scholarly journals Role of the Carotid Bodies in the Hypertensive and Natriuretic Responses to NaCl Load in Conscious Rats

2018 ◽  
Vol 9 ◽  
Author(s):  
Elaine Fernanda da Silva ◽  
Aryanne Batista Soares de Melo ◽  
Eulício de Oliveira Lobo Júnior ◽  
Karla Lima Rodrigues ◽  
Lara Marques Naves ◽  
...  

1994 ◽  
Vol 267 (5) ◽  
pp. H1713-H1718 ◽  
Author(s):  
Y. Fujisawa ◽  
A. Miyatake ◽  
Y. Hayashida ◽  
Y. Aki ◽  
S. Kimura ◽  
...  

Hypotensive hemorrhage decreases heart rate (HR) and renal sympathetic nerve activity (RSNA). Hemorrhage is a potent stimulus for arginine vasopressin (AVP) release; therefore, AVP may contribute to such inhibitory action of HR and RSNA during hemorrhage. We evaluated the roles of vasopressin on the regulation of blood pressure (BP), HR, and RSNA during hemorrhage using nonpeptide and selective V1- and V2-receptor antagonists (OPC-21268 and OPC-31260) in conscious rats. After hemorrhage (20 ml/kg body wt) BP decreased by 62 +/- 10 mmHg along with bradycardia (-110 +/- 15 beats/min) and renal sympathoinhibition (-50 +/- 8). Pretreatment of V1-receptor antagonist (5 mg/kg iv) did not affect the initial fall of BP but attenuated subsequent BP recovery. Bradycardic and renal sympathoinhibitory responses following hemorrhage were abolished (-14 +/- 24 beats/min and -7 +/- 9) by V1-receptor antagonist. Pretreatment of V2-receptor antagonist (1 mg/kg iv) did not affect the response of BP; however, it did slightly strengthen bradycardia and prolong renal sympathoinhibition. Hemorrhage increased the plasma AVP concentration more than 50-fold. These results indicate that when the plasma concentration of AVP is extremely high during hemorrhage, vasopressin via V1 receptor contributes to BP recovery by the peripheral vasoconstriction and exerts an inhibitory action on RSNA, and vasopressin via V2 receptor exerts opposite stimulatory action on RSNA.



Author(s):  
Stuart M. Tomares ◽  
Owen S. Bamford ◽  
Laura M. Sterni ◽  
Robert S. Fitzgerald ◽  
John L. Carroll


2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Elizabeth B Oliveira‐Sales ◽  
Marie Ann Toward ◽  
Ruy Ribeiro Campos ◽  
Julian FR Paton




2002 ◽  
Vol 167 (4) ◽  
pp. 1887-1891 ◽  
Author(s):  
Bao Jun Gu ◽  
Osamu Ishizuka ◽  
Yasuhiko Igawa ◽  
Osamu Nishizawa ◽  
Karl-Erik Andersson


Endocrinology ◽  
1987 ◽  
Vol 120 (5) ◽  
pp. 2186-2188 ◽  
Author(s):  
Hiroshi Itoh ◽  
Kazuwa Nakao ◽  
Takayuki Yamada ◽  
Narito Morii ◽  
Shozo Shiono ◽  
...  


1992 ◽  
Vol 262 (6) ◽  
pp. G1121-G1126 ◽  
Author(s):  
B. Bonaz ◽  
L. Martin ◽  
E. Beurriand ◽  
M. Manier ◽  
J. Hostein ◽  
...  

The role of the locus ceruleus (LC) in the control of migrating myoelectric complex (MMC) was investigated in rats with lesions induced by injections of 6-hydroxydopamine (6-OHDA). Control animals received the vehicle alone. MMC was recorded in conscious rats chronically fitted with electrodes. After 6-OHDA was injected into the LC, lesions of the LC were total, partial (mostly rostral), or ineffective. The MMC period was significantly longer in animals with a total or partial lesion but was unchanged in animals with an ineffective lesion. No lesion of other brain noradrenergic nuclei was observed. The longer MMC period is comparable to that obtained after intracerebroventricular injection of 6-OHDA, which is responsible for a more diffuse destruction of brain noradrenergic systems, including LC itself. Bilateral lesions of the central tegmental tract, which carries ascending noradrenergic axons from the medullary and pontine cell groups outside the LC, do not alter the MMC cycle. Consequently, the LC is most likely the major brain noradrenergic candidate for modulating the MMC pattern in rats.



2001 ◽  
Vol 280 (4) ◽  
pp. R1162-R1168 ◽  
Author(s):  
René H. Worck ◽  
Dennis Staahltoft ◽  
Thomas E. N. Jonassen ◽  
Erik Frandsen ◽  
Hans Ibsen ◽  
...  

Simultaneous blockade of systemic AT1 and AT2 receptors or converting enzyme inhibition (CEI) attenuates the hypoglycemia-induced reflex increase of epinephrine (Epi). To examine the role of brain AT1 and AT2 receptors in the reflex regulation of Epi release, we measured catecholamines, hemodynamics, and renin during insulin-induced hypoglycemia in conscious rats pretreated intracerebroventricularly with losartan, PD-123319, losartan and PD-123319, or vehicle. Epi and norepinephrine (NE) increased 60-and 3-fold, respectively. However, the gain of the reflex increase in plasma Epi (Δplasma Epi/Δplasma glucose) and the overall Epi and NE responses were similar in all groups. The ensuing blood pressure response was similar between groups, but the corresponding bradycardia was augmented after PD-123319 ( P < 0.05 vs. vehicle) or combined losartan and PD-123319 ( P < 0.01 vs. vehicle). The findings indicate 1) brain angiotensin receptors are not essential for the reflex regulation of Epi release during hypoglycemia and 2) the gain of baroreceptor-mediated bradycardia is increased by blockade of brain AT2 receptors in this model.



2001 ◽  
Vol 120 (5) ◽  
pp. A74
Author(s):  
Ayhan Bozkurt ◽  
Mustafa Deniz ◽  
Nese Imeryuz ◽  
Nefise Barlas Ulusoy ◽  
Berrak C. Yegen


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