragmatic length and FRC in upright dogs are thus actively determined. The present data also indicate that by relaxing at end expiration, the expiratory muscles make a substantial contribution to tidal volume in upright dogs; in the 80 degrees head-up posture, this contribution would amount to approximately 60% of tidal volume.

Adrenal medullary responses to repeated hemorrhage in conscious dogs

1986 ◽  
Vol 251 (6) ◽  
pp. R1193-R1199
Author(s):  
M. P. Lilly ◽  
W. C. Engeland ◽  
D. S. Gann
Keyword(s):  
Blood Volume ◽  
Activity Patterns ◽  
Environmental Influences ◽  
Conscious Dogs ◽  
Catecholamine Secretion ◽  
Hormonal Responses ◽  
Pentobarbital Sodium ◽  
Daily Feeding ◽  
Anesthetized Dogs

Potentiated adrenal responses to the second of two identical hemorrhages spaced 24 h apart are seen in the pentobarbital sodium-anesthetized dog. Although pentobarbital effectively reduces environmental influences, barbiturates affect hemodynamic and hormonal responses and preclude normal daily feeding and activity patterns. To determine the role of anesthesia in these earlier results, we prepared awake trained dogs with chronic adrenal venous catheters. Animals were bled 8.7-21.8% of measured blood volume [131] over 3 min, and peripheral and adrenal blood was sampled. Blood was reinfused 1 h later, and the dogs were fed. The protocol was repeated 24 h later. Dogs with small hemorrhage (11.6 +/- 2.3% blood vol; n = 9) showed no difference in catecholamine secretion on the 2 days. Dogs with large hemorrhage (18.9 +/- 2.1% blood vol; n = 9) showed a greater epinephrine and norepinephrine secretory response to hemorrhage on day 2. No differences were detected in the hemodynamic response to bleeding on the 2 days. Whereas potentiation was seen in epinephrine and norepinephrine responses to a second 10% hemorrhage in anesthetized dogs, larger hemorrhage was needed to elicit this effect in awake dogs. Thus potential adrenal medullary responses to repeated hemorrhage occur in both awake and pentobarbital-anesthetized dogs, but important differences in the threshold and manifestation of this effect are seen.

Carotid sinus baroreceptor control of splanchnic resistance and capacity

1988 ◽  
Vol 255 (6) ◽  
pp. H1305-H1310 ◽  
Author(s):  
M. J. Brunner ◽  
A. S. Greene ◽  
A. E. Frankle ◽  
A. A. Shoukas
Keyword(s):  
Blood Volume ◽  
Vascular Resistance ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Constant Flow ◽  
Vascular Bed ◽  
Anesthetized Dogs ◽  
Reflex Control ◽  
Baroreceptor Reflex Control ◽  
Sinus Pressure

The contribution of the splanchnic vascular bed in the carotid sinus baroreceptor reflex control of vascular resistance and capacity was studied in nine pentobarbital-anesthetized dogs. The splanchnic circulation was vascularly isolated in an unopened abdomen and perfused at constant flow and venous pressure. Decreasing carotid sinus pressure from 200 to 50 mmHg resulted in a 72% increase in splanchnic vascular resistance and a decrease in splanchnic blood volume of 4.7 ml/kg. Changes in splanchnic inflow from 0 to 70 ml.min-1.kg-1 resulted in linear changes in splanchnic arterial pressure. Increasing carotid sinus pressure significantly decreased the slope (P less than 0.005) and intercept (P less than 0.025) of the splanchnic pressure-flow relationship. It is concluded that in the dog, the splanchnic vascular bed contributes a major portion of blood volume mobilized by the carotid sinus reflex.

Role of carotid sinus baroreflex in attenuating systemic arterial pressure variability studied in anesthetized dogs

1994 ◽  
Vol 266 (2) ◽  
pp. H720-H729 ◽  
Author(s):  
T. Yoshida ◽  
Y. Harasawa ◽  
T. Kubota ◽  
H. Chishaki ◽  
T. Kubo ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Amplitude Spectrum ◽  
Low Frequency ◽  
Systemic Arterial Pressure ◽  
Open Loop ◽  
Frequency Range ◽  
Carotid Sinus Baroreflex ◽  
Anesthetized Dogs

Attenuation of systemic arterial pressure (SAP) variability by the carotid sinus baroreflex (CSBR) was quantified in nine anesthetized, vagotomized dogs. SAP amplitude spectrum was compared between open-loop [SAPo(f)] and closed-loop [SAPc(f)] operation of the CSBR. At 0.002 Hz, SAPc amplitude was 3.5 +/- 2.2 (SD) mmHg, and SAPo was 9.6 +/- 3.5 mmHg (P < 0.01). At 0.02 Hz, SAP(c) amplitude was 2.8 +/- 1.2 mmHg, and SAPo was 4.3 +/- 1.2 mmHg (P < 0.05). At higher frequencies, SAPo(f) was indistinguishable from SAPc(f). With the opened CSBR, intracarotid sinus pressure (CSP) was pseudorandomly varied, and the resulting SAP responses were recorded to determine the transfer function from CSP to SAP [HCSP.SAP(f)]. From SAPo(f) and the determined HCSP.SAP(f), we estimated SAP(f) if the CSBR was closed [SAPc,est(f)] and compared it with SAPc(f). These two spectra were similar in each dog over a frequency range of 0.002–0.15 Hz, the differences between SAPo(f) and SAPc(f) being reconcilable with HCSP.SAP(f). Although the anesthetized state and vagotomy may have distorted the transfer characteristics of the CSBR from those in conscious (with the intact vagi) states, the results of the present study indicate that the CSBR attenuated SAP variability mainly in a low-frequency range below 0.02 Hz and that this attenuation was attributable to the transfer properties of the CSBR.

scholarly journals Role of ETB receptors and nitric oxide in adrenal catecholamine secretion in anesthetized dogs

1999 ◽  
Vol 277 (4) ◽  
pp. R1051-R1056 ◽  
Author(s):  
Akio Hosokawa ◽  
Takahiro Nagayama ◽  
Kimiya Masada ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Splanchnic Nerve ◽  
Inhibitory Effect ◽  
Catecholamine Secretion ◽  
Anesthetized Dogs ◽  
Nos Inhibitor ◽  
Neuronal Nos ◽  
Endothelin B ◽  
Oxide Synthase

We examined the effects of sarafotoxin 6c (S6c), an endothelin-B (ETB) receptor agonist, on adrenal catecholamine secretion in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered intra-arterially into the adrenal gland through the phrenicoabdominal artery. Infusion of S6c attenuated increases in adrenal catecholamine output induced by splanchnic nerve stimulation. The inhibitory effect of S6c on the catecholamine secretion response was suppressed with a selective ETB receptor antagonist N- cis2,6-dimethylpiperidinocarbonyl-l-γ-methylleucyl-d-1-methoxycarbonyltryptophanyl-d-norleucine (BQ-788), a nitric oxide synthase (NOS) inhibitor N ω-nitro-l-arginine methyl ester, and a neuronal NOS inhibitor 7-nitroindazole monosodium salt (7-NINA). Similar results were obtained with the catecholamine secretion response induced by injection of ACh. 7-NINA alone did not affect these catecholamine secretion responses. These results suggest that ETB receptors play an inhibitory role in adrenal catecholamine secretion by activating neuronal NOS, whereas neuronal NOS is unlikely to be involved in regulation of adrenal catecholamine secretion in the absence of simultaneous ETB receptor stimulation.

Characterization of noradrenergic transmission at the dorsal motor nucleus of the vagus involved in reflex control of fundus tone

2008 ◽  
Vol 294 (3) ◽  
pp. R720-R729 ◽  
Author(s):  
Melissa A. Herman ◽  
Mark Niedringhaus ◽  
Alisa Alayan ◽  
Joseph G. Verbalis ◽  
Niaz Sahibzada ◽  
...  
Keyword(s):  
Quantitative Analysis ◽  
Motor Nucleus ◽  
Inhibit Activity ◽  
Dorsal Motor Nucleus ◽  
Noradrenergic Innervation ◽  
Cervical Vagotomy ◽  
Reflex Control ◽  
Intravenous Atropine

Quantitative analysis of innervation to dorsal motor nucleus of the vagus (DMV) fundus-projecting neurons indicates that ∼17% of input neurons are noradrenergic. To determine whether this small percentage of neurons innervating DMV output to the stomach is physiologically relevant, we evaluated the role of norepinephrine at the DMV in mediating a vagovagal reflex controlling the fundus. A strain gauge was sutured onto the fundus of isoflurane-anesthetized rats to monitor changes in tone evoked by esophageal distension (ED). ED produced a decrease in fundus tone of 0.31 ± 0.02 g ( P < 0.05), which could be reproduced after a 30-min interval between distensions. Bilateral cervical vagotomy and/or pretreatment with intravenous atropine methylbromide prevented the reflex-induced fundus relaxation. In contrast, intravenous NG-nitro-l-arginine methyl ester had no effect. Bilateral microinjection of α2-adrenoreceptor antagonists (yohimbine and RS-79948) into the DMV also prevented the response. Before microinjection of α2-adrenoreceptor antagonists, ED decreased fundus tone by 0.33 ± 0.05 g ( P < 0.05). After antagonist microinjection, ED decreased fundus tone by only 0.05 ± 0.06 g ( P > 0.05). Bilateral microinjection of prazosin into the DMV had no effect on the response. Microinjection of norepinephrine into the DMV mimicked the effect of ED and was also prevented by prior microinjection of an α2-adrenoreceptor antagonist. Our results indicate that noradrenergic innervation of DMV fundus-projecting neurons is physiologically important and suggest that norepinephrine released at the DMV acts on α2-adrenoreceptors to inhibit activity in a cholinergic-cholinergic excitatory pathway to the fundus.

Reflex suppression of renin release by ventricular receptors with vagal afferents

1977 ◽  
Vol 233 (2) ◽  
pp. H181-H184 ◽  
Author(s):  
M. D. Thames
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Left Coronary Artery ◽  
Vagal Afferents ◽  
Renin Release ◽  
Volume Depletion ◽  
Veratrum Alkaloids ◽  
Anesthetized Dogs ◽  
Reflex Control

Intracoronary injection of veratrum alkaloids is known to stimulate ventricular receptors with vagal afferents resulting in bradycardia and hypotension. This study examined the role of veratrum-sensitive ventricular receptors in the control of renin secretion in eight chloralose-anesthetized dogs. Hemorrhage of 10% caused renin release to increase significantly from a control of 778 to 1,971 ng/min. Arterial pressure and renal blood flow did not change significantly. The augmented release of renin during volume depletion was virtually abolished by injection of cryptenamine (2 microgram/kg) into the main left coronary artery, falling from 1,971 to 269 ng/min by 4 min after the cryptenamine injection. Blood pressure decreased significantly from 130 mmHg before to 111 mmHg after injection. Renal blood flow did not change significantly. This reflex suppression of renin release by excitation of ventricular receptors was abolished by vagotomy. These data indicate that ventricular receptors with vagal afferents participate in the reflex control of renin release.

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