Vascular α2-adrenoceptors can mediate nerve stimulation-evoked contractions

1985 ◽  
Vol 68 (s10) ◽  
pp. 117s-120s ◽  
Author(s):  
James R. Docherty ◽  
Lisa Hyland

1. It is now established that α2-adrenoceptors can be present on vascular smooth muscle as targets for exogenous agonists, but some controversy exists as to whether these vascular α2-receptors may also be the target for neurally released noradrenaline. 2. In human saphenous vein we have found evidence that the α2-antagonist yohimbine in low concentrations (0.01 μmol/l) can significantly inhibit stimulation-evoked contractions, whereas the α1-antagonist prazosin is more than ten times less potent. 3. It is concluded that, at least in some tissues, neuro-effector transmission can be mediated by vascular α2-adrenoceptors.

2011 ◽  
Vol 15 (8) ◽  
pp. 1695-1702 ◽  
Author(s):  
Guanghong Jia ◽  
Anshu Aggarwal ◽  
Amanuel Yohannes ◽  
Deepak M. Gangahar ◽  
Devendra K. Agrawal

1989 ◽  
Vol 256 (3) ◽  
pp. H607-H612
Author(s):  
M. P. Owen ◽  
M. C. Taphorn ◽  
J. G. Walmsley

A comparative study of the adrenergic control of two sequential rabbit intrarenal arteries of differing diameter [intrarenal branch artery (IRBA)-unstretched lumen diameter (ULD) approximately 300 microns and interlobar artery (ILA)-ULD approximately 250 microns] has been conducted. The neurogenic contractile response of isolated segments in relation to the maximum response to l-norepinephrine (NE) was minimal (8 Hz response approximately 30% of maximum contraction) and similar in both types of arteries. Phentolamine (PTA) (10(-6) M) blocked neurally evoked contractions of the IRBAs at 2, 4, and 8 Hz and of the ILAs at 2 and 4 Hz. (8 Hz responses were not entirely blocked in 3 out of 8 ILAs.) The sensitivity to exogenous NE decreased with a decrease in intrarenal vessel diameter, whereas the maximum active smooth muscle cell stress to NE was greater than 3 X 10(5) N/m2 for each vessel. All arterial segments constricted in response to histamine (H) and NE with equal maximal effects; however, sensitivity to H was greater in the smaller artery (ILA). The comparative contractile responses to nerve stimulation and exogenous NE in sequential renal arteries contrasts to the pattern of these responses in sequential arteries in any other rabbit regional bed previously studied (pulmonary and ear vasculature).


1990 ◽  
Vol 68 (10) ◽  
pp. 1346-1350 ◽  
Author(s):  
Yong-Yuan Guan ◽  
Chiu-Yin Kwan ◽  
Edwin E. Daniel

The relationship between the postsynaptic α1-adrenoceptor reserve and the sensitivity of vasoconstriction induced by α-adrenoceptor agonists to the dihydropyridine Ca2+ entry blocker nifedipine was investigated in isolated muscle strips of dog mesenteric artery (DMA) and saphenous vein (DSV). The amplitudes of the contractile responses of DMA induced by phenylephrine were the same as those in DSV in the presence and in the absence of extracellular Ca2+. The use of 3 × 10−9 M phenoxybenzamine to irreversibly block the α1-adrenoceptors revealed a marked difference in the size of the α1-adrenoceptor reserve between DMA (40%) and DSV (7%). In spite of a larger receptor reserve, the contractile responses induced by phenylephrine in DMA were more sensitive to nifedipine compared with those in DSV. These results suggest that the postsynaptic α1-adrenoceptor reserve in vascular smooth muscle, at least in DMA and DSV, does not play an important role in buffering the inhibitory effect of nifedipine on the contractile response to a full agonist of α1-adrenoceptors. Other factors, such as the difference in the membrane depolarizing effect, the ability to utilize intracellular Ca2+ for contraction, and the possible existence of α1-adrenoceptor subtypes, may contribute to the different inhibitory effects of nifedipine on these blood vessels.Key words: adrenoceptors, nifedipine, smooth muscle, calcium, saphenous vein, mesenteric artery.


1995 ◽  
Vol 29 (1) ◽  
pp. 15-21 ◽  
Author(s):  
Kelvin G. M. Brockbank ◽  
Mark G. Davies ◽  
Shirley M. Fields ◽  
Per-Otto Hagen

Sign in / Sign up

Export Citation Format

Share Document