Steroid potentiation of responses to sympathomimetic amines in aortic strips

Abstract

Hydrocortisone potentiates responses to adrenaline and noradrenaline in aortic strips by inhibiting their inactivation by catechol-O-methyl transferase (Kalsner, 1969). It was of interest to determine whether other steroid hormones also enhance responses to catecholamines and decrease their rate of inactivation by 0-methylation. In the present study the effects of 17f-oestradiol, progesterone and desoxycorticosterone on responses to a variety of sympathomimetic amines were investigated. MethodsRabbit aortic strips, prepared according to Furchgott (1960), were suspended under 2 g tension in 15 ml. chamibers containing Krebs-Henseleit (Krebs) solution

Effect of steroids on β‐adrenoceptor‐mediated relaxation of pig bronchus

“…This is to be expected given that Iso is the preferred substrate for both extraneuronal uptake and for COMT (Gillespie, 1973;Guldberg & Marsden, 1975;Trendelenburg, 1980). Kalsner (1969) suggested that cortisol-induced potentiation of vascular responses to catecholamines may be due to inhibition of COMT or extraneuronal uptake. This steroid was shown to inhibit both COMT and uptake in cat heart (Cornish & Goldie, 1980).…”

“…17,B-Oestradiol, progesterone, testosterone, corticosterone, deoxycorticosterone and cortisol-HS are potent inhibitors of extraneuronal catecholamine uptake (Kalsner, 1969;Salt, 1972;Cornish etal., 1978) Of these steroids, only 17p-oestradiol is known also to inhibit the neuronal uptake of catecholamines (Iversen & Salt, 1970;Salt, 1972;Cornish et al, 1978). Normetanephrine (4-22 ElM) is known to inhibit selectively extraneuronal uptake by approximately 50% (Burgen & Iversen, 1965;Mireyless & Foster, 1973;Major, Sauerwein & Graefe, 1978).…”

“…The underlying mechanism of steroid-induced potentiation of catecholamine responses has been attributed variously to adrenoceptor sensitization (Besse & Bass, 1966;Yard & Kadowitz, 1972;Brine, Cornish & Miller, 1979), inhibition of catecholamine uptake (Kaumann, 1972;Pun et al, 1973;Goldie, 1976) and inhibition of catechol-0-methyl transferase (COMT) (Kalsner, 1969;Cornish & Goldie, 1980). Indeed, each of these mechanisms may be involved depending upon the tissue, species and steroid used.…”

“…Various steroids potentiate the actions of catecholamines both in vivo (Fritz & Levine, 1951;Schmid, Eckstein & Abboud, 1967;Pun, McCulloch & Rand, 1973;Shenfield, Hodson, Clarke & Paterson, 1975;Goldie, 1980) and in vitro (Kalsner, 1969;Kaumann, 1972;Goldie, 1976;Cornish, Goldie & Miller, 1978;Hackney & Szentivanyi, 1980). The underlying mechanism of steroid-induced potentiation of catecholamine responses has been attributed variously to adrenoceptor sensitization (Besse & Bass, 1966;Yard & Kadowitz, 1972;Brine, Cornish & Miller, 1979), inhibition of catecholamine uptake (Kaumann, 1972;Pun et al, 1973;Goldie, 1976) and inhibition of catechol-0-methyl transferase (COMT) (Kalsner, 1969;Cornish & Goldie, 1980).…”

On the Mechanism of Pancuronium‐induced Super‐sensitivityto Noradrenaline in Rat Smooth Muscle

“…Quintana (1977) suggested that the steroidal structure of pancuronium might confer some of the properties exhibited by the corticosteroids and some of their derivatives. These drugs promote an acute NA supersensitivity in cardiac and arterial smooth muscle, 17 ,B-oestradiol being the most potent (see, for instance Kalsner, 1969;Iversen & Salt, 1970). However, it is interesting that the response of the rat vas deferens to corticosteroids is atypical; 17 P-oestradiol is a potent non-competitive antagonist of NA on this preparation (Tomlinson unpublished).…”