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peptides (מקור פרסום )
Eimerl, J., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
Bayorh, M.A., Morehouse School of Medicine, Department of Pharmacology, Atlanta, GA 30310, United States
Zukowska-Grojec, Z., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
Faden, A.I., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
Ezra, D., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
Feuerstein, G., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
The effects of substance K (SK), a newly discovered tachykinin, on the cardiovascular and sympathetic system were evaluated in the pithed rat preparation and in the in situ domestic pig heart. In pithed rats, SK (10 nmol/kg, IV) produced a triphasic mean blood pressure (MAP) response: short depressor, short pressor (+11±1 mmHg), and prolonged depressor phase (-9±1 mmHg, n=9-24, p<0.001). Neither effect was significantly affected by pretreatment with propranolol (2 mg/kg) or phentolamine (1 mg/kg). The pressor response was accompanied by increased heart rate (HR): 41±4 beats/min, while lower doses produced a decrease: -8±2 beats/min (p<0.01). Propranolol abolished the increase in HR. SK inhibited the pressor response evoked by electrical stimulation of the spinal cord (SCS) and by Arg8-vasopressin (AVP). SK increased circulating levels of epinephrine and norepinephrine but did not change release of catecholamines evoked by SCS. Direct intracoronary injections of SK (0.3-100 nmol, intact pig heart) increased coronary blood flow; higher doses decreased MAP and increased HR. These results indicate that: (1) SK can produce pressor and depressor effects in the rat and is a potent coronary dilator in the pig. (2) In the pithed rat SK causes catecholamine release which mediates its cardiac accelerator effect and it antagonizes adrenergic and non-adrenergic pressor stimuli. © 1985.
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Substance K: Vascular and cardiac effects in rat and pig
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Eimerl, J., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
Bayorh, M.A., Morehouse School of Medicine, Department of Pharmacology, Atlanta, GA 30310, United States
Zukowska-Grojec, Z., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
Faden, A.I., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
Ezra, D., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
Feuerstein, G., Neurobiology Research Division, Department of Neurology Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799, United States
Substance K: Vascular and cardiac effects in rat and pig
The effects of substance K (SK), a newly discovered tachykinin, on the cardiovascular and sympathetic system were evaluated in the pithed rat preparation and in the in situ domestic pig heart. In pithed rats, SK (10 nmol/kg, IV) produced a triphasic mean blood pressure (MAP) response: short depressor, short pressor (+11±1 mmHg), and prolonged depressor phase (-9±1 mmHg, n=9-24, p<0.001). Neither effect was significantly affected by pretreatment with propranolol (2 mg/kg) or phentolamine (1 mg/kg). The pressor response was accompanied by increased heart rate (HR): 41±4 beats/min, while lower doses produced a decrease: -8±2 beats/min (p<0.01). Propranolol abolished the increase in HR. SK inhibited the pressor response evoked by electrical stimulation of the spinal cord (SCS) and by Arg8-vasopressin (AVP). SK increased circulating levels of epinephrine and norepinephrine but did not change release of catecholamines evoked by SCS. Direct intracoronary injections of SK (0.3-100 nmol, intact pig heart) increased coronary blood flow; higher doses decreased MAP and increased HR. These results indicate that: (1) SK can produce pressor and depressor effects in the rat and is a potent coronary dilator in the pig. (2) In the pithed rat SK causes catecholamine release which mediates its cardiac accelerator effect and it antagonizes adrenergic and non-adrenergic pressor stimuli. © 1985.
Scientific Publication
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