[Characteristics of alpha2-adrenoceptor mediated contractile response in isolated aortae of rats].

In order to investigate the characteristics of vascular alpha(2)-adrenoceptor (alpha(2)-AR) and its relation to alpha(1)-AR, isolated Wistar rat (10 weeks) aortae were used as a model for testing contractile function in vivo. It was found that both alpha(1) and alpha(2)-AR (mainly alpha(1)-AR) mediated the contractile response. While alpha(1)-AR enhanced the contractile response mediated by alpha(2)-AR, alpha(2)-AR had no effect on that mediated by alpha(1)-AR. When alpha(1)-AR was irreversibly blocked and the activity of alpha(2)-AR remained intact, the contractile response mediated by alpha(2)-AR was no longer observed. The contractile response only reappeared in the presence of KCl of the threshold level, and the extent of the maximum contraction decreased, compared with control (with alpha(1)-AR being intact). The results show that there exists a functional alpha(2)-AR in rat aorta, however, the contractile effect of which depends on the stimulation of alpha(1)-AR.

Differences of desensitization and hypersensitization between alpha 1A- and alpha 1B-adrenoceptors in rat isolated blood vessels.

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.

[Neuropeptide Y reduces desensitization of alpha 1-adrenoceptors in rat blood vessels].

Vasoconstrictive responses to norepinephrine (NE) in isolated rat aorta and renal artery were respectively taken to represent the biological responses mediated by alpha 1B and alpha 1A subtype adrenoceptor (AR). After blood vessels were incubated with 10 mumol/L NE for 2 h, alpha 1-AR mediated vasocontraction was desensitized significantly, alpha 1B-AR being more marked than alpha 1A-AR. In the presence of 0.5 mumol/L neuropeptide Y (NPY), desensitization of alpha 1B-AR was attenuated significantly. In rat aorta the NE-mediated contraction comprised both phasic and tonic elements. After the incubation with NE, the phasic contraction period was prolonged but magnitude decreased, while no change was found for the tonic contraction. In the presence of NPY, the changes of phasic contraction caused by NE preincubation disappeared. It is suggested that retardation and reduction of intracellular Ca2+ release were involved in the mechanism for desensitization of alpha 1B-AR.