Differential activation of alpha 1- and alpha 2-adrenoceptors on microvascular smooth muscle during sympathetic nerve stimulation.

Abstract

The relative contribution of postjunctional Gi-and a2-adrenoceptors to constriction of microvessels was examined during sympathetic nerve stimulation and sympathetic escape (difference between peak and steady-state constriction). Large arterioles (120±4 ,um control diameter) and venules (174±6 ,um) and small arterioles (13+±4 ,um) were examined in rat cremaster skeletal muscle during stimulation of the cremaster efferent innervation (decentralized lumbar sympathetic chain, 0.5-16 Hz, 2-minute train). The muscle was suspended in a tissue bath, and diameter was measured with intravital microscopy. Frequency-response curves were obtained after vehicle (prazosin or rauwolscine) was added to the bath. In large arterioles, prazosin (10-7 M) significantly attenuated constriction by 60-80%; a fivefold higher concentration had no additional effect. In contrast, rauwolscine (1 to 5 x 10-7 M) had no effect. Venules evidenced minimal response to nerve stimulation. In small arterioles, rauwolscine (5 x 10-7 M) significantly attenuated constriction by 50-60%, while prazosin (10-M) had no effect. These data suggest that for large arterioles, which are known to possess both receptors, a1l-adrenoceptors are preferentially stimulated by nerve-released norepinephrine. In contrast, sympathetic constriction of small arterioles is mediated by a2-adrenoceptors. Compared with large arterioles, small arterioles exhibited greater peak and steady-state constriction at all frequencies, with maximal responses achieved over the 0.5-4 Hz range. Large arterioles exhibit graded constriction over the entire frequency range. Sympathetic escape exhibited a small, negatively correlated frequency dependence for large arterioles, tended to be greater for small arterioles, and was more evident in large arterioles during aV2-adrenoceptor constriction at low-frequency stimulation. This distinct neural control of large resistance vessels by a1-adrenoceptors and small terminal arterioles by a2-adrenoceptors may allow neurogenic regulation of these vessel segments to be differentially susceptible to modulation by other extrinsic and intrinsic vasoactive controls that preferentially interact with al-and av2-adrenergic contractile mechanisms. (Circulation Research 1991;68:232-244) V ascular smooth muscle can possess al-and a2-adrenoceptors that both mediate contraction.1-4 Whether postjunctional a1-and a2-adrenoceptors subserve distinct physiological roles is unknown. Several earlier studies of whole animals or regional vascular beds revealed preferential blockade by a2-antagonists of pressor responses to blood-borne norepinephrine (NE), whereas a1-antagonists prefer-

Neurogenic double‐peaked vasoconstriction of human gastroepiploic artery is mediated by both α1‐ and α2‐adrenoceptors

“…Similar results have been obtained in rat skeletal muscle vascular beds (Ohyanagi et al, 1991). In this study, we noticed that the a 2 -adrenoceptor-mediated component did not increase following an increase in the frequency of stimulation, showing a relatively restricted constrictor response.…”

Postexercise α-adrenergic receptor hyporesponsiveness in hypertensive rats is due to nitric oxide

“…Furthermore, in this study, we failed to investigate the role of ␣ 2 -adrenergic receptors in the control of vascular tone (12). It is well documented that sympathetic nerve stimulation produces substantial vasoconstriction in skeletal muscle via ␣ 1 -and ␣ 2 -adrenergic receptors (34,43). Similarly, both ␣ 1 -and ␣ 2 -adrenergic receptors contribute to sympathetic vasoconstriction in skeletal muscle at rest and during exercise (2).…”

Neural control of muscle blood flow during exercise

“…In resting muscles, sympathetic nerve stimulation constricts all resistance vessels. Increasing the stimulus frequency of SNA from 0.5 Hz through 16 Hz produces a full range of vasoconstriction mediated primarily through the release of norepinephrine (5,21,50,60,95). However, there is a rank order of responsiveness to SNA that varies with location in the resistance network.…”

“…When SNA is sustained (2-3 min) in resting muscle, distal arterioles have a tendency to "escape" from sympathetic vasoconstriction and exhibit a secondary relaxation (5,27,60). In contrast, vasoconstriction is sustained in proximal arterioles and feed arteries (50,95).…”