Coronary vasoconstriction induced by vasopressin. Production of myocardial ischemia in dogs by constriction of nondiseased small vessels.

Maturi, Mary F.; Martin, Staci; Markle, David R.; Maxwell, M; Burruss, C R; Speir, Edith; Greene, R. R.; Ro, Young Moo; Vitale, Dino Franco; Green, M V

doi:10.1161/01.cir.83.6.2111

Cited by 76 publications

(36 citation statements)

References 31 publications

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“…ECG changes induced by vasopressin indicated a subendocardiac ischemia (17). Vasopressin is considered to be a vasoconstrictor of the coronary artery (18). An increase in oxygen supply due to coronary vasodilatation or antispasmodic action is crucial to inhibit these ECG changes.…”

Section: Discussionmentioning

confidence: 99%

Antiischemic Properties of Fasudil in Experimental Models of Vasospastic Angina

Satoh

Ikegaki

Asano

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-We studied the antiischemic properties of fasudil, a Rho-kinase inhibitor, in conscious rabbits with coronary vasospasm induced by vasopressin and endothelin. Pretreatment with fasudil (0.3 and 3 mg/kg) attenuated the maximum elevation of the T-wave elicited by endothelin. Pretreatment with fasudil inhibited the T-wave elevation elicited by vasopressin. Fasudil and hydroxy fasudil, an active metabolite of fasudil, relaxed the endothelin-, U-46619-, 5-hydroxytryptamine-or histamine-induced contraction in swine coronary arterial strips. Fasudil and hydroxy fasudil significantly prevented the reduction in coronary flow by vasopressin in the Langendorff perfused rat heart. Fasudil was effective in protecting the heart against vasopressin and endothelin-induced myocardial ischemic change in conscious rabbits, and this beneficial effect can be attributed to its action of ameliorating the severe contraction of arteries. The inhibition of Rho-kinase may have implications for the development of novel therapeutic strategies for vasospastic angina in patients.

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Section: Discussionmentioning

confidence: 99%

Antiischemic Properties of Fasudil in Experimental Models of Vasospastic Angina

Satoh

Ikegaki

Asano

et al. 2001

Japanese Journal of Pharmacology

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“…Therefore, V1a-dependent vasoconstriction that increases afterload, ventricular stress, 25 and cardiac hypertrophy 26 may result in systemic vascular resistance and a decrease in cardiac output and contractility. 27 Several investigators have shown a V1a receptor-mediated coronary vasoconstrictor response to vasopressin, 28 which is an effect that seems to be dose dependent. The activation of V1b receptors may play an additional role.…”

Section: Clinical Researchmentioning

confidence: 99%

Copeptin Levels Associate with Cardiovascular Events in Patients with ESRD and Type 2 Diabetes Mellitus

Fenske

Wanner

Allolio

et al. 2011

Journal of the American Society of Nephrology

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In ESRD, the neurohormone arginine vasopressin (AVP) may act primarily through V1a and V1b receptors, which promote vasoconstriction, myocardial hypertrophy, and release of adrenocorticotropic hormone. The preanalytical instability of AVP limits the investigation of whether this hormone associates with cardiovascular events, but the stable glycopeptide copeptin may serve as a surrogate because it is co-secreted with AVP from the posterior pituitary. Here, we studied whether copeptin predicts cardiovascular risk and mortality in ESRD. We measured copeptin at baseline in 1241 hemodialysis patients with type 2 diabetes participating in the German Diabetes and Dialysis Study. The median copeptin level was 81 pmol/L (interquartile range, 81 to 122 pmol/L). In Cox regression analyses, compared with patients with copeptin levels in the lowest quartile (Յ51 pmol/L), patients with copeptin levels in the highest quartile (Ͼ122 pmol/L) had a 3.5-fold increased risk for stroke (HR, 3.48; 95% CI: 1.71 to 7.09), a 73% higher risk for sudden death (HR, 1.73; 95% CI: 1.01 to 2.95), a 42% higher risk for combined cardiovascular events (HR, 1.42; 95% CI: 1.06 to 1.90), and a 48% higher risk for all-cause mortality (HR, 1.48; 95% CI: 1.15 to 1.90). In contrast, we did not detect significant associations between copeptin levels and risks for myocardial infarction or death caused by congestive heart failure. In conclusion, copeptin levels strongly associate with stroke, sudden death, combined cardiovascular events, and mortality in hemodialysis patients with type 2 diabetes. Whether vasopressin receptor antagonists will improve these outcomes requires further studies. 22: 782-790, 201122: 782-790, . doi: 10.1681 Arginine vasopressin (AVP) is a key neurohormone in the human body, with numerous important physiologic activities including regulation of BP, fluid volume, and serum osmolality. AVP acts via three G protein-coupled receptors, namely the V1a (vasoconstriction and myocardial hypertrophy), the V1b (release of adrenocorticotropic hormone), and the V2 receptor (water retention in the renal collecting duct). Despite its suggested importance in the pathogenesis of cardiovascular disorders, 1,2 the evaluation of AVP secretion is difficult because of its preanalytical instability. Copeptin, a 39-amino acid glycopeptide that comprises the Cterminal part of the AVP precursor, is co-secreted with AVP from the neurohypophysis and is a stable and sensitive surrogate marker for AVP release, making it much easier to measure. 3 Dialysis patients are at a very high risk of death (about 20% per year) 4 . Thus, the identification of new risk factors with the potential of applying inter- J Am Soc Nephrol

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“…Moreover, pharmacological doses of AVP reduce cardiac output independently of the increase in coronary vascular resistance. [15]. Lastly, in isolated rat heart, when coronary perfusion is maintained constant, low concentrations of AVP enhance the myocardial contractility, whereas an opposite effect is observed at high AVP concentrations (500 pg/mL) [16].…”

Section: Discussionmentioning

confidence: 96%

Terlipressin infusion induces Tako-Tsubo syndrome in a cirrhotic man with hepato-renal syndrome

et al. 2011

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Coronary vasoconstriction induced by vasopressin. Production of myocardial ischemia in dogs by constriction of nondiseased small vessels.

Abstract: Thus, vasopressin produces myocardial ischemia by constricting small, nondiseased coronary arteries severely enough to overcome the competition from normal coronary regulation, and this ischemic event is not mediated by prostaglandin products.

Cited by 76 publications

References 31 publications

Antiischemic Properties of Fasudil in Experimental Models of Vasospastic Angina

Antiischemic Properties of Fasudil in Experimental Models of Vasospastic Angina

Copeptin Levels Associate with Cardiovascular Events in Patients with ESRD and Type 2 Diabetes Mellitus

Terlipressin infusion induces Tako-Tsubo syndrome in a cirrhotic man with hepato-renal syndrome

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