Regular ArticleDysfunction of Soluble Guanylyl Cyclase in Aorta and Kidney of Goto–Kakizaki Rats: Influence of Age and Diabetic State
References (29)
- et al.
Impaired nitric oxide-mediated vasodilation in patients with non-insulin-dependent diabetes mellitus
J. Am. Coll. Cardiol.
(1996) - et al.
Activation of purified guanylate cyclase by arachidonic acid requires absence of enzyme-bound heme
Biochim. Biophys. Acta
(1987) - et al.
Contribution of the renin–angiotensin system to subsensitivity of soluble guanylyl cyclase in TGR(mREN2)27 rats
Eur. J. Pharmacol.
(2000) - et al.
Association of prolonged hyperglycemia with glomerular hypertrophy and renal basement membrane thickening in the Goto Kakizaki model of non-insulin-dependent diabetes mellitus
Am. J. Kidney Dis.
(2001) - et al.
Hypertension and antihypertensive therapy as risk factors for type 2 diabetes mellitus
N. Engl. J. Med.
(2000) - et al.
Impaired endothelium-dependent vasodilation in patients with insulin-dependent diabetes mellitus
Circulation
(1993) - et al.
Impaired endothelium-dependent and independent vasodilation in patients with type 2 (non-insulin-dependent) diabetes mellitus
Diabetologia
(1992) - et al.
Impaired endothelium-dependent and independent dilation of forearm resistance arteries in men with diet-treated non-insulin-dependent diabetes: Role of dyslipidaemia
Clin. Sci. (Colch.)
(1996) - et al.
A new form of guanylyl cyclase is preferentially expressed in rat kidney
Biochemistry
(1990) - et al.
The spontaneous-diabetes rat: A model of noninsulin dependent diabetes mellitus
Proc. Jpn. Acad.
(1981)
Beta-cell insensitivity to glucose in the GK rat, a spontaneous nonobese model for type II diabetes
Diabetes
Abnormal insulin secretion and glucose metabolism in pancreatic islets from the spontaneously diabetic GK rat
Diabetologia
Changes in islet blood flow in rats with NIDDM
Diabetologia
Insulin-induced activation of glycerol-3-phosphate acyltransferase by a chiro-inositol-containing insulin mediator is defective in adipocytes of insulin-resistant, type II diabetic, Goto–Kakizaki rats
Proc. Natl. Acad. Sci. USA
Cited by (63)
Nitric oxide resistance in type 2 diabetes: Potential implications of HNO donors
2023, Nitric Oxide in Health and Disease: Therapeutic Applications in Cancer and Inflammatory DisordersFactors influencing the soluble guanylate cyclase heme redox state in blood vessels
2022, Vascular PharmacologyCitation Excerpt :Although these findings are not sufficient, the influence on the sGC heme redox state in blood vessels may vary depending on the duration and/or type of hypertension. Diabetes is accompanied by a decrease in DEA/NO [NO donor]-stimulated cGMP accumulation but not by a change in protoporphyrin IX [porphyrin]-stimulated cGMP accumulation in thoracic aortas of Goto-Kakizaki rats [79]. Similarly, a study using a streptozotocin-induced diabetes model in rats found that the relaxant response of thoracic aortas to DEA/NO [NO donor] is attenuated by diabetes, whereas the response to HMR-1766 [sGC activator] remains unchanged; the former is arguably caused by the scavenging of NO, but not by a shift in the sGC heme redox balance [80].
Frailty and sarcopenia as the basis for the phenotypic manifestation of chronic diseases in older adults
2016, Molecular Aspects of MedicineCitation Excerpt :Evidence from animal models suggests that the severity of vascular dysfunction increases in aged diabetic animals with respect to those only diabetic or only aged. Old type 2 diabetic rats show an exacerbated reduction of endothelium-dependent relaxations in aorta, mesenteric artery and corpus cavernosum (Gür et al., 2005; Miyata et al., 1992; Witte et al., 2002). With respect to age-matched lean non-diabetic (LETO) rats, endothelial vasodilation is significantly reduced in obese diabetic (OLETF) rats at 20 weeks and further reduced at 40 weeks of age, an impairment that was prevented by performing physical activity (Bunker et al., 2010).
Diabetes mellitus associated cardiovascular signalling alteration: A need for the revisit
2013, Cellular SignallingThe specific VPAC2 agonist Bay 55-9837 increases neuronal damage and hemorrhagic transformation after stroke in type 2 diabetic rats
2013, NeuropeptidesCitation Excerpt :Thus, it is possible that the reported efficacy was still mediated by direct VPAC2-mediated neuroprotection, although “by passing” those systemic side effects that led to brain hemorrhage in our study. Although no side effects of Bay 55-9837, except at very high doses, were reported by Tsutsumi et al. (Tsutsumi et al., 2002), the high rate of mortality and hemorrhages in our study could possibly be attributed to the combination of the following factors: the diabetic GK rats develop severe endothelial dysfunction over time, which leads to decreased arterial relaxation (Kazuyama et al., 2009) and increased blood pressure (Witte et al., 2002). GK rats have been reported to exhibit significant alterations in cerebral vasculature (Beauquis et al., 2010), which-together with the above hypertension–may underlie their increased propensity for hemorrhagic transformations after stroke (Ergul et al., 2007).
Vascular nitric oxide resistance in type 2 diabetes
2023, Cell Death and Disease
- 1
To whom correspondence should be addressed. Fax: +49 621 33 00 333. E-mail: [email protected].