The relationship between hypertension and central serotonergic nervous system activity in spontaneously hypertensive rats

1988 ◽  
Vol 11 (4) ◽  
pp. 301-307
Author(s):  
Sung Jin Kim ◽  
Kwang Ho Ko
Keyword(s):  
Nervous System ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
System Activity ◽  
Nervous System Activity ◽  
The Relationship

Changes of Blood Pressure Rhythm and Clock Protein Expression Levels in Spontaneously Hypertensive Rats After Ischemia-Reperfusion

2021 ◽  
Author(s):  
Jing Jin ◽  
Yumeng Liu ◽  
Jing Huang ◽  
Dong Zhang ◽  
Jian Ge ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Protein Expression ◽  
Circadian Clock ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Expression Levels ◽  
The Relationship ◽  
Clock Protein

Abstract Objective A variety of circadian patterns of blood pressure after ischemic stroke in patients with essential hypertension appear to be a potential risk of stroke recurrence, but the mechanism is still unclear. This study intends to reveal the changes in blood pressure rhythm and circadian clock protein expression levels in spontaneously hypertensive rats (SHR) after ischemia-reperfusion, and the relationship between the two. Methods Using the SHR middle cerebral artery occlusion experimental model, the systolic blood pressure was continuously monitored for 24 hours after the operation to observe the blood pressure rhythm. The rat tail vein blood was taken every 3h, and the serum CLOCK, BMAL1, PER1 and CRY1 protein expression levels were detected by Elisa. Pearson correlation analysis counted the relationship between SHR blood pressure rhythm and circadian clock protein fluctuation after ischemia-reperfusion. Results The proportion of abnormal blood pressure patterns in the SHR + tMCAO group was significantly higher than that in the SHR group, the serum CLOCK expression was relatively constant, and the circadian rhythm of BMAL1, PER1 and CRY1 protein expression changed significantly. Pearson analysis showed that PER1 protein level was negatively correlated with dipper (r = -0.565, P = 0.002) and extreme-dipper (r = -0.531, P = 0.001) blood pressure, and was significantly positively correlated with non-dipper blood pressure (r = 0.620, P < 0.001). Conclusion The rhythm pattern of blood pressure after ischemia-reperfusion in SHR is obviously disordered, and it is closely related to the regulation of Per1 gene.

Enhancement of the Anti-Hypertensive Effect of Methyldopa and other Anti-Hypertensive Drugs by Carbidopa in Spontaneously Hypertensive Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 407s-410s
Author(s):  
A. Scriabine ◽  
C. T. Ludden ◽  
C. A. Stone ◽  
R. J. Wurtman ◽  
C. J. Watkins
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Specific Radioactivity ◽  
Acid Decarboxylase ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Amino Acid Decarboxylase ◽  
Aromatic Amino Acid Decarboxylase ◽  
Nervous System Activity ◽  
Biochemical Studies ◽  
Tyrosine Content

1. A peripheral inhibitor of l-aromatic amino acid decarboxylase, carbidopa [(—)-l-α-hydrazino-3,4-dihydroxy-α-methylbenzenepropanoic acid monohydrate], at doses up to 25 mg/kg intraperitoneally or 30 mg/kg orally had no effect on directly recorded arterial pressure of spontaneously hypertensive rats derived from the Wistar/Okamoto strain. It enhanced, however, the anti-hypertensive effects of methyldopa, hydrallazine, guanethidine and clonidine, and, to a lesser extent, reserpine and hydrochlorothiazide. The mechanism of this enhancement is presently unknown, but biochemical studies support the assumption that carbidopa is likely to reduce sympathetic nervous system activity. 2. The conversion of [3H]tyrosine (given intraperitoneally) to dopa (3,4-dihydroxyphenylalanine) and catecholamines was measured in the hearts and adrenals of control rats and animals pretreated with carbidopa (100 mg/kg, intraperitoneally). Carbidopa significantly decreased the accumulation of 3H-labelled catecholamines in both organs and increased their total tyrosine content and the specific radioactivity of tyrosine.

Role of the sympathetic nervous system in the alcohol–guanabenz hemodynamic interaction

1992 ◽  
Vol 70 (9) ◽  
pp. 1217-1224 ◽  
Author(s):  
Abdel A. Abdel-Rahman ◽  
Robert G. Carroll ◽  
Mahmoud M. El-Mas
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Spontaneously Hypertensive Rats ◽  
Specific Interaction ◽  
Plasma Catecholamines ◽  
Hypotensive Effect ◽  
Plasma Catecholamine ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Sympathetic Nervous

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.

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