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.

Blood pressure reducing effects of Phalaris canariensis in normotensive and spontaneously hypertensive rats

2012 ◽  
Vol 90 (2) ◽  
pp. 201-208 ◽  
Author(s):  
Clévia Santos Passos ◽  
Lucimeire Nova Carvalho ◽  
Roberto Braz Pontes ◽  
Ruy Ribeiro Campos ◽  
Olinda Ikuta ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Antihypertensive Agent ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Antihypertensive Effect ◽  
Treatment Interruption ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Baseline Levels ◽  
Phalaris Canariensis

The birdseed Phalaris canariensis (Pc) is popularly used as an antihypertensive agent. The aqueous extract of Pc (AEPc) was administered in adult normotensive Wistar rats and spontaneously hypertensive rats (SHR) and in prehypertensive young SHR (SHRY, 3 weeks old). Animals received AEPc (400 mg·kg–1·day–1, by gavage) for 30 days, then groups were divided into 2 subgroups: one was treated for another 30 days and the other received water instead of AEPc for 30 days. AEPc reduced systolic blood pressure (SBP) in both adult groups; however, treatment interruption was followed by a gradual return of the SBP to baseline levels. SHRY became hypertensive 30 days after weaning. AEPc minimized the increase in SBP in SHRY, but blood pressure rose to levels similar to those in the untreated group with treatment interruption. There were no changes in renal function, diuresis, or Na+ excretion. Pc is rich in tryptophan, and the inhibition of the metabolism of tryptophan to kynurenine, a potential vasodilator factor, prevented the blood pressure reducing effect of AEPc. Moreover, AEPc significantly reduced sympathoexcitation. Data indicate that the metabolic derivative of tryptophan, kinurenine, may be a mediator of the volume-independent antihypertensive effect of Pc, which was at least in part mediated by suppression of the sympathetic tonus.

Response of blood pressure and cardiac myosin polymorphism to swimming training in the spontaneously hypertensive rat

1982 ◽  
Vol 60 (8) ◽  
pp. 1098-1103 ◽  
Author(s):  
Heinz Rupp ◽  
Ruthard Jacob
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Swimming Training ◽  
Myosin V ◽  
Spontaneously Hypertensive ◽  
Myosin Isoenzyme

Cardiac muscle can adapt to different functional demands, as evidenced by polymorphism of myosin. Pressure load in spontaneously hypertensive rats induced a shift of the myosin isoenzymes towards myosin V3 (18% V1, 27% V2, 55% V3) relative to normotensive Wistar rats (49% V1, 29% V2, 22% V3). A swimming routine with Wistar rats resulted in a shift towards myosin V1 (72% V1, 18% V2, 10% V3). The training effect is not restricted to normotensive rats, since spontaneously hypertensive rats subjected to the same swimming routine exhibited a myosin isoenzyme pattern (38% V1, 31% V2, 31% V3) approaching that of the sedentary Wistar rats. Swimming training can, therefore, prevent the myosin isoenzyme redistribution towards myosin V3 found in sedentary spontaneously hypertensive rats. Furthermore, systolic blood pressure was significantly reduced (130 ± 8 mmHg (1 mmHg = 133.322 Pa)) in the swim-trained compared with the sedentary spontaneously hypertensive rats (157 ± 12 mmHg). The training-induced changes in myosin polymorphism and systolic blood pressure are, at least partially, attributed to substantially normalized sympathetic activity. The functional relevance of swimming training in the spontaneously hypertensive rat is seen in the increased potential of coping with situations requiring fast contraction which may occur during sudden physical exertion or emotional stress.

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