Plasma catecholamine concentrations in normotensive rats of different strains and in spontaneously hypertensive rats under basal conditions and during cold exposure

Life Sciences ◽  
1982 ◽  
Vol 31 (19) ◽  
pp. 2137-2143 ◽  
Author(s):  
Giovanni B. Picotti ◽  
Michele O. Carruba ◽  
Carla Ravazzani ◽  
Gian Pietro Bondiolotti ◽  
Mosè Da Prada
1992 ◽  
Vol 70 (9) ◽  
pp. 1217-1224 ◽  
Author(s):  
Abdel A. Abdel-Rahman ◽  
Robert G. Carroll ◽  
Mahmoud M. El-Mas

The present study evaluated the contribution of the sympathetic nervous system to the adverse hemodynamic action of ethanol on hypotensive responses in conscious unrestrained spontaneously hypertensive rats. Ethanol caused a dose-related attenuation of the hypotensive effect of guanabenz. An equivalent hypotensive response to sodium nitroprusside was not influenced by ethanol, which indicates a potential specific interaction between ethanol and guanabenz. Alternatively, it is possible that a preexisting high sympathetic nervous system activity, which occurred during nitroprusside infusion, may mask a sympathoexcitatory action of ethanol. Further, ethanol (1 g/kg) failed to reverse the hypotensive effect of the ganglionic blocker hexamethonium. This suggests that a centrally mediated sympathoexcitatory action of ethanol is involved, at least partly, in the reversal of hypotension. In addition, the antagonistic interaction between ethanol and guanabenz seems to take place within the central nervous system and involves opposite effects on central sympathetic tone. Finally, changes in plasma catecholamines provide supportive evidence for the involvement of the sympathetic nervous system in this interaction. In a separate group of conscious spontaneously hypertensive rats, ethanol (1 g/kg) reversed the guanabenz-evoked decreases in blood pressure and plasma catecholamine levels. It is concluded that (i) ethanol adversely interacts with centrally acting antihypertensive drugs through a mechanism that involves a directionally opposite effect on sympathetic activity, and (ii) a sympathetically mediated pressor effect of ethanol is enhanced in the presence of an inhibited central sympathetic tone.Key words: spontaneously hypertensive rats, ethanol, catecholamines, guanabenz, hexamethonium.


1979 ◽  
Vol 20 (5) ◽  
pp. 729-729 ◽  
Author(s):  
Chun Ho Pak ◽  
Masato Matsunaga ◽  
Kenichi Morimoto ◽  
Akira Hara ◽  
Chuichi Kawai

1985 ◽  
Vol 3 (1) ◽  
pp. 63-66 ◽  
Author(s):  
Yukio Yamori ◽  
Katsumi Ikeda ◽  
Elliott C. Kulakowski ◽  
Richard McCarty ◽  
Walter Lovenberg

1988 ◽  
Vol 255 (5) ◽  
pp. H1018-H1023 ◽  
Author(s):  
R. M. Thornton ◽  
J. M. Davidson ◽  
S. Oparil

This study sought to determine whether spontaneously hypertensive rats (SHR) on a high-NaCl diet have an enhanced pressor response to acute cold exposure and to define the peripheral mechanisms involved in the enhanced pressor response. SHR and normotensive Wistar-Kyoto (WKY) rats that had been on 1 and 8% NaCl diets for 3 wk were subjected to cold exposure. After a 30-min control period, animals were exposed to cold (6 +/- 2 degrees C) for 90 min. Mean arterial pressure (MAP), heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured continuously. In a separate group of SHR on 1 and 8% NaCl diets, an arginine vasopressin (AVP) V1 receptor antagonist (10 micrograms/kg iv) was given before cold exposure, and MAP was measured throughout cold exposure. Plasma AVP was measured before and during cold exposure in a separate group of SHR. During cold exposure, there was a significant increase (P less than 0.05) in MAP (25 mmHg) in SHR on the 8% NaCl diet only. In contrast, HR and LSNA increased similarly during cold exposure in both SHR and WKY on the two diets. AVP was similar in both SHR groups (7.1 pg/ml for 1% vs. 6.1 pg/ml for 8%) before cold exposure, but during cold exposure it increased in the 8% NaCl SHR only, reaching 17.6 pg/ml at 90 min. The AVP V1 antagonist completely abolished the cold stress-induced rise in MAP in SHR. Thus SHR on a high-NaCl diet have an enhanced pressor response to acute cold exposure compared with SHR on a normal NaCl diet.(ABSTRACT TRUNCATED AT 250 WORDS)


Author(s):  
Camila Lidiane de Morais ◽  
Dora Maria Grassi Kassisse ◽  
Filipy Borghi ◽  
Carolina Silva ◽  
Priscila Cristina da Silva

Angiotensin II (AII) produced by Renin-Angiotensin-Aldosterone System (RAAS) through the classical pathway have been associated with the regulation of adipocyte glycolytic and lipolytic metabolism. This pathway can be potentiated by the increase of catecholamines. The Wistar-Kyoto (WKY) and Spontaneously Hypertensive Rats (SHR) strains exhibet high catecholamines pattern and have different adipocyte profiles. This work aims to evaluate the influence of AII in the production of glycerol and lactate from these different strains.


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