? 2-adrenoceptors in rat resistance vessels

Abstract

In pithed rats increases in blood pressure were induced by i.v. injections of the alpha 1-agonist methoxamine and the alpha 2-agonists clonidine, oxymetazoline and B-HT 920. The pressor responses were further analyzed by repeated measurements of cardiac output with the thermodilution technique and by calculation of total peripheral vascular resistance. During the pressor phase both vascular resistance and cardiac output were found to be elevated. This indicates that increases in both haemodynamic variables contributed to the pressure rise. Under the assumption that elevated vascular resistance reflected constriction of arterioles and elevated cardiac output constriction of capacitance vessels via increased venous return to the heart, and considering that the magnitude of the increase of both haemodynamic parameters was similar for all three agonists, the results suggest the existence of both alpha 1- and alpha 2-adrenoceptors in resistance as well as in capacitance vessels of rats. For alpha 2-adrenoceptors in resistance vessels this conclusion was supported by the finding that the calcium antagonists verapamil and/or tiapamil virtually abolished the increases of blood pressure and vascular resistance in response to clonidine, oxymetazoline or B-HT 920, but not to methoxamine. The calcium antagonists did not affect the increases in cardiac output, irrespective of which type of alpha-agonist was administered. While the present results support the existence of alpha 2-adrenoceptors in resistance vessels of the rat, they do not allow a firm conclusion as to their occurrence in rat capacitance vessels.

Blockade by nifedipine of responses to intravenous bolus injection or infusion of α1‐and α2‐adrenoceptor agonists in the pithed rat

“…Since the best estimates of this in pithed rats of this size, obtained by three separate methods, are approximately 15 to 25 ml min-' (e.g. Gerold & Haeusler, 1983;Kaufman & Vollmer, 1985;Hiley & Thomas, 1987), this suggests that at least 75% of intravenously infused NA is lost before it reaches the arterial side of the systemic circulation.…”

Direct effects of alpha 2-adrenergic receptor stimulation on intravascular systemic capacity in the dog.

“…Evidence for the decrease in vascular capacitance found in the present study was not seen in the canine studies by Zandberg et al 18 and by Woodman and Vatner. 19 The dose of the a 2 -agonist employed in the present study was high compared with that used in either of the latter two studies but lower than that used by Eisner et al 16 Other studies have definitively demonstrated that there are postsynaptic a 2 -adrenergic receptors in arteries of several mammalian species including humans, with both a,-and a 2 -adrenergic arterial receptors. 5 ' a> M Dog and humans appear to have both a,-and a 2 -adrenergic receptors in the arterial and venous circulations. '…”

“…In the pithed rat, Gerold and Haeusler 16 have shown that the administration of three distinct cr 2 -agonists results in an increase in both systemic vascular resistance and cardiac output. The latter effect is consistent with an increase in venous return secondary to constriction of the capacitance vasculature.…”

Postjunctional α2‐adrenoceptors mediate venoconstriction in the hindquarters circulation of anaesthetized cats

“…From those studies, it appears that there are a2-adrenoceptors in the systemic venous circulation of pithed rats (Gerold & Haeusler, 1983;Kalkman et al, 1984), although it has been suggested that there are no functional 02-adrenoceptors in the systemic venous circulation of pithed cats (Kalkman et al, 1984) or spinalized, ganglion-blocked dogs (Zandberg et al, 1984). This was because neither B-HT 920 nor B-HT 933 elevated cardiac output in these preparations.…”

“…Blood pressure measurements indicate changes predominantly in resistance and cardiac function, the latter of which could be due to either intrinsic cardiac factors (e.g. heart rate, contractility) or changes in venous return (Gerold & Haeusler, 1983). However, the relative contribution of each component cannot be readily determined, although the measurement of perfusion pressure (under constant flow) will indicate changes in only resistance function.…”