Acute and Chronic Effects of Exercise on Baroreflexes in Spontaneously Hypertensive Rats

Hypertension ◽  
1997 ◽  
Vol 30 (3) ◽  
pp. 714-719 ◽  
Author(s):  
Gustavo José Justo Silva ◽  
Patricia Chakur Brum ◽  
Carlos Eduardo Negrão ◽  
Eduardo Moacyr Krieger
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Chronic Effects ◽  
Acute And Chronic Effects

scholarly journals Chronic effects of arotinolol (S-596) in spontaneously hypertensive rats.

1985 ◽  
Vol 8 (1) ◽  
pp. 50-55 ◽  
Author(s):  
KOICHIRO KISHI ◽  
KOICHIRO KAWASHIMA ◽  
HIROFUMI SOKABE ◽  
KEN SAITO
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Chronic Effects

Chronic and selective vasopressin blockade in spontaneously hypertensive rats

1994 ◽  
Vol 267 (6) ◽  
pp. R1467-R1471 ◽  
Author(s):  
H. Okada ◽  
H. Suzuki ◽  
Y. Kanno ◽  
Y. Yamamura ◽  
T. Saruta
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Hypertensive Rats ◽  
Control Groups ◽  
Receptor Antagonists ◽  
Spontaneously Hypertensive ◽  
Chronic Effects ◽  
V2 Receptor ◽  
V2 Antagonist

Chronic effects of orally available, nonpeptide vasopressin V1 and V2 receptor antagonists on conscious spontaneously hypertensive rats (SHR) were investigated. SHR and Wistar rats were divided into four groups, groups S-1 to S-4 and W-1 to W-4, respectively. Groups S-1 and W-1 were untreated as control. Groups S-2 and W-2 were treated with V1 antagonist, groups S-3 and W-3 received V2 antagonist, and groups S-4 and W-4 were treated with both of V1 and V2 antagonists. V1 and/or V2 antagonists did not affect degree of blood pressure of W-2, W-3, and W-4 rats, and V1 antagonist, alone or combined with V2 antagonist, slightly reduced increases in blood pressure of S-2 and S-4 rats without significance. However, V2 antagonist induced significantly massive and hyposmolar urine in W-3 rats compared with that in S-3 rats. In conclusion, in SHR, circulating vasopressin contributes to increases in blood pressure via either V1 or V2 receptors less than expected from previous studies with antibodies or peptide antagonists.

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