Increased total and regional vascular resistance produced by propranolol.
Propranolol when administered acutely causes little change in blood pressure and a decrease in cardiac output. Blood pressure is maintained due to increased vascular resistance. The purpose of this investigation was to determine if increased vascular resistance after propranolol occurs uniformly among various tissues and if increased resistance is due to reflex vasoconstriction. Total and regional vascular resistance were determined with the radioactive microsphere technique in dogs anesthetized with chloralose. Intravenous propranolol, 1 mg/kg, caused little change in blood pressure, cardiac rate, cardiac output and total and regional vascular resistance 30 min after administration. These changes were not different than changes after saline injection. In dogs pretreated with the alpha adrenergic receptor antagonist, dibozane, i.v. propranolol did not affect cardiac rate or blood pressure but reduced cardiac output and increased total peripheral resistance. Vascular resistance in brain, heart, lung, duodenum and skin was  increased whereas kidney, spleen and muscle vascular resistance was not significantly changed. It is concluded that increased vascular resistance produced by propranolol does not occur uniformly among tissues. Increased vascular resistance after propranolol is not due to reflex activation of alpha adrenergic receptors but may involve alterations in unidentified vasoconstrictor or vasodilator influences in certain vascular beds.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D005260:Female; D008297:Male; D009928:Organ Specificity; D010879:Piperazines / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology*; D012039:Regional Blood Flow / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects*
D010879:Piperazines; C100216:dibozane; D011433:Propranolol