Experimental diabetes induces hyperreactivity of rabbit renal artery to 5-hydroxytryptamine

Miranda, Francisco Javier Noya; Alabadí, José A.; Lloréns, Silvia; Apodaca, Rosa F. Ruiz de; Centeno, José M.; Alborch, Enrique

doi:10.1016/s0014-2999(02)01438-3

Cited by 25 publications

(24 citation statements)

References 43 publications

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“…The renal production of thromboxane A 2 and prostacyclin is increased in diabetic rats (Okumura et al, 2000). In contrast, other studies show a decreased formation of vasoconstrictor prostanoid in rat mesenteric arterial bed in response to methoxamine (Makino and Kamata, 1998), rabbit carotid arteries in response to acetylcholine (Miranda et al, 2000a) or 5-hydroxytryptamine (Miranda et al, 2000b), and rabbit renal arteries in response to 5-hydroxytryptamine (Miranda et al, 2002) in diabetes. These data support the specificity of the changes in modulatory mechanisms of the arterial response to endothelin-1 mentioned above, and show that changes in vascular reactivity induced by diabetes may vary depending on the species, vascular bed, and stimuli studied.…”

Section: Discussionmentioning

confidence: 86%

“…Endothelial thromboxane A 2 modulates the response to endothelin-1 of dog basilar artery (Shirahase et al, 1991), rat hepatic vascular bed (Kurihara et al, 1992), and aorta from hypertensive rats (Taddei and Vanhoutte, 1993). Recently, we have reported that the endothelium modulates the response of the rabbit carotid artery to acetylcholine (Miranda et al, 2000a) and 5-hydroxytryptamine (Miranda et al, 2000b) and that of the rabbit renal artery to 5-hydroxytryptamine (Miranda et al, 2002) by releasing both NO and a vasoconstrictor prostanoid. Because in both indomethacinand furegrelate-treated arteries from diabetic rabbits the EC 50 values were increased with respect to those obtained in the corresponding arteries from control rabbits, it can be deduced that indomethacin and furegrelate were more effective at inhibiting responses in diabetic than in control arteries.…”

Section: Discussionmentioning

confidence: 99%

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Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1

Lloréns

Miranda

Alabadí

et al. 2004

European Journal of Pharmacology

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The influence of diabetes on regulatory mechanisms and specific receptors implicated in the contractile response of isolated rabbit carotid arteries to endothelin-1 was examined. Endothelin-1 induced a concentration-dependent contraction that was greater in arteries from diabetic rabbits than in arteries from control rabbits. Endothelium removal or N G -nitro-L-arginine enhanced contractions in response to endothelin-1 only in control arteries, without modifying the endothelin-1 response in diabetic arteries. Indomethacin, furegrelate (thromboxane A 2 inhibitor), or cyclo-(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123; endothelin ET A receptor antagonist) inhibited the contractions in response to endothelin-1, the inhibition being greater in diabetic arteries than in control arteries. 2,6-Dimethylpiperidinecarbonyl-g-methyl-Leu-N in -(methoxycarbonyl)-D-Trp-D-Nle (BQ-788; endothelin ET B receptor antagonist) enhanced the contraction elicited by endothelin-1 in control arteries and displaced to the right the contractile curve for endothelin-1 in diabetic arteries. In summary, diabetes induces hyperreactivity of the rabbit carotid artery to endothelin-1 by a mechanism that at least includes: (1) enhanced activity of muscular endothelin ET A receptors; (2) impairment of endothelin ET B receptor-mediated nitric oxide (NO) release; and (3) enhancement of the production of thromboxane A 2 .

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Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1

Lloréns

Miranda

Alabadí

et al. 2004

European Journal of Pharmacology

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“…Whereas previous studies have shown that contractile responses are altered in Type I and Type II diabetes (15,19,25,32,33,35,37,38,42,43,45,48), relatively few studies have examined mechanisms that produce these changes (15,43). Activity of Rho kinase appears to be enhanced under pathophysiological conditions, including subarachnoid hemorrhage and hypertension (5,30).…”

Section: Discussionmentioning

confidence: 99%

Cerebral vascular dysfunction in TallyHo mice: a new model of Type II diabetes

Didion¹,

Lynch²,

Faraci³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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.-The purpose of this study was to characterize vascular responses and to examine mechanisms of vascular dysfunction in TallyHo mice, a new polygenic model of Type II diabetes. Responses of cerebral arterioles and carotid arteries were examined in vivo by using a cranial window and in vitro by using tissue baths, respectively. Dilatation of cerebral arterioles (baseline diameter ϭ 33 Ϯ 1 m) in response to acetylcholine, but not to nitroprusside, was markedly reduced (P Ͻ 0.05) in TallyHo mice. Responses of cerebral arterioles to acetylcholine in TallyHo mice were restored to normal with polyethylene glycol-superoxide dismutase (100 U/ml; a superoxide scavenger). Responses to acetylcholine were also greatly impaired (P Ͻ 0.05) in the carotid arteries from TallyHo mice. Phenylephrine-and serotonin-, but not to KCl-or U46619-, induced contraction was increased two-to fourfold (P Ͻ 0.05) in carotid arteries of TallyHo mice. Responses to phenylephrine and serotonin were reduced to similar levels in the presence of Y-27632 (an inhibitor of Rho kinase; 3 mol/l). These findings provide the first evidence that vascular dysfunction is present in TallyHo mice and that oxidative stress and enhanced activity of Rho kinase may contribute to altered vascular function in this genetic model of Type II diabetes. carotid artery; cerebral circulation; endothelium; microcirculation EPIDEMIOLOGICAL STUDIES suggest that there is a marked increase in the number of vascular complications in patients with diabetes (21,22,51). For example, results from the Framingham study have found a two-to fourfold increased risk associated with diabetes and the development of other cardiovascular risk factors, including atherosclerosis, carotid artery disease, and stroke (21). Although Type II diabetes accounts for the majority (ϳ90%) of diabetes in humans (3), relatively little is known regarding vascular responses and mechanisms that produce vascular dysfunction in Type II diabetes compared with Type I diabetes.Whereas studies using ob/ob (leptin-deficient) and db/db (leptin receptor-deficient mice) have provided much insight into vascular alterations in the genetic models of Type II diabetes (8,19,25,42,(43)(44)(45)(46), such monogenic deficiencies in leptin and the leptin receptor are rare and are not always associated with the development of diabetes in humans (14). TallyHo mice represent a newly defined polygenetic model of Type II diabetes and are characterized by hyperglycemia, hyperinsulinemia, hyperlipidemia, and moderate obesity (23,

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“…[7][8][9] Several reports by our research team [10][11][12] and others 3,[13][14][15] have found that alterations in vasocontraction induced by 5-HT were observed in patients with cardiovascular diseases as well as in those with diabetes. An accumulating body of evidence suggests that 5-HT plays a role in the development of diabetic complications.…”

mentioning

confidence: 92%

Effect of Long-Term Diabetes on Serotonin-Mediated Contraction in Carotid Arteries from Streptozotocin-Induced Diabetic Male and Female Rats

Watanabe

Matsumoto

Ando

et al. 2016

Biological & Pharmaceutical Bulletin

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An accumulating body of evidence suggests that males and females differ in vascular function in arteries under pathophysiological states. In this study, we tested whether there was a sex difference associated with serotonin (5-hydroxytryptamine, 5-HT)-mediated contraction in the carotid arteries of long-term streptozotocin (STZ)-induced diabetic rats [viz. 23 or 24 weeks after STZ (65 mg/kg, intravenously (i.v.)) injection starting at 8 weeks old of rats]. In the control group, the 5-HT-and high-K -induced contractions were greater in females than in males. In both sexes, treatment with STZ led to a decrease of 5-HT-induced contraction in carotid arteries compared to controls. In STZ-induced diabetic rats, the carotid arterial 5-HTinduced contraction was greater in female rats than in diabetic male rats. The high-K -induced contraction was greater in diabetic female rats than in either age-matched female controls or diabetic male rats. Expression of the 5-HT 2A receptor, which is the main receptor for 5-HT-induced contraction in rat carotid arteries, was similar among the four groups. These results suggest that decreased 5-HT-induced carotid arterial contraction is seen in both sexes under long-term STZ-induced diabetic conditions. Further, this reduction seems to be weaker in females than in males. This alteration of 5-HT-induced contraction may be partly associated with increased voltage-dependent Ca 2 channel activity.Key words carotid artery; contraction; serotonin; sex difference; streptozotocin Although women generally develop cardiovascular diseases several years later than men, this benefit may be diminished in diabetic individuals. The results of numerous epidemiological studies investigating the relationship between sex and the development of cardiovascular disease in diabetics have been inconsistent.1,2) Alterations in the responsiveness of blood vessels to various hormones and/or neurotransmitters in patients of both sexes with diabetes mellitus are well established. [3][4][5][6] However, there is confounding evidence of vascular function between diabetics of both male and females.The neurotransmitter serotonin [5-hydroxytriptamine (5-HT)] is an important factor that is involved in the regulation of several vascular functions, including blood flow, blood pressure, and vascular tone, in pathophysiological states. 7-9)Several reports by our research team [10][11][12] and others 3,[13][14][15] have found that alterations in vasocontraction induced by 5-HT were observed in patients with cardiovascular diseases as well as in those with diabetes. An accumulating body of evidence suggests that 5-HT plays a role in the development of diabetic complications. For example, sarpogrelate, an antagonist of the 5-HT 2A receptor, has beneficial effects against diabetic nephropathy, neuropathy, and diabetes-associated vascular dysfunction, including arterial stiffness and arteriosclerosis, in diabetic patients and animal models. [16][17][18][19] This relevant evidence suggests that the manipulation of 5-HT function c...

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Experimental diabetes induces hyperreactivity of rabbit renal artery to 5-hydroxytryptamine

Cited by 25 publications

References 43 publications

Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1

Different role of endothelin ETA and ETB receptors and endothelial modulators in diabetes-induced hyperreactivity of the rabbit carotid artery to endothelin-1

Cerebral vascular dysfunction in TallyHo mice: a new model of Type II diabetes

Effect of Long-Term Diabetes on Serotonin-Mediated Contraction in Carotid Arteries from Streptozotocin-Induced Diabetic Male and Female Rats

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