Differences of desensitization and hypersensitization between alpha 1A- and alpha 1B-adrenoceptors in rat isolated blood vessels
Abstract
AIM:
To study the differences of the agonist-induced desensitization and the reserpinization-induced hypersensitization between alpha 1A- and alpha 1B-adrenoceptors (AR) mediated vasoconstriction.
METHODS:
The thoracic aortae, mesenteric, and renal arteries of rats were isolated. The cumulative-concentration response-curve (CCRC) of vasoconstriction for NE was recorded. NE activated only alpha 1-AR since the perfusing Krebs solution contained propranolol 1 mumol . L-1 and yohimbine 0.1 mumol . L-1 to block beta- and alpha 2-AR. CCRC for NE was made, preparations were pretreated with CEC 50 mumol . L-1 for then washed, and CCRC for NE was repeated. After i.p. reserpine 4 mg . g-1 i.p., the rats were killed, the thoracic aortae and renal arteries were taken, CCRC for NE was compared with the corresponding blood vessels in control rats.
RESULTS:
Pretreatment with CEC caused reductions of the NE-induced maximal constriction by 82.5 +/- 3.0% (P < 0.01) and 54.2 +/- 9.5% (P < 0.01) in thoracic aortae and mesenteric arteries, respectively, but no effect in renal arteries. Preincubation with NE caused the alpha 1-AR mediated-vasoconstriction diminished 14.4 +/- 5.9, 1.8 +/- 0.8 and 7.3 +/- 1.8 times in aortae, renal arteries, and mesenteric arteries, respectively. In reserpinized rats, the contraction in renal arteries induced by NE increased by 56%, but showed no change in aortae.
CONCLUSION:
Alpha 1B-AR mediated vasoconstriction is easier to be desensitized, while alpha 1A-AR mediated vasoconstriction is easier to be hypersensitized in rats.
Keywords:
To study the differences of the agonist-induced desensitization and the reserpinization-induced hypersensitization between alpha 1A- and alpha 1B-adrenoceptors (AR) mediated vasoconstriction.
METHODS:
The thoracic aortae, mesenteric, and renal arteries of rats were isolated. The cumulative-concentration response-curve (CCRC) of vasoconstriction for NE was recorded. NE activated only alpha 1-AR since the perfusing Krebs solution contained propranolol 1 mumol . L-1 and yohimbine 0.1 mumol . L-1 to block beta- and alpha 2-AR. CCRC for NE was made, preparations were pretreated with CEC 50 mumol . L-1 for then washed, and CCRC for NE was repeated. After i.p. reserpine 4 mg . g-1 i.p., the rats were killed, the thoracic aortae and renal arteries were taken, CCRC for NE was compared with the corresponding blood vessels in control rats.
RESULTS:
Pretreatment with CEC caused reductions of the NE-induced maximal constriction by 82.5 +/- 3.0% (P < 0.01) and 54.2 +/- 9.5% (P < 0.01) in thoracic aortae and mesenteric arteries, respectively, but no effect in renal arteries. Preincubation with NE caused the alpha 1-AR mediated-vasoconstriction diminished 14.4 +/- 5.9, 1.8 +/- 0.8 and 7.3 +/- 1.8 times in aortae, renal arteries, and mesenteric arteries, respectively. In reserpinized rats, the contraction in renal arteries induced by NE increased by 56%, but showed no change in aortae.
CONCLUSION:
Alpha 1B-AR mediated vasoconstriction is easier to be desensitized, while alpha 1A-AR mediated vasoconstriction is easier to be hypersensitized in rats.