Cardiac actions of central but not peripheral urotensin II are prevented by β-adrenoceptor blockade

S. G. Hood, A. M.D. Watson, C. N. May

Research output: Contribution to journalArticleResearchpeer-review

25 Citations (Scopus)

Abstract

Urotensin II (UII) is a highly conserved peptide that has potent cardiovascular actions following central and systemic administration. To determine whether the cardiovascular actions of UII are mediated via β-adrenoceptors, we examined the effect of intravenous (IV) propranolol on the responses to intracerebroventricular (ICV) and IV administration of UII in conscious sheep. Sheep were surgically instrumented with ICV guide tubes and flow probes or cardiac sympathetic nerve recording electrodes. ICV UII (0.2 nmol/kg over 1 h) caused prolonged increases in heart rate (HR; 33 ± 11 beats/min; P < 0.01), dF/dt (581 ± 83 L/min/s; P < 0.001) and cardiac output (2.3 ± 0.4 L/min; P < 0.001), accompanied by increases in coronary (19.8 ± 5.4 mL/min; P < 0.01), mesenteric (211 ± 50 mL/min; P < 0.05) and iliac (162 ± 31 mL/min; P < 0.001) blood flows and plasma glucose (7.0 ± 2.6 mmol/L; P < 0.05). Propranolol (30 mg bolus followed by 0.5 mg/kg/h IV) prevented the cardiac responses to ICV UII and inhibited the mesenteric vasodilatation. At 2 h after ICV UII, when HR and mean arterial pressure (MAP) were increased, cardiac sympathetic nerve activity (CSNA) was unchanged and the relation between CSNA and diastolic pressure was shifted to the right (P < 0.05). The hyperglycemia following ICV UII was abolished by ganglion blockade but not propranolol. IV UII (20 nmol/kg) caused a transient increase in HR and fall in stroke volume; these effects were not blocked by propranolol. These results demonstrate that the cardiac actions of central UII depend on β-adrenoreceptor stimulation, secondary to increased CSNA and epinephrine release, whereas the cardiac actions of systemic UII are not mediated by β-adrenoreceptors and probably depend on a direct action of UII on the heart.

Original languageEnglish
Pages (from-to)1248-1256
Number of pages9
JournalPeptides
Volume26
Issue number7
DOIs
Publication statusPublished - 1 Jul 2005
Externally publishedYes

Keywords

  • Cardiac contractility
  • Cardiac sympathetic nerve activity
  • Ganglion blockade
  • Hyperglycemia
  • Propranolol
  • Regional blood flow

Cite this

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title = "Cardiac actions of central but not peripheral urotensin II are prevented by β-adrenoceptor blockade",
abstract = "Urotensin II (UII) is a highly conserved peptide that has potent cardiovascular actions following central and systemic administration. To determine whether the cardiovascular actions of UII are mediated via β-adrenoceptors, we examined the effect of intravenous (IV) propranolol on the responses to intracerebroventricular (ICV) and IV administration of UII in conscious sheep. Sheep were surgically instrumented with ICV guide tubes and flow probes or cardiac sympathetic nerve recording electrodes. ICV UII (0.2 nmol/kg over 1 h) caused prolonged increases in heart rate (HR; 33 ± 11 beats/min; P < 0.01), dF/dt (581 ± 83 L/min/s; P < 0.001) and cardiac output (2.3 ± 0.4 L/min; P < 0.001), accompanied by increases in coronary (19.8 ± 5.4 mL/min; P < 0.01), mesenteric (211 ± 50 mL/min; P < 0.05) and iliac (162 ± 31 mL/min; P < 0.001) blood flows and plasma glucose (7.0 ± 2.6 mmol/L; P < 0.05). Propranolol (30 mg bolus followed by 0.5 mg/kg/h IV) prevented the cardiac responses to ICV UII and inhibited the mesenteric vasodilatation. At 2 h after ICV UII, when HR and mean arterial pressure (MAP) were increased, cardiac sympathetic nerve activity (CSNA) was unchanged and the relation between CSNA and diastolic pressure was shifted to the right (P < 0.05). The hyperglycemia following ICV UII was abolished by ganglion blockade but not propranolol. IV UII (20 nmol/kg) caused a transient increase in HR and fall in stroke volume; these effects were not blocked by propranolol. These results demonstrate that the cardiac actions of central UII depend on β-adrenoreceptor stimulation, secondary to increased CSNA and epinephrine release, whereas the cardiac actions of systemic UII are not mediated by β-adrenoreceptors and probably depend on a direct action of UII on the heart.",
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Cardiac actions of central but not peripheral urotensin II are prevented by β-adrenoceptor blockade. / Hood, S. G.; Watson, A. M.D.; May, C. N.

In: Peptides, Vol. 26, No. 7, 01.07.2005, p. 1248-1256.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

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N2 - Urotensin II (UII) is a highly conserved peptide that has potent cardiovascular actions following central and systemic administration. To determine whether the cardiovascular actions of UII are mediated via β-adrenoceptors, we examined the effect of intravenous (IV) propranolol on the responses to intracerebroventricular (ICV) and IV administration of UII in conscious sheep. Sheep were surgically instrumented with ICV guide tubes and flow probes or cardiac sympathetic nerve recording electrodes. ICV UII (0.2 nmol/kg over 1 h) caused prolonged increases in heart rate (HR; 33 ± 11 beats/min; P < 0.01), dF/dt (581 ± 83 L/min/s; P < 0.001) and cardiac output (2.3 ± 0.4 L/min; P < 0.001), accompanied by increases in coronary (19.8 ± 5.4 mL/min; P < 0.01), mesenteric (211 ± 50 mL/min; P < 0.05) and iliac (162 ± 31 mL/min; P < 0.001) blood flows and plasma glucose (7.0 ± 2.6 mmol/L; P < 0.05). Propranolol (30 mg bolus followed by 0.5 mg/kg/h IV) prevented the cardiac responses to ICV UII and inhibited the mesenteric vasodilatation. At 2 h after ICV UII, when HR and mean arterial pressure (MAP) were increased, cardiac sympathetic nerve activity (CSNA) was unchanged and the relation between CSNA and diastolic pressure was shifted to the right (P < 0.05). The hyperglycemia following ICV UII was abolished by ganglion blockade but not propranolol. IV UII (20 nmol/kg) caused a transient increase in HR and fall in stroke volume; these effects were not blocked by propranolol. These results demonstrate that the cardiac actions of central UII depend on β-adrenoreceptor stimulation, secondary to increased CSNA and epinephrine release, whereas the cardiac actions of systemic UII are not mediated by β-adrenoreceptors and probably depend on a direct action of UII on the heart.

AB - Urotensin II (UII) is a highly conserved peptide that has potent cardiovascular actions following central and systemic administration. To determine whether the cardiovascular actions of UII are mediated via β-adrenoceptors, we examined the effect of intravenous (IV) propranolol on the responses to intracerebroventricular (ICV) and IV administration of UII in conscious sheep. Sheep were surgically instrumented with ICV guide tubes and flow probes or cardiac sympathetic nerve recording electrodes. ICV UII (0.2 nmol/kg over 1 h) caused prolonged increases in heart rate (HR; 33 ± 11 beats/min; P < 0.01), dF/dt (581 ± 83 L/min/s; P < 0.001) and cardiac output (2.3 ± 0.4 L/min; P < 0.001), accompanied by increases in coronary (19.8 ± 5.4 mL/min; P < 0.01), mesenteric (211 ± 50 mL/min; P < 0.05) and iliac (162 ± 31 mL/min; P < 0.001) blood flows and plasma glucose (7.0 ± 2.6 mmol/L; P < 0.05). Propranolol (30 mg bolus followed by 0.5 mg/kg/h IV) prevented the cardiac responses to ICV UII and inhibited the mesenteric vasodilatation. At 2 h after ICV UII, when HR and mean arterial pressure (MAP) were increased, cardiac sympathetic nerve activity (CSNA) was unchanged and the relation between CSNA and diastolic pressure was shifted to the right (P < 0.05). The hyperglycemia following ICV UII was abolished by ganglion blockade but not propranolol. IV UII (20 nmol/kg) caused a transient increase in HR and fall in stroke volume; these effects were not blocked by propranolol. These results demonstrate that the cardiac actions of central UII depend on β-adrenoreceptor stimulation, secondary to increased CSNA and epinephrine release, whereas the cardiac actions of systemic UII are not mediated by β-adrenoreceptors and probably depend on a direct action of UII on the heart.

KW - Cardiac contractility

KW - Cardiac sympathetic nerve activity

KW - Ganglion blockade

KW - Hyperglycemia

KW - Propranolol

KW - Regional blood flow

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SP - 1248

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