scholarly journals Inhibitory Effect of Cilnidipine on Pressor Response to Acute Cold Stress in Spontaneously Hypertensive Rats

1995 ◽  
Vol 69 (2) ◽  
pp. 119-125 ◽  
Author(s):  
Masahiro Hosono ◽  
Tohru Hiruma ◽  
Kiyoshi Watanabe ◽  
Yutaka Hayashi ◽  
Haruo Ohnishi ◽  
...  
Keyword(s):  
Cold Stress ◽  
Spontaneously Hypertensive Rats ◽  
Pressor Response ◽  
Inhibitory Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals The effects of pertussis toxin-treatment on integrated vasoactive response of vascular system in spontaneously hypertensive rats

2008 ◽  
pp. 137-139
Author(s):  
S Čačányiová ◽  
F Kristek ◽  
J Kuneš ◽  
J Zicha
Keyword(s):  
Pertussis Toxin ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Vascular System ◽  
Pressor Response ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
The Right ◽  
Hypotensive Response

We investigated the effect of pertussis toxin (PTX) on hypotensive response induced by acetylcholine (ACh) and bradykinin (BK) and on noradrenaline (NA)-induced pressor response in spontaneously hypertensive rats (SHR). Fifteenweek-old Wistar rats and age-matched SHR were used. Half of SHR received PTX (10 µg/kg/i.v.) and the experiments were performed 48 h later. After the anesthesia the right carotid artery was cannulated in order to record blood pressure (BP). The hypotensive response to ACh was enhanced in SHR compared to Wistar rats. After pretreatment of SHR with PTX the hypotensive response to ACh was reduced compared to untreated SHR and it was also diminished in comparison to Wistar rats. Similarly, the hypotensive response to BK was also decreased after PTX pretreatment. The pressor response to NA was increased in SHR compared to Wistar rats. NA-induced pressor response was considerably decreased after PTX pretreatment compared to untreated SHR. In conclusion, the enhancement of hypotensive and pressor responses in SHR was abolished after PTX pretreatment. Our results suggested that the activation of PTXsensitive inhibitory Gi proteins is involved in the regulation of integrated vasoactive responses in SHR and PTX pretreatment could be effectively used for modification of BP regulation in this type of experimental hypertension.

Abstract P150: Sex Difference of Hypertension in Spontaneously Hypertensive Rats: Role of Mitochondrial Oxidative Stress

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Rodrigo O Maranon ◽  
Carolina Dalmasso ◽  
Chetal N Patil ◽  
Jane F Reckelhoff
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Sex Difference ◽  
Spontaneously Hypertensive Rats ◽  
Pressor Response ◽  
Premenopausal Women ◽  
Hypertensive Rats ◽  
Mitochondrial Oxidative Stress ◽  
Spontaneously Hypertensive ◽  
Mitochondrial Superoxide

Men have higher blood pressure (BP) than premenopausal women. Pressor response to oxidative stress may be a major contributor to the sex difference in BP control. Mitochondrial oxidative stress is associated with hypertension; however, whether mitochondrial oxidative stress plays a role in the sex difference in BP is unknown. In the present study, we tested the hypothesis that mitochondrial oxidative stress contributes to the sex difference in BP regulation in spontaneously hypertensive rats (SHR). Young intact (iYMSHR) and castrated males (cYMSHR), and females SHR (YFSHR) (3 mos of age) were implanted with radiotelemeters, and after a 4 day baseline BP, were treated with mitoTempo (0.75 mg/kg/d, sc minipumps), a specific scavenger of mitochondrial superoxide, for 7 days. Following 10 days washout of mito-tempo, rats were treated with Tempol (30 mg/kg/day, po drinking water) for 7 days. iYMSHR have higher blood pressure (by telemetry) than cYMSHR and YFSHR (148±1 mmHg, n=5, vs 132±1 mmHg, n=5, and 139±1 mmHg, n=5; p<0.01, respectively). MitoTempo reduced BP by 6% in iYMSHR (147±1 vs 139±1, n=5; p<0.05) compared to females (3%: 139±1 vs 136±1; n=5; p: NS) and castrated males (4.5%: 132±1 vs 126±1, n=5; p<0.05). After 10 days washout, tempol reduced BP only in iYMSHR (144±1 vs 130±1 mmHg, n=5; p<0.05). Our results suggest that mitochondrial oxidative stress may contribute to BP regulation in male SHR, but has no effect in females. The data also suggest that the presence of testosterone is necessary for the pressor response to oxidative stress in males since Tempol had no effect on BP in castrated males. Further studies examining the effect of steroid hormones and mitochondria in BP regulation are necessary to elucidate the importance of mitochondrial oxidative stress on sex difference of hypertension.

Vasopressin V2 receptor enhances gain of baroreflex in conscious spontaneously hypertensive rats

1999 ◽  
Vol 276 (3) ◽  
pp. R872-R879 ◽  
Author(s):  
Donella B. Sampey ◽  
Louise M. Burrell ◽  
Robert E. Widdop
Keyword(s):  
Receptor Antagonist ◽  
Spontaneously Hypertensive Rats ◽  
Pressor Response ◽  
Receptor Subtype ◽  
Hypertensive Rats ◽  
Receptor Antagonists ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Baroreflex Function ◽  
Shr And Wky Rats

The aim of the present study was to determine the receptor subtype involved in arginine vasopressin (AVP)-induced modulation of baroreflex function in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats using novel nonpeptide AVP V1- and V2-receptor antagonists. Baroreceptor heart rate (HR) reflex was investigated in both SHR and WKY rats which were intravenously administered the selective V1- and V2-receptor antagonists OPC-21268 and OPC-31260, respectively. Baroreflex function was assessed by obtaining alternate pressor and depressor responses to phenylephrine and sodium nitroprusside, respectively, to construct baroreflex curves. In both SHR and WKY rats baroreflex activity was tested before and after intravenous administration of vehicle (20% DMSO), OPC-21268 (10 mg/kg), and OPC-31260 (1 and 10 mg/kg). Vehicle did not significantly alter basal mean arterial pressure (MAP) and HR values or baroreflex function in SHR or WKY rats. The V1-receptor antagonist had no significant effect on resting MAP or HR values or on baroreflex parameters in both groups of rats, although this dose was shown to significantly inhibit the pressor response to AVP (5 ng iv; ANOVA, P < 0.05). In SHR but not WKY rats the V2-receptor antagonist significantly attenuated the gain (or slope) of the baroreflex curve (to 73 ± 3 and 79 ± 7% of control for 1 and 10 mg/kg, respectively), although AVP-induced pressor responses were also attenuated with the higher dose of the V2-receptor antagonist. These findings suggest that AVP tonically enhances baroreflex function through a V2 receptor in the SHR.

scholarly journals Age-related differences in pressor response to norepinephrine (NE) and tyramine (Ty) in spontaneously hypertensive rats (SHR)

1988 ◽  
Vol 46 ◽  
pp. 128
Author(s):  
Yoshiko Masubuchi ◽  
Toshio Kumai ◽  
Taiichiro Ohno ◽  
Masami Tanaka ◽  
Minoru Watanabe ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Pressor Response ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Age Related

Vasopressin receptors and inositol trisphosphate production in blood vessels of spontaneously hypertensive rats

1989 ◽  
Vol 67 (3) ◽  
pp. 232-239 ◽  
Author(s):  
Richard Larivière ◽  
Johanne Baribeau ◽  
Jean St-Louis ◽  
Ernesto L. Schiffrin
Keyword(s):  
Blood Pressure ◽  
Phospholipase C ◽  
Binding Sites ◽  
Spontaneously Hypertensive Rats ◽  
Pressor Response ◽  
Inositol Trisphosphate ◽  
Normal Density ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Phosphoinositide Breakdown

To understand the regulation of vasopressin (AVP) receptors in spontaneous hypertension, we investigated the pressor response of AVP in the perfused mesenteric vasculature, AVP binding sites in the membrane preparation of the same vascular bed, and the production of inositol trisphosphate (InsP3) stimulated by AVP in the aorta of spontaneously hypertensive rats (SHR), Wistar–Kyoto rats (WKY), and Wistar rats (WR) at different ages (4–16 weeks). Plasma AVP concentrations were similar in SHR, WKY, and WR at all ages. The density of AVP vascular binding sites was significantly higher in WKY than in SHR and WR at 12 weeks. Receptor affinity was similar in all strains. The pressor response of the mesenteric vasculature to AVP was similar in the three strains of rats at 4 weeks (prehypertensive stage) and increased progressively in SHR compared with WKY and WR at 8 and 12 weeks of age by 43 and 35%, respectively, and by more than 80% at 16 weeks of age (established hypertensive stage). There was no difference in vascular sensitivity to AVP. A significantly increased pressor response to a supramaximal dose of norepinephrine was also found at 16 weeks in SHR, but not in younger rats. InsP3 production in the aorta in response to AVP was increased in SHR at 8, 12, and 16 weeks, compared with WKY and WR. These results suggest that the vascular response to AVP is increased in SHR, in spite of decreased or normal density of binding sites compared with WKY or WR. The increased responsiveness to AVP in SHR may be mediated in part by the enhanced activity of AVP receptor-coupled phospholipase C, resulting in increased membrane phosphoinositide breakdown and inositol trisphosphate production, which may play a role in the elevation of blood pressure in SHR.Key words: vascular reactivity, vasopressin binding sites, phosphoinositide breakdown, phospholipase C, high blood pressure.

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