Inotropic and electrophysiological effects of histamine on human ventricular heart muscle.

1 The inotropic effects of impromidine have been studied and compared with those of histamine on human isolated left ventricular preparations stimulated at I Hz. Both drugs caused concentrationrelated increases in force of contraction and were of similar potency, although the maximum response to impromidine was markedly and significantly less than that to histamine. 2 The positive inotropic responses of impromidine were inhibited by cimetidine 1 x 10-5M, consistent with histamine H2-receptor involvement. 3 Impromidine 1 x 10-4 M inhibited maximal responses to histamine to a level equal to the maximal impromidine response; however, impromidine did not inhibit responses to isoprenaline. 4 Positive inotropic activity and inhibition ofmaximal responses to histamine occurred over a similar impromidine concentration-range. 5 Impromidine displaced histamine concentration-response curves to the right, whereas mepyramine had no effect on responses to histamine. 6 It is concluded that impromidine has positive inotropic activity on the human ventricle, that the response is mediated via histamine H2-receptors, and that impromidine is a partial agonist compared with histamine.

Section: Introductionmentioning

confidence: 61%

Impromidine is a partial histamine H₂‐receptor agonist on human ventricular myocardium

English

Gristwood²,

Owen³

et al. 1986

“…It is of interest to point out the report by Eckel, Gristwood, Nawrath, Owen & Satter (1982) who showed that the positive inotropic action of histamine on human isolated myocardium was antagonized by cimetidine alone, an indication of an H2-receptor mediated response. The concentration range for the positive inotropic action was similar to the range reported in this paper for histamine induced relaxation.…”

Section: Discussionmentioning

confidence: 99%

Effects of histamine and the histamine antagonists mepyramine and cimetidine on human coronary arteries in vitro

Godfraind

Miller

1983

1The effects of histamine have been studied on human isolated coronary artery preparations taken from hearts ranging in age from 9 to 73 years. 2 Histamine in large concentrations (100 jiM) contracted arteries which were without tone or spontaneous activity and sometimes induced rhythmic contractile activity. If spontaneous rhythmic activity was present it was enhanced by histamine. The contractile effects of histamine were inhibited by mepyramine but not by cimetidine. 3 Arteries which were contracted by depolarization responded with relaxation to histamine concentrations lower than those required to evoke a contraction; arteries from younger hearts were more sensitive than those from older hearts. 4 Mepyramine potentiated the maximal relaxant effect of histamine in arteries from hearts of all ages but cimetidine had very little effect. 5 In the presence of mepyramine, cimetidine antagonized the relaxant effect of histamine, shifting the concentration-effect curve to the right. 6 It is concluded that human coronary arteries contain both H1-and H2-type receptors, the HI-receptors mediating contraction. The relaxant effects of histamine can only be inhibited by a combination of both H1-and H2-receptor antagonists.

“…For example, the application of al-adrenoceptor agonists induces a strong positive inotropic effect in the rabbit ventricle (Schumann et al, 1974), whereas in human ventricular heart muscle it has almost no effect (Jakob et al, 1988). Conversely, histamine markedly increases the force of contraction in human ventricular heart muscle (Eckel et al, 1982) but is devoid of any effects in the cat ventricle (Flynn et al, 1979). With respect to cholinergic and purinergic effects in the heart, there is circumstantial evidence from several earlier studies that both acetylcholine (Trautwein et al, 1962;Sleator & de Gubareff, 1964;Ten Eick & Singer, 1979) and adenosine (de Gubareff & Sleator, 1965;BOhm et al, 1985;Lee & Chang, 1985;Marmo et al, 1986;Genovese & Levi, 1987) can alter cardiac function in the human heart.…”

Section: Discussionmentioning

confidence: 99%

“…The procedures for mounting specimens from human heart muscle and the techniques for measuring both force of contraction and action potential parameters have been described in detail (Eckel et al, 1982;Jakob et al, 1988).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Functional role of cholinoceptors and purinoceptors in human isolated atrial and ventricular heart muscle

Jakob¹,

Oelert²,

Rupp³

et al. 1989

The effects of cholinergic and purinergic stimulation on action potential, force of contraction and 86Rb efflux were investigated in human atrial and ventricular heart muscle. In atrial heart muscle, carbachol and (−)‐N6‐(R‐phenyl‐isopropyl)‐adenosine (R‐PIA) and 5′‐(N‐ethyl)‐carboxamido‐adenosine (NECA) evoked transient decreases of action potential duration and force of contraction; the steady‐state effects on force of contraction were virtually identical to control values. In the presence of propranolol, steady‐state values after carbachol, R‐PIA or NECA amounted to about 50% of control values. In ventricular heart muscle, carbachol, NECA and R‐PIA did not significantly affect the action potential configuration or force of contraction. Carbachol, NECA and R‐PIA induced a maintained depression of the positive inotropic response to isoprenaline in both atrial and ventricular heart muscle. The rate constant of 86Rb efflux was slightly increased by carbachol, NECA and R‐PIA in atrial (10–20%) but not in ventricular heart muscle. In the presence of isoprenaline, carbachol, NECA and R‐PIA did not significantly affect the rate constant of 86Rb efflux in both atrial and ventricular heart muscle. Isoprenaline alone increased the rate constant of 86Rb by about 25% in both tissues.