Acute and chronic effects of ethanol on papillary muscles from spontaneously hypertensive rats

1996 ◽  
Vol 302 (1-3) ◽  
pp. 61-67 ◽  
Author(s):  
Ricardo A. Brown ◽  
Adedapo O. Savage ◽  
Thomas C. Lloyd
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Papillary Muscles ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Chronic Effects ◽  
Acute And Chronic Effects

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

Tolerance to hypoxia of myocardium from adult and aged spontaneously hypertensive rats

1987 ◽  
Vol 252 (6) ◽  
pp. H1096-H1104 ◽  
Author(s):  
W. W. Brooks ◽  
J. S. Ingwall ◽  
C. H. Conrad ◽  
C. Holubarsch ◽  
O. H. Bing
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Energy Charge ◽  
High Energy ◽  
Left Ventricular ◽  
Adenylate Energy Charge ◽  
Papillary Muscles ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Tolerance To Hypoxia

Myocardial mechanics and high-energy phosphate content [ATP and creatine phosphate (CrP)] of isolated left ventricular papillary muscle preparations from male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were compared at 6 and 18 mo of age. In comparison with oxygenated (95% O2-5% CO2) glucose-supplied (5.5 mM) papillary muscles from hearts of WKY rats, papillary muscles from hypertrophied hearts of the 18-mo-old SHR exhibited a prolonged time to peak tension, electromechanical delay time, and an increase in resting tension measured at the apex of the length-tension curve. Adenine nucleotide (ATP and ADP) contents of oxygenated papillary muscles were not significantly different between SHR and WKY strains at 6 or 18 mo of age, but CrP content of hearts from adult WKY and SHR were higher than for aged WKY and SHR rats. For up to 30 min of hypoxia (95% N2-5% CO2), muscles from the 18-mo-old SHR and WKY rats demonstrated improved tolerance to hypoxia compared with muscles from younger animals. However, at 60 min of hypoxia the 18-mo-old SHR demonstrated lower active tension and adenylate energy charge [(1/2 ADP + ATP)/(ATP + ADP + AMP)]. At higher glucose concentrations (22 mM), both 18-mo-old WKY and SHR demonstrated improved tolerance to hypoxia; moreover, the differences between strains were no longer evident. Following reoxygenation with 5.5 mM glucose, contracture tension and CrP content recovered to near prehypoxic control levels, whereas developed tension and ATP content remained moderately depressed for all groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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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