The contribution of postjunctional α1 and α2- adrenoceptors and P2-purinoceptors to the neuroeffector response was examined in isolated segments of human subcutaneous resistance arteries. Electrical field stimulation (EFS, 20 V, 0.2 ms, 1-25 Hz) elicited a maximum contractile response which was 38.2 ± 1.6% of that elicited by exogenously applied (5 µM)noradrenaline (n = 56). Tetrodotoxin (1 µM), used to inhibit neurotransmission, reduced the electrically evoked response to 24.7 ± 4.4% (n = 10) of the control response. The α1-adrenoceptor antagonist prazosin (1 µM)reduced the maximum EFS contractile response to 64.8 ± 5.5% of the control response (n = 17). Application of the α2-adrenoceptor antagonist yohimbine (0.1 µM)reduced the maximum EFS response to 68.2 ± 8.2 % of the control response (n = 9). In the presence of prazosin plus yohimbine at the above-mentioned concentrations the maximum response to EFS was reduced to 47.6 ± 6.7 % (n = 11). Responses following α-blockade were not statistically different from those in the presence of tetrodotoxin, but the mean responses indicate that a non-adrenergic component to the EFS response cannot be discounted. Desensitisation of P2-purinoceptors with αβ-methylene ATP had no effect on responses to EFS; therefore under the conditions studied these receptors do not appear to be involved in neurotransmission. These results confirm the presence of postjunctional α1-and α2-adrenoceptors in human resistance arteries and for the first time demonstrate that the postjunctional α2-adrenoceptor is important in modulating vascular responses elicited by intramural sympathetic nerve fibres.
1. Chemical renal medullectomy was performed in Wistar rats by intraperitoneal injection of 2-bromoethylamine hydrobromide (200 mg/kg body weight). The effect of this treatment upon blood pressure and mesenteric vascular reactivity and morphology was studied 3 weeks after treatment. 2. Blood pressure was significantly raised in medullectomized rats. The indirect systolic pressures (means +/- SEM) were 112 +/- 2.4 mmHg (14.9 +/- 0.32 kPa) and 123 +/- 3.5 mmHg (16.4 +/- 0.5 kPa) (P less than 0.02) for control (n = 12) and medullectomized (n = 12) rats, respectively. However, there were no significant changes in the morphology of the mesenteric resistance vessels. 3. Maximum pressor responses and Ca2+ sensitivities were unchanged in these vessels compared with controls, but the sensitivity to noradrenaline was significantly reduced. Noradrenaline pD2 (= -log ED50) values (means +/- SEM) were 5.87 +/- 0.03 and 5.69 +/- 0.08 (P less than 0.05) for control (n = 12) and medullectomized (n = 12) rats, respectively. 4. This study demonstrates that in this model of hypertension the noradrenaline sensitivity is reduced in mesenteric resistance vessels, but there are no detectable morphological changes associated with the rise in blood pressure.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.