Cardiovascular responses to acute stress in young-to-old spontaneously hypertensive rats.

Yamamoto, J.; Nakai, Masatsugu; Nishizaki, Takashi

doi:10.1161/01.hyp.9.4.362

Cited by 44 publications

(20 citation statements)

References 34 publications

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“…15,46). It should also be noted in this context that plasma catecholamines in SHR and WKY of different ages do not differ, but the increment seen after stress is greater in SHR (10). In view of our findings, catecholamines also seem to be less likely candidates for the observed changes in SHR islet blood flow.…”

Section: Wky Shrsupporting

confidence: 42%

“…The increased vascular resistance in SHR is not associated with any marked changes in organ blood perfusion compared with control rats (9,10). However, the blood flow responses to endothelium-derived vasoactive substances are enhanced with regard to vasoconstrictors (11), but attenuated with regard to the effects of the vasodilators (12,13).…”

Section: Introductionmentioning

confidence: 86%

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The pancreatic islets in spontaneously hypertensive rats: islet blood flow and insulin production

Iwase

Sandler²,

Carlsson³

et al. 2001

European Journal of Endocrinology

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The aim of the study was to investigate if hypertension affects pancreatic islet blood flow and endocrine function. For this purpose, spontaneously hypertensive rats (SHR) were compared with normotensive control Wistar±Kyoto rats (WKY). Both islet size and islet cell replication in 4-monthold SHR was increased compared with WKY. The (pro)insulin biosynthesis was reduced in islets isolated from SHR, whereas the insulin content was unchanged. A hyperinsulinemic response to glucose in vivo was observed in 4-and 12-month-old SHR. Pancreatic blood flow, measured using a microsphere technique, was lower in SHR than in WKY in rats aged 5 weeks, 4 months or 1 year. Islet blood flow was lower in 4-month-old and 1-year-old SHR. In 4-month-old animals, islet blood flow was unaffected by administration of enalaprilate and prazosin in both strains, but was markedly decreased by the administration of N G -methyl-L-arginine. It was concluded that the islets of SHR have a decreased insulin production in vitro and a decreased islet blood perfusion. The reasons for this are likely to be multifactorial. Because SHR maintained an essentially normal glucose tolerance, an adaptation of the b-cells to the metabolic and hemodynamic changes imposed by hypertension occurred.

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Section: Wky Shrsupporting

confidence: 42%

Section: Introductionmentioning

confidence: 86%

The pancreatic islets in spontaneously hypertensive rats: islet blood flow and insulin production

Iwase

Sandler²,

Carlsson³

et al. 2001

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…Increased oxidative stress and increased basal PKC activity have also been described in experimental models of agerelated pathologies such as hypertension and diabetes (Banday et al, 2007;Marwaha and Lokhandwala, 2006). WKY rats used in this study, is a well studied normotensive strain with no age-related alterations of blood pressure values (Bing et al, 2002;Loch et al, 2009;Moura et al, 2005;Yamamoto et al, 1987). The proposed mechanism was that increased ROS production stimulated PKC-δ via activation of NF-B (Banday et al, 2007).…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Renal aging in WKY rats: Changes in Na+,K+-ATPase function and oxidative stress

Silva¹,

Pinto²,

Simão³

et al. 2010

Experimental Gerontology

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It has been suggested that alterations in Na + ,K + -ATPase mediate the development of several aging-related pathologies, such as hypertension and diabetes. Thus, we evaluated Na + ,K + -ATPase function and H 2 O 2 production in the renal cortex and medulla of Wistar Kyoto (WKY) rats at 13, 52 and 91 weeks of age. Creatinine clearance, proteinuria, urinary excretion of Na + and K + and fractional excretion of Na + were also determined.The results show that at 91 weeks old WKY rats had increased creatinine clearance and did not have proteinuria. Despite aging having had no effect on urinary Na + excretion, urinary K + excretion was increased and fractional Na + excretion was decreased with age. In renal proximal tubules and isolated renal cortical cells, 91 weeks old rats had decreased Na + ,K + -ATPase activity when compared to 13 and 52 weeks old rats. In renal medulla, 91 weeks old rats had increased Na + ,K + -ATPase activity, paralleled by an increase in protein expression of α 1 -subunit of Na + ,K + -ATPase. In addition, renal H 2 O 2 production increased with age and at 91 weeks of age renal medulla H 2 O 2 production was significantly higher than renal cortex production.The present work demonstrates that although at 91 weeks of age WKY rats were able to maintain Na + homeostasis, aging was accompanied by alterations in renal Na + ,K + -ATPase function. The observed increase in oxidative stress may account, in part, for the observed changes. Possibly, altered Na + ,K + -ATPase renal function may precede the development of age-related pathologies and loss of renal function.

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“…However, stress is another common characteristic of the hypertensive models that respond to orexin inhibition, namely BPH/2J mice and SHR. Both have exaggerated cardiovascular reactivity to stress 34,35 and stressinduced hypertensive rats, where hypertension is induced by chronic exposure to stressful stimuli. 12 Thus, it would be interesting to know whether patients with stress-related forms of hypertension also have overactive orexinergic systems.…”

Section: Perspectivesmentioning

confidence: 99%

Contribution of Orexin to the Neurogenic Hypertension in BPH/2J Mice

et al. 2016

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BPH/2J mice are a genetic model of hypertension which were selectively bred for elevated blood pressure (BP) in the 1970s alongside a normotensive strain (BPN/3J).1 Recent studies suggest that the hypertension in BPH/2J mice is caused by enhanced activation of the sympathetic nervous system (SNS) because ganglion blockade causes a greater depressor response in BPH/2J mice compared with BPN/3J controls. 2,3 Importantly, cardiovascular regulatory forebrain regions within the hypothalamus and amygdala display markedly greater neuronal activity in BPH/2J compared with BPN/3J mice during the dark-active period of the 24-hour light cycle.2 Furthermore, lesions of the medial amygdala reduced the hypertension and SNS overactivity in BPH/2J mice. 4 Thus the central nervous system seems to play a crucial role in driving the sympathetically mediated hypertension in this model.A gene array approach has been used to identify differential expression of genes in the hypothalamus between BPH/2J and BPN/3J mice. 5,6 An important finding was that expression of the orexin precursor gene (hcrt) in BPH/2J mice was more than double that of normotensive mice in early and established hypertension. Thus, hcrt could potentially contribute to the development and maintenance of BPH/2J hypertension.5 Furthermore, BPH/2J mice have ≈4-fold greater expression of the hcrt gene in the hypothalamus during the dark-active period compared with light period when mice are predominantly inactive or asleep. 6 Characteristics of the BPH/2J mouse strain, such as high BP, tachycardia, greater locomotor activity, overactivity of the SNS, 2 and exaggerated cardiovascular reactivity to stressful stimuli, 7 could all be reflective of a greater activity of the orexinergic neurons. Indeed, orexin is capable of increasing BP, heart rate (HR), and SNS activity.8 Orexinergic neurons originate in the hypothalamus and project to a wide range of brain regions, but in terms of sympathetic control of BP, the Abstract-BPH/2J mice are a genetic model of hypertension associated with an overactive sympathetic nervous system.Orexin is a neuropeptide which influences sympathetic activity and blood pressure. Orexin precursor mRNA expression is greater in hypothalamic tissue of BPH/2J compared with normotensive BPN/3J mice. To determine whether enhanced orexinergic signaling contributes to the hypertension, BPH/2J and BPN/3J mice were preimplanted with radiotelemetry probes to compare blood pressure 1 hour before and 5 hours after administration of almorexant, an orexin receptor antagonist. Mid frequency mean arterial pressure power and the depressor response to ganglion blockade were also used as indicators of sympathetic nervous system activity. Administration of almorexant at 100 (IP) and 300 mg/ kg (oral) in BPH/2J mice during the dark-active period (2 hours after lights off) markedly reduced blood pressure (−16.1±1.6 and −11.0±1.1 mm Hg, respectively; P<0.001 compared with vehicle). However, when almorexant (100 mg/ kg, IP) was administered during the light-inactive pe...

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Cardiovascular responses to acute stress in young-to-old spontaneously hypertensive rats.

Cited by 44 publications

References 34 publications

The pancreatic islets in spontaneously hypertensive rats: islet blood flow and insulin production

The pancreatic islets in spontaneously hypertensive rats: islet blood flow and insulin production

Renal aging in WKY rats: Changes in Na+,K+-ATPase function and oxidative stress

Contribution of Orexin to the Neurogenic Hypertension in BPH/2J Mice

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